2011 Public Comments on the National Plan for Alzheimer's Disease and the National Alzheimer's Project Act

07/01/2015

Table of Contents

DECEMBER 2011 COMMENTS

NOVEMBER 2011 COMMENTS

OCTOBER 2011 COMMENTS

SEPTEMBER 2011 COMMENTS

AUGUST 2011 COMMENTS

JUNE 2011 COMMENTS


DECEMBER 2011 COMMENTS

DATE:  December 30, 2011

SUBJECT:  info for Advisory Council-December

I am hopeful that you will see that the attachment is included in the summary of input for the month of December 2011. I look forward to attending the January meeting of the NAPA Advisory Council.

Thank you,

Mary Hogan

ATTACHMENT:

My name is Mary Hogan. I am one of 8 older siblings of the late Bill Hogan. I submit this request to you today, December 30, 2011, in honor of my brother and hopefully for other families who are facing the challenges related to Down syndrome and Alzheimer's disease.

In January 2006, at the age of 45, Bill was diagnosed with dementia, Alzheimer's type. Over the course of the next 4 years his journey became far more complex. He experienced a very rapid deterioration during the last 13 months of his life and died of chronic aspiration pneumonia on February 25, 2010, two months shy of his 50th birthday. My brother was a member of a subgroup of individuals with Down syndrome that develop AD early, decline rapidly and face a premature death. This has been a great loss for our family and Bill's community at large.

Extraordinary efforts to advocate for Bill were required during the final years of his life. Active advocacy was sometimes lonely and often a frustrating process. Obstacles for advocacy increased significantly after Bill's diagnosis of Alzheimer's disease. Our experience is most likely replicated in other families as well.

I write to you today to request the following considerations for the National Alzheimer Project Act Advisory Council on Alzheimer's Research, Care and Services:

  1. People with Intellectual Disabilities, and their caregivers, should be included in future planning with the same access to appropriate care and support as individuals in the general population. The growing incidence of Alzheimer's disease will be mirrored in the ID population, most especially with individuals with DS who have a far greater likelihood of developing this insidious disease by age 60. Inclusion in any future planning will be ensure that this often marginalized group will have access to appropriate care across their lifetime.
  2. Most often individuals with ID, including those with DS, are cared for by their families well into their adult lives, often by aging family members. Recognition of the need to enhance support for this group of caregivers will be critical in the future. I ask that NAPA Advisory Council recognize the need for improved dementia care for individuals with intellectual disabilities in conjunction with increased support for family members as caregivers and advocates.
  3. Since individuals with Down syndrome are at increased risk for developing Alzheimer's disease, families, caregivers, agencies, medical providers and researchers will need to work together to maintain their "quality of life". Families facing DS/AD need access to information about both disease process and advocacy. I suggest a review of what has been produced by Alzheimer's Australia and the Australian government as a sample of what might be provided.
  4. A consortium of providers (i.e. Alzheimer's Association, Health and Human Services, the Administration on Developmental Disabilities or Administration on Aging, UCEDD, families, and advocacy organizations, etc.) should disseminate best practice guidelines related to adults with intellectual disabilities and dementia. This will include training and education for care providers across a multitude of settings. I suggest careful consideration of the forthcoming document produced by the National Task Group on Intellectual Disabilities and Dementia Practices.

I am hopeful that in this day of limited funding the needs of all people with Alzheimer's disease will be addressed creatively and with the greatest of compassion and that the National Alzheimer Project Act Advisory Council will provide leadership and direction for the future.

I thank you for the considering this request.

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DATE:  December 30, 2011

SUBJECT:  Input on the National Plan for Alzheimer's Disease

Attached are the CAMD suggestions for consideration for the National Plan for Alzheimer's Disease.

Neil, it was nice to see you at NINDS' recent Parkinson's meeting, and hope your recovery continues expeditiously.

Best of the New Year to you both!

Lynn D. Hudson, Ph.D.
Director, Coalition Against Major Diseases (CAMD)
Chief Science Officer, Critical Path Institute
Tucson, AZ
http://www.c-path.org

ATTACHMENT: 

Presently there are no approved treatment to slow the progression of Alzheimer's disease (AD) or cure this devastating disease. Filling the AD drug pipeline will require facilitating translation of basic research discoveries and increasing collaboration with the FDA and international regulatory agencies. The Critical Path Institute, working in a public-private partnership with the FDA, created the Coalition Against Major Diseases (CAMD) to identify improved methods and tools that accelerate drug development in neurodegenerative conditions such as Alzheimer's disease. NIA contributes to the consensus science for AD drug development tools in CAMD, as do our 16 member companies and other key stakeholders.

The goal of improving the drug development process for Alzheimer's disease can be addressed by incorporating the following actions into the National Plan for Alzheimer's Disease:

  1. Widespread adoption and use of the AD data standards developed by the Clinical Data Interchange Standards Consortium (CDISC) to facilitate data sharing. These CDISC AD data standards should be used in all new and ongoing federally-funded and industry-sponsored AD clinical trials. While the FDA currently encourages sponsors to use CDISC standards when submitting data, the ability for the FDA to require such standards in applications should be considered. The AD data standards should be frequently updated and expanded to cover any new measures.
  2. Construction of a comprehensive AD clinical natural history database that could be mined by qualified investigators. This database should contain both control and active intervention arms of clinical trials and include trials of failed drugs. For optimal data mining, the data should be deposited in CDISC format with legacy data remapped to the AD data standards. Such a database, whether constructed by a foundation or a public-private partnership, would need to address privacy and informed consent concerns as well as liability issues. Moreover, a mechanism to protect proprietary, confidential data would need to be built in. Incentives for pharmaceutical companies to submit deidentified and appropriately coded treatment arm data include immediate access to a rick source of pooled data. Data mining of the AD clinical database should provide information on which biomarkers accurately track disease progression and response or non-response to treatment. This aggregated mega-database should also offer valuable insights for repurposing drugs.
  3. Regulatory qualification of biomarkers that can be applied to testing new AD drugs. Progress in developing AD drugs has been hampered by the lack of biomarkers qualified by regulatory agencies for testing efficacy, particularly in the earliest stages of the disease. While AD researchers have identified some tantalizing candidates, providing the level of evidence needed for FDA qualification typically requires additional evidence and analysis. Such efforts are beyond the scope and resources of individual companies or academic researchers, and are best carried out through a public-private partnership/consortium model (e.g. ADNI, CAMD).
  4. Development of analytic standards and reliable methods for measuring AD biomarkers. The lack of standardization for imaging modalities and/or assays of CSF analytes can prevent the FDA from accepting a biomarker for use in AD clinical trials. Standardization of analytic methods, together with establishing a resource of appropriate reference samples, should be a national priority.
  5. Development of quantitative disease progression models to inform the design of AD clinical trials and evaluate new medicines. Mathematical models offer ways to differentiate between symptomatic and disease-modifying drug effects, determine the optimal sample sizes and sampling times, identify subpopulations with unique characteristics, assess the impact of baseline disease severity on drug response, and more. In short, models can prevent a good drug from failing, and keep bad drugs off the market. Modeling and simulation tools can be built using the clinical data of a large AD database, such as the one constructed by CAMD that contains ~ 6000 AD patients enrolled in the control arm of clinical trials. Even larger databases with cognitively normal controls and patients at the earliest stages of the disease, along with richer sources of biomarker information on these patients, should be constructed to facilitate the decision-making process in prevention trials as well as AD clinical trials. These quantitative disease models need to be evaluated by the FDA and accepted as "fit for use" so that the pharmaceutical companies can better design AD clinical trials.

Each of these drug development tools fall within the "precompetitive space", where the knowledge gained and time saved can benefit individual company efforts to bring new drugs to the market. The National Plan for Alzheimer's Disease would benefit by incorporating these action items to spur the development of safe and effective medicines for the prevention and treatment of Alzheimer's disease.

Thank you for the opportunity to provide input on the National Plan for Alzheimer's Disease.

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DATE:  December 21, 2011

SUBJECT:  comments for NAPA Advisory Council

Please advise about the status of on-going comments. Can I assume that you continue to take comments each month and that they are sent to advisory council for review?

Mary Hogan

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DATE:  December 8, 2011

SUBJECT:  NCCDP

We would be interested in being on the Advisory Council for Alzheimer's research Care and Services. Is this possible?

NCCDP ALZHEIMER'S DEMENTIA STAFF EDUCATION WEEKFEBRUARY 14TH TO 21ST.Register at the top right of home page and begin downloading Now to March 1st. Free staff in-services includes power point, hand outs, staff pre and post tests. The tool kit includes, Proclamation, Alzheimer's Bill of Rights and Alzheimer's Pledge and so much more. Fantastic in-service on Sexuality and Intimacy and Dementia. See http://www.nccdp.org

Sandra Stimson, CALA, ADC, CDP, CDCMExecutive Director National Council of Certified Dementia Practitionershttp://www.nccdp.org

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DATE:  December 5, 2011

SUBJECT:  January NAPA Advisory Council meeting

My name is Mary Hogan and I am interested in attending the January 2012 NAPA Advisory Council meeting. I am wondering if this is possible.

I was a guardian/caregiver for my 49 year old brother who had down syndrome and died of complications of Alz. disease. I have a vested interest in the Council activities and national plan and have worked with Matt Janicki on the National Task Group on Intellectual Disabilities and Dementia Practices. Please see the attached article and you will understand my commitment to this important cause.

Hopefully I will have an opportunity to be present for this important meeting.

Thank you for your consideration.

Mary Hogan

ATTACHMENT:   Down Syndrome newsletter.pdf

Available as separate links:
Down Syndrome News, Vol. 34, 2011, #2 Down Syndrome News: Remembering Bill

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NOVEMBER 2011 COMMENTS

DATE:  November 29, 2011

SUBJECT:  FW: Bipartisan letter to Sec. Sebelius regarding Draft National Alzheimer's Plan

I have attached a letter from Rep. Markey and Rep. Smith, Co-chairs of the Alzheimer's Taskforce and House authors of the National Alzheimer's Project Act (NAPA), with their recommendations for the National Alzheimer's Plan.

Please forward this letter to any any all staff working on NAPA, both at HHS and elsewhere.

We thank you for all of the work you are doing to implement the law and are excited to see the draft plan soon!

Thank you,

MaryAlice Parks

Legislative Correspondent and New Media Specialist

Office of Rep. Ed Markey (MA -07)

Washington, DC

ATTACHMENT:  

As the Co-founders and Co-chairs of the Bipartisan Congressional Taskforce on Alzheimer's Disease and House authors of the National Alzheimer's Project Act (NAPA), we are writing to urge the Department of Health and Human Services (HHS) to continue its swift and efficient implementation of the Act. NAPA is intended to be transformative, creating a groundbreaking, far-reaching, and thoughtful National Alzheimer's Plan to improve care for Alzheimer's patients across the country and ultimately cure this disease.

We applaud the ongoing work of the Nation Alzheimer's Project Act's Advisory Council and federal agency working groups. We are pleased to hear that a draft National Alzheimer's Plan required by the law will be read by early next year. As you know, several of the largest Alzheimer's advocacy, care, and research organizations have submitted ideas and priorities for the National Alzheimer's Plan.1 We hope that the agencies working to develop the draft plan will strongly consider these various proposals.

We provide below our recommendations for your consideration as you prepare the National Alzheimer's Plan:

1. Increase medical research funding and coordination

As millions of baby-boomers age and retire, Alzheimer's is becoming a national pandemic, threatening to undermine our Medicare and Medicaid systems. Today the federal government spends $93 billion out of Medicare to care for Alzheimer's patients -- almost one out of every five Medicare dollars (18%) each year. This money pays for hospitalizations, doctor visits, and drugs associated with the disease. An additional $37 billion comes out of the Medicaid budget every year -- more than one out every 10 Medicaid dollars (11%). Taken together, that's $130 billion every year from Medicare and Medicaid that is spent on this one disease alone.

In addition, nearly 15 million caregivers provide approximately 17 billion hours of unpaid care to family members and friends with Alzheimer's, which represents a large drain on the time and the resources of families and employers. Now more than ever, we need to accelerate research breakthroughs in the causes, treatments and prevention of this disease and reduce the emotional and financial burden of Alzheimer's on families and federally-funded programs.

Basic research is our best hope for understanding the fundamentals of this disease and finding a cure. Currently, Alzheimer's research is underfunded across the federal government, academia and the private sector. According to data from HHS, Alzheimer's disease receives a franction of the research funding at the National Institutes of Health (NIH) compared to other diseases. Today, the NIH spends about $6 billion a year on cancer research and $3 billion a year on AIDS research. Alzheimer's has five times as many victims as AIDS, yet receives only $469 million in research funding a year -- less than 1/6 the amount spent on AIDS research.

Deaths from AIDS, cancer, and heart disease have fallen in the last decade. As a nation, we should learn from our past successes. Prioritizing and funding medical research has lead to breakthroughs and treatments and ultimately saved lives. In the same way, we must expand funding for basic medical research for Alzheimer's disease, which continues to have a dramatically increasing number of patients every year across the country.2

It is also our hope that in drafting the National Alzheimer's Plan, HHS will also explore ways to better coordinate research and grants dollars within the centers and institutes of the NIH. Currently, over a dozen institutes at the NIH support or conduct Alzheimer's related research. Perhaps there is a need for an institute focused solely on the disease or a way to enhance data sharing amongst researchers. Whatever the solutions, the National Alzheimer's Plan should include concrete ideas to guarantee that all money, given through grants or used internally, is spent effectively and in coordination with other research projects in support of a larger research agenda.

In addition, we urge HHS to consider innovative projects to facilitate research and therapy development across public and private sectors. For instance, HHS should consider the feasibility of increasing accessibility to lumbar punctures for patients in order to develop national databases and registries for at risk patients. Cerebral spinal fluid tests are proven to identify those at high risk of Alzheimer's disease.3 Increasing access to this screening technique would help facilitate entries into clinical trials, and, once therapies have been developed, identify those who should receive such therapies.

2. Incent private sector research and development

Biopharmaceutical companies have approximately 21,000 ongoing clinical drug trials in the U.S., yet only 100 of them are focused on Alzheimer's disease. It is our hope that new incentives for pharmaceutical companies to invest in research and therapy development, including the development of new drugs, devices, biological products, biomarkers, or diagnostic tools, are included in the National Alzheimer's Plan.

Federal agencies have adopted methods in the past for encouraging research and therapy development under adverse conditions, including: extended market exclusively for demonstrably effective treatments, priority review or fast-tracking by the Food and Drug Administration for treatments in the pipeline, review of guidelines regarding clinical trials, and patent life reform. It is our hope that the benefits and consequences of all methods are thoughtfully examined and considered in this case.

In addition, we urge HHS to consider ways to increase public-private partnerships for research and therapy development including possible strategic investments in start-up or growth companies engaged in advanced research and novel therapeutics, especially those companies willing to match funds from HHS.

3. Expand public awareness efforts

The National Alzheimer's Plan should call on relevant government agencies to work with local and state governments to develop public awareness campaigns around Alzheimer's disease, in the way HHS and the Centers of Disease Control have spearheaded public awareness campaigns in the past. It is our hope that the campaigns would focus on: the symptoms of Alzheimer's disease, the importance of diagnosis, how to access clinical trials, and the availability of resources and services for patients, families and caregivers.

4. Provide reimbursement for comprehensive diagnosis

Reports estimate that as few as 19 percent of people with Alzheimer's disease have a documented diagnosis of their condition in their primary care medical record.4 African-American and Hispanic populations are even less likely to be diagnosed than whites despite being at higher risks for Alzheimer's disease.

Medicare currently covers diagnostic evaluations and some imaging tests. However, if the signs of dementia have not been detected in the first place, a diagnostic evaluation is not conducted. Furthermore, after a diagnosis has been made, time constraints and lack of reimbursement often preclude a necessary discussion with the newly diagnosed patients and their caregivers regarding the diagnosis, treatment options, and support services available. As a result, many people with dementia and their families are not effectively connected to resources to help them manage the condition and avoid crises.

With an early diagnosis, patients and families can prepare for the oncoming symptoms of the disease. Facilitating conversations between doctors and caregivers and providing resources for patients' families can help mitigate the number of hospitalizations and complications for patients and ultimately bring down Medicare costs.

H.R. 1386, the Health Outcomes Planning and Evaluation Act (HOPE) for Alzheimer's, which we co-authored, proposes that the Centers for Medicare And Medicaid Services develop a new Medicare reimbursement code for a comprehensive diagnosis of Alzheimer's disease to help drive best practices among doctors. This includes reimbursement of the following: screening of dementia, diagnostic evaluation, discussion with doctor and caregiver, and medical record documentation.

5. Expand outcome-oriented care programs and dementia training for healthcare professionals

Models such as Independence at Home (IAH) and Resources for Enhancing Caregiver Health (REACH) have proven to improve the quality of care for patients and reduce health care costs by keeping patients in the comfort of their own homes longer and coordinating care services. IAH, currently a demonstration project slated to begin January 2012, creates a team of doctors, nurses, social workers, pharmacists, physical therapists and others to provide proactive care in the home for seniors with multiple chronic conditions like Alzheimer's, Parkinson's, and congestive heart failure. As you know, there are more than 57 million Amerians living with multiple chronic illnesses in our country. These patients typically have numerous prescriptions written by an array of doctors, and struggle to visit their physicians when they need care. IAH aims to end the current disjointed approach of caring for these patients. Such successful programs that reduce costs and improve health care outcomes should be considered in the National Alzheimer's Plan and enacted across the country to support caregivers and increase access to quality care for all patients.5

In addition, it is our hope that the National Alzheimer's Plan will call on federal agencies to work with state and local governments to increase Alzheimer's and dementia training for health care professionals, social workers, employees of long-term care facilities and law enforcement. Increased training and education could dramatically improve the treatment of Alzheimer's patients and help avoid unnecessary costs and harm as the result of wrongful diagnosis and mistreatment.

6. Encourage State Plans

30 states currently have or are in the process of developing plans for supporting Alzheimer's patients.6 The Massachusetts Executive Office of Elder Affairs, for example, established a committee of experts to evaluate services and resources available to Alzheimer's patients and their caregivers and develop a strategy for improving care. Their initial reports focused on the need to diagnose patients early, connect patients and their families to available resources, and facilitate at-home care.

The challenges associated with Alzheimer's disease are too varied and far-reaching for the federal government to tackle alone. From improving transportation services for patients in rural neighborhoods to assisting in the creation of new adult daycare centers, state and local governments are well positioned to improve the day-to-day care of Alzheimer's patients. In order to fully support the millions of Americans with Alzheimer's disease and their families struggling to care for them, we need local and state governments involved in developing appropriate service models.

For these reasons, we hope the National Alzheimer's Plan will encourage states to assess the services they currently provide and develop plans for caring for the growing number of patients in the future. In addition, the National Alzheimer's Plan should look for ways the federal government can support or reward state efforts to improve and coordinate care, especially if states develop innovative solutions with measurable cost-savings or improvements in care.

Caring for the aging baby-boomers will be one of the greatest tests of our society. Today, over 5 millions Americans and their families are struggling with Alzheimer's disease. Unless we find a way to prevent, slow, or cure this disease, in less than one generation those struggles will nearly triple, as millions more Americans face the prospect of an Alzheimer's diagnosis. We must change our current trajectory. NAPA was intended to outline innovative and large-scale strategies for improving care for our senior citizens, to which we owe so much, and ultimately find a cure for this devastating disease. We encourage HHS and its partnering federal agencies to continue their diligent, timely, and thoughtful work to implement NAPA and draft this historic National Alzheimer's Plan.

Sincerely,

Edward J. Markey
U.S. Representative

Chris Smith
U.S. Representative

NOTES

  1. See: Leaders Engaged in Alzheimer's Disease (LEAD). A Path Forward http://c3320830.r30.cf0.rackcdn.com/LEAD-ThePathAhead-2011-11-01.pdf; Alzheimer's Association, Alzheimer's from the Frontlines http://www.alz.org/document_custom/napareport.pdf; Alzheimer's Association, No Time to Waste http://www.alzfdn.org/documents/No%20Time%20to%20Waste%20Report-10-11.pdf.
  2. See: http://report.nih.gov/rcdc/categories/ and LEAD, A Path Forware: 10.
  3. Richard J. Perrin, Anne M. Fagan, and David M. Holtzman, "Multimodal techniques for diagnosis and prognosis of Alzheimer's disease," Nature 461:15 (Oct. 2009).
  4. "Implementing a screening and diagnosis program for dementia in primary care," General Internal Medicine (2005) http://www.ncbi.nlm.nih.gov/pubmed/16050849.
  5. R. Meyer, "Consider Medical Care at Home," Geriatrics (June 2009); S. Okie, "Home Delivery: Bringing Primary Care into the Household," New England Journal of Medicine (Dec. 2008).
  6. See: http://www.alz.org/join_the_cause_state_plans.asp.

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DATE:  November 22, 2011

SUBJECT:  Written Comments from SWHR

Please find the attached comments from the Society for Women's Health Research (SWHR). If you have any questions or have problems opening the document, please let me know.

Sincerely,

Leslie Stevens, MA

Senior Government Relations Associate

Society for Women's Health Research (SWHR)

Washington, DChttp://www.swhr.org

ATTACHMENT:

The Society for Women's Health Research (SWHR) is writing to the Advisory Council on Alzheimer's Research, Care, and Services in regards to the National Alzheimer's Project Act (NAPA). SWHR has key scientific recommendations that it believes the Advisory Council should consider as it is establishing an integrated national plan to overcome Alzheimer's disease.

SWHR, a national non-profit organization based in Washington, D.C., is widely recognized as the thought leader in research on sex differences and is dedicated to improving women's health through advocacy, education, and research. SWHR appreciates the work NAPA is and will be doing to focus our nation's resources on Alzheimer's disease. While Alzheimer's disease is a disease of the brain, the brains of men and women are inherently different. It is common knowledge that men and women think differently; however, recent scientific discoveries have demonstrated that the difference goes beyond thought processes. Sex differences have been observed in the anatomy of the brain, behavioral traits, and in the physiological responses of the nervous system to outside stimuli and internal perturbation. These differences are also noted in the aging process and for the degenerative diseases such as Alzheimer's and Parkinson's disease.

SWHR believes that sex differences in Alzheimer's disease are critical to scientific advancements in diagnosing and treating the disease and need to be a part of the plan's scope. In October 2011, SWHR convened a one-day scientific roundtable of experts to discuss what is known about sex and gender differences in Alzheimer's disease, from both a basic and clinical science perspective as well as those of the caregiver and what research questions needed to be answered for progress to be made in the disease for all who are impacted. From the meeting it was clear that Alzheimer's disease research must account for sex as a basic biological variable and include sex-specific analyses and would be an extremely useful component of a national strategic plan to combat Alzheimer's disease. Key research recommendations from the roundtable that NAPA should include:

  • Research on the rate of progression of Alzheimer's Disease, specifically examining sex differences in the transition from normality to early stages of disease to dementia, and from dementia to outcomes.
  • Research on the influence of sex steroids, bioenergetic vulnerabilities, synaptic function, and cognition in the brain as it relates to Alzheimer's disease.
  • Re-examination of existing data for potential sex differences to help define the etiology of Alzheimer's disease and publishing sex-specific results.
  • Research on the differential impact of the caregiving role on men and women and design interventions to provide more effective services

Significant differences exist between men and women who suffer from Alzheimer's disease. Larry Cahill, Ph.D., an associate professor in the Department of Neurobiology and Behavior at the University of California, Irvine, explained in a paper published in Nature Reviews Neuroscience that "Alzheimer's disease-related neurofibrillary pathology associated with abnormally phosphorylated tau protein differs in the hypothalamus of men and women: up to 90 percent of older men show this pathology, whereas it is found in only 8-10 percent of age-matched women." Abnormalities caused by Alzheimer's disease may differ between the sexes and result in different symptoms or behavioral problems for men and women with the disease and may lead to the need for different treatment decisions.

Furthermore, Biology of Sex Differences (BSD) published research on sex differences of certain brain cells and their response to inflammation in the article, "Sex Differences in the Inflammatory Response of Primary Astrocytes to Lippolysaccharide" on July 12, 2011. Sex differences in incidence, age of onset, symptoms or outcome are evident in many neurological and psychiatric disorders. Astrocytes, one of the glial cells of the brain, show sex difference in number of cells, function, and differentiation. Glial cells are involved with physical support for neurons, while others regulate the internal environment of the brain, and provide nutrients to neurons of the brain.

With the increasing number of known sex differences found in research in Alzheimer's disease, SWHR recommends gaining a better understanding of the relationship between pathology and how disease presentation affects men and women differently leading to future sex-specific therapies for the disease.

Through our research recommendations above, SWHR seeks to put before the Advisory Council on Alzheimer's Research, Care, and Services the need to advance more targeted therapies in Alzheimer's disease for both men and women. This will lead to a greater understanding of risk factors for both men and women and more sex specific treatment of cognitive aging, Alzheimer's disease and other dementias.

Should the Advisory Council have any questions or would like more information please contact Eileen Resnick, Director of Scientific Programs at SWHR, at 202-496-5010 or Eileen@swhr.org.

Sincerely,

Phyllis Greenberger, MSW
President and CEO

References

Boston University (2008, March 18). One In Six Women, One In Ten Men At Risk For Alzheimer's Disease In Their Lifetime. ScienceDaily. Retrieved November 17, 2011, from http://www.sciencedaily.com/releases/2008/03/080318114824.htm

Society for Women's Health Research (SWHR) (2008, December 20). Alzheimer's Disease: Women Affected More Often Than Men. ScienceDaily. Retrieved November 17, 2011, from http://www.sciencedaily.com/releases/2008/12/081220085057.htm

Santos-Galindo, M., Acaz-Fonseca, E., Bellini, M. J., & Garcia-Segura, L. M. (2011). Sex differences in the inflammatory response of primary astrocytes to lipopolysaccharide. Biological Sex Differences , 2(7),

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DATE:  November 20, 2011

SUBJECT:  Informed Consent Question

How exactly can these clinical trials be conducted on individuals with cognitive disorders? How do they give informed consent ?

A guardians should NEVER be allowed to give consent for testing and for that matter no person other than the subject who will be tested should be allowed to give informed consent for clinical trials.

Can the proxy individual who is giving informed consent feel the physiological consequences? I think not and this practice is in violation of international human research testing laws I believe.

What is being done to protect the incapacitated from being placed involuntarily into clinical trials?

Latifa S. Ring

National Organization To Stop Elder Abuse and Guardianship Abuse (NOTEGA)

http://www.stopelderabuse.net

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DATE:  November 14, 2011

SUBJECT:  NAPA

CAUSES AND PREVENTION CAN BE DISCLOSED WITH STATISTICS! I am an 84 year old woman and a member of a genetic-Alzheimer's family. In my lifetime I am aware of eight family members who have been victims of Alzheimer's, the last three in my generation. Like so many families, I have watched my mother and my sister slowly lose their identities to this tragedy.

In the 21 years since an autopsy specified my mother's AD, dementia-research has mostly consisted of the very limited success of pharmaceutical trials, and more recently, gene-testing. This tunnel-vision has resulted in many family's continuing tragedies.

Currently, researchers are seeking new ways to identify pre-symptomatic members of such genetic families. They are searching for methods to identify those at high-risk, who are not yet experiencing cognitive impairments, so as to test "preventive" medications or life-styles.

There is no need of evaluating pre-clinical subjects, when critical diagnostic testing and histories already exist, or can be researched, for those who have already been diagnosed with dementia.

Current testing is uncovering conditions that may be causing dementia; injuries, diet, diseases, pathologies, environment, without the additional knowledge of possible linkage to commonality!

It is time to invest in a "National/International Registry" to uncover the comparative histories of millions of patients. A computerized dignostic framework and guiding terminology needs to be created, to organize a vital public-reference as an ongoing global study of all brain diseases.

Gerta FarberBerkeley, CA

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DATE:  November 12, 2011

SUBJECT:  National Alzheimer's Project Act [NAPA] - Editorial re: recommendations for action plan

Please find attached the pdf of an editorial concerning NAPA in the current issue of Alzheimer's & Dementia: Journal of the Alzheimer's Association. This document includes a set of recommendations for consideration by NAPA's Advisory Council [and/or the Secretary, DHHS] in drafting the National Strategic Plan.

I have also attached the draft of a memorandum concerning PAS2020 effort to formulate a specific recommendation to NAPA concerning a national initiative to establish 'public-private partnership' for discovery-development of treatments for AD.

Let me know your thoughts on these two items

Best regards,

Zaven S. Khachaturian, PhDPresidentPAD2020 -- The Campaign to Prevent Alzheimer's Disease by 2020Potomc, MD

ATTACHMENT:   ZK Editorial on NAPA NOV2011 ALZDEM.pdf   Draft Memo re Public-Private partnerships - NAPA - 26OCT11.doc

Available as separate links:
Prospects for Designating Alzheimer's Disease Research a National Priority Alzheimer’s & Dementia: Editorial Prospects for designating Alzheimer’s disease research a national priority
Perspective: Public-Private Partnerships to Develop Treatments Perspective Public-Private Partnerships to Develop Treatments

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DATE:  November 8, 2011

SUBJECT:  Thx for msg

Report's posted at alz.org/napa. I've attached a copy. We'll send out as attachment to AC members later today as well.

Best,Rob

ATTACHMENT:   NAPA_Report_110311.pdf

Available as separate links:
Alzheimer's from the Frontlines: Challenges a National Alzheimer's Plan Must Address Alzheimer’s from the Frontlines: Challenges a National Alzheimer’s Plan Must Address

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DATE:  November 3, 2011

SUBJECT:  Report for NAPA Advisory Council: The Path Ahead: A Framework for a Transformative National Plan to Defeat Alzheimer's Disease

Attached please find the report entitled The Path Ahead: A Framework for a Transformative National Plan to Defeat Alzheimer's Disease. This report provides a series of recommendations developed by Leaders Engaged on Alzheimer's Disease (LEAD) around research, clinical care, long-term care and support services, and drug discovery and development for consideration by the Advisory Council as it develops a national strategic plan for Alzheimer's disease.

We would greatly appreciate it if you can please distribute the attached report and cover letter to the members of the Advisory Council for their review.

Thank you,

Patrick Fritz

ATTACHMENT #1:  

Available as separate links:
The Path Ahead: A Framework for a Transformative National Plan to Defeat Alzheimer's Disease The Path Ahead: A Framework for a Transformative National Plan to Defeat Alzheimer’s Disease

ATTACHMENT #2:

Enclosed please find the report entitled The Path Ahead: A Framework for a Transformative National Plan to Defeat Alzheimer's Disease. This report provides a series of recommendations developed by Leaders Engaged on Alzheimer's Disease (LEAD) around research, clinical care, long-term care and support services, and drug discovery and development for consideration by the Advisory Council as it develops a national strategic plan for Alzheimer's disease.

LEAD was created to bring together stakeholders from all segments of the Alzheimer's-serving community - including government, business, and civic sectors -- to increase attention to and awareness of Alzheimer's disease, its care, treatment, prevention, research, and eventual cure. As you know, the increasing prevalence of this disease and the costs of caring for its victims is creating a grave and growing public health, fiscal and economic concern for our nation. With the goal of changing the trajectory of Alzheimer's disease, LEAD convened representatives from more than 40 organizations to develop strategies and recommendations focused on reducing costs, improving care and preventing Alzheimer's disease. We believe that these recommendations, if implemented, offer our best hope to save millions of American lives and trillions of taxpayer and family dollars in the coming decades otherwise lost to Alzheimer's disease.

LEAD members and participants, including nationally renowned experts representing the full range of voices of the Alzheimer's-serving community, actively supported the passage of NAPA and are now willing to be a resource to the Advisory Council as it moves forward with the development and implementation of a strategic plan. We respectfully submit our recommendations in the attached report for consideration and stand ready to support the Advisory Council efforts as the national plan is developed.

Should you have questions or require additional information about this report, please contact Sally Sachar, Chief Operating Officer of USAgainstAlzheimer's at (202) 360-2043, ssachar@usagainstalzheimers.org, or Sue Peschin, Vice President of Public Policy for the Alzheimer's Foundation of America, at 202466-0590, speschin@alzfdn.org. We look forward to working with you on this important effort.

Respectfully,

George Vradenburg
Chair & Co-Founder
USAgainstAlzheimer's

Eric J. Hall
Founding President & Chief Executive Officer
Alzheimer's Foundation of America

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OCTOBER 2011 COMMENTS

DATE:  October 20, 2011

SUBJECT:  FROM ERIC HALL/AFA REPORT TO NAPA!

I am extremely pleased to forward a copy of No Time to Waste, AFA's recommendations in connection with the National Alzheimer's Project Act. The report will be posted shortly on our website and released on PR Newswire.

Eric J. HallPresident and Chief Executive OfficerAlzheimer's Foundation of AmericaNew York, NYhttp://www.alzfdn.org

ATTACHMENT:   NoTimetoWasteReport-Final10-11.pdf

Available as separate links:
No Time to Waste: Recommendations for an Integrated National Plan to Overcome Alzheimer's Disease No Time to Waste: Recommendations for an Integrated National Plan to Overcome Alzheimer's Disease

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  October 19, 2011

SUBJECT:  NAPA National Plan Recommendations

Thank you for the opportunity to submit recommendations for the NAPA National Plan. Attached are our recommendations that focus on the unbefriended elderly. We hope their needs will be addressed in the final plan. Please contact me if you need any additional information.

Thanks again,

Kathy Cubit Director of Advocacy InitiativesCenter for Advocacy for the Rights and Interests of the Elderly (CARIE)Director of Advocacy Initiatives Philadelphia, PAhttp://www.carie.org, http://www.caregivergps.org

ATTACHMENT:  

NAPA National Plan Recommendations

The Center for Advocacy for the Rights and Interests of the Elderly (CARIE) is pleased to submit the following recommendations for inclusion in the NAPA National Plan. CARIE is a non-profit organization dedicated to improving the quality of life for frail older adults by working to protect their rights and promote awareness of their needs and concerns. Since 1977, CARIE has been providing advocacy services and options counseling for older adults and their caregivers. CARIE coordinates the Dorothy S. Washburn Legislative Committee comprised of legal, health and human services professionals as well as older adults who advocate to improve public policy impacting older adults and their caregivers.

CARIE is concerned about the issue of unbefriended elderly, more specifically, those with Alzheimer’s disease and other dementia who do not have a caregiver or responsible party to help them. There have been problems with these older adults being prematurely admitted to nursing facilities or being denied in-home services because of concern about liability. CARIE requests that the NAPA National Plan begin to address the needs of this population. There should be a dialogue about how to best strike a balance between preserving autonomy and allowing consumers to take some risks versus ensuring safety through more protective measures. While there is an abundance of information about Alzheimer’s disease and related dementia and support for caregivers, there is little, if any, information for those who do not have a caregiver or responsible party. There is enough anecdotal evidence to assume that not all older adults have family or close friends available to help.

CARIE’s Dorothy S. Washburn Legislative Committee makes the following recommendations for the NAPA National Plan:

Recommendations

  1. Include the issue and needs of unbefriended elderly in the NAPA National Plan and encourage the inclusion of the needs of this population in state plans.
  2. Implement an epidemiological study to identify the scope of the problem.
  3. Implement research to help identify best practices for ways to ensure early diagnosis for unbefriended elderly. Issues related to stigma and cultural differences should be addressed. Quality assessments should be readily available in all communities for consumers who are becoming concerned about symptoms.
  4. Design and fund demonstration projects to identify best practices and practical, cost-effective models for service delivery. There should be a balance between consumers’ safety and their need for autonomy. Different needs, preferences and values should be considered. Models should be tested among various cultural groups to identify potential variance with approaches. Identify benchmarks and performance measures that foster good outcomes.
  5. Research, design and implement clinical tools to help assess the decision-making capacity of individuals and work to maximize autonomy and ensure individuals are engaged and involved in making decisions to the greatest extent possible.
  6. Identify and utilize an ethical framework for assessment, planning and service delivery to ensure autonomy to the best extent possible as well as cultural considerations.
  7. Identify best practices for health care professionals, social workers, and paraprofessionals needed to work with this population including competencies and knowledge needed.
  8. Create training programs and help implement best practices for public safety officials such as police and fire fighters, emergency management personnel, and postal workers to help them identify those in need as well as where to turn for further assistance. Information should include but not be limited to what to do for someone who is found wandering.
  9. Develop strategies to prevent financial exploitation and premature guardianships for those in the early stages of Alzheimer’s disease or other dementia. Ensure access to legal services.
  10. Create, test, and implement model community educational programs to increase public awareness and decrease stigma.

Please contact Kathy Cubit at CARIE for more information.

Available as separate links:
NAPA National Plan Recommendations NAPA National Plan Recommendations

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  October 12, 2011

SUBJECT:  From Ross Schriftman, Alzheimer's Plan Comments

For two years I cared for my Mom with Alzheimers. In her memory and to help people understand the need for long term care planning and the relationship of sons caring for moms with the disease I wrote, "My Million Dollar Mom." Here is the the link to information about the book: http://www.buybooksontheweb.com/product.aspx?ISBN=0-7414-6713-5

Research is very important. However, I see no mention of an effort to get Americans to plan ahead for the need for long term care. This must be part of an overall approach. Care giver subsidies will NOT work as an answer. With the budget constraints where will the money came from? What about care giver burn out. Family members need PROFESSIONAL care to assist them in caring the their loved ones. ONLY long term care insurance can provide enough dollars to pay for the services of home care agencies. Without a robust long term care insurance market the number of home care agencies thriving will be diminished and the burden will get worse not better.

I urge you to support education and incentives to encourage Americans to plan with their families for their future needs for care. The purchase long term care insurance, putting their legal documents in order and having a well thought out plan of how, who and where they should be cared for is essential.

Finally, on the budget side, as a long term care insurance agent my clients (including my Mom) have received more than $2 million in benefits from their policies. That is money their families did not have to lay out. That is money that our overly strained Medicaid budget did not have to come up with.

Please include advanced planning as part of this program.

Thank you for your consideration.

Sincerely,

Ross Schriftman, RHU, LUTCF, ACBC, MSAAHorsham, PA

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SEPTEMBER 2011 COMMENTS

DATE:  September 30, 2011

SUBJECT:  Comments for the Council

The single most staggering dilemma facing our Nation today is the upcoming tsunami of "boomers" barreling down upon us that will become victims of Alzheimer's!

At this time, Right Now, visionary leadership is absolutely essential in order to effectively direct action that will lessen the hardship that will be experienced by millions so stricken as well as their loved ones. Decisive action towards implementing screening that will diagnose severity with appropriate treatment being scheduled at the time of screening.

While the emphasis remains on "The Cure" we cannot afford to lose sight of the here and now and the fact that today there are meds available that will lessen the impact of this mind-robbing malady and provide relief for friends and loved one of these individuals in the way of quality of life extensions. Early detection must be recognized as a priority concern.

Florida, with its huge Elder population, leads the Nation in this devastating and incurable disease. It is projected that in just a few years this amount may increase three fold. Now s the time for action/Further delays will be a reflection of an abdication of responsibility.

As a caregiver who has experienced first handthe horrific loss of individuality by those who have no control of this I stand firmly for immediate priority action to alleviate the suffering associated with Alzheimer's. As a civilized society we can do no less to insure the respect and dignity of these souls.

Austin R CurryExecutive DirectorElder Care Advocacy of Florida

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DATE:  September 29, 2011

SUBJECT:  National Alzheimers Plan

Dear Advisory Council, for the past 7 years my siblings and I have been assisting my mother manage the challenges of Alzheimersdisease. I am a veteran of the nursing/psychiatric field with training in Geriatric Mental Health. When our mother began to show signs of the disease I urged her doctor to do a mini mental exam. At the time she scored below 20 and I believe this was due in part to the fact that she is Spanish speaking only and the test was designed for the English speaker. And I don't believe she comprehended its purpose and mostly joked around with the questions and answers. The fact remained that she missed all the critical orientation questions and her recent memory was severely impaired. Today she remains coherent, jovial and she converses easily. She has some difficulty with remote and recent memory, and item recognition, but she still recognizes familiar faces and is able to do most familiar tasks. She can still prepare simple meals, make coffee, and perform all ADLs. Recently, she has shown signs of new memory formation. These memories are based on new information obtained a month or two prior. The new memories are usually linked to an emotional response, eg; something she enjoys or wants to do. The new memories are formed after she has asked the same question repeatedly and it has been answered each time as though it was being asked for the first time. She has been on a combination of drugs called Namenda and Aricept, as well as the chewable version of Melatonin that only Trader Joes sells. She does not experience sundowning and sleeps 8 or 9 hours per night. She experiences one waking about 4 am when she takes another Melatonin and sleeps until 8 or 9 am. The geriatric mental health training I participated in was offered by the University Of Washington School of Social Work, it featured a wonderful section on a program called the Beyond Love Project. The project workbook was written by Moyra Jones and it is a community based model that can be adopted by any community. The Beyond Love Project utilizes the collaborative effort of various medical and legal professionals, as well a community volunteers to teach caregivers to care for themselves and their loved ones with compassion. It provides tools to assist caregivers in recognizing the stages ofdementing disorders, as well as the limitations and challenges of each stage. I have been working on distribution of pamphlets that are produced by the Dept of Health and Human Services to encourage education and early detection. But I am one person and it is not enough. Our Medical professionals are the first line of defense and often they are not aware of the early signs. My mother's own doctor said to me in horror "how did I not see this? I've known this woman for 10 years." I responded "she presents well doesn't she?" The truth is, like any other disease, the only way for a medical professional to detect this disease is by testing for it. My point here is that a Mini Mental Exam should be as standard as a colonoscopy or prostate exam at 55. Thank you for your time and I look forward to hearing about the new plan and I hope to be a part of bringing much needed services to my community. In the meantime, I will continue my efforts to bring awareness, education and support and advocacy to my community.

Laura Villegas

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DATE:  September 29, 2011

SUBJECT:  Alzheimer's National Advisory Council / participation

I am writing because I would like to become involved in advocacy work on behalf of U.S. citizens suffering from Alzheimer's. I was the sole caretaker for my mother, who passed away in February 2010; I began my long, sometimes difficult, but very rewarding journey with her in 1999. She was housed for several years in assisted living facilities, and my experience clearly showed me that Alzheimer's patients are not receiving the specialized care they deserve. Further, I also learned about traumatic housing transfer issues, and the need for the Alzheimer's patient to have one-on-one care daily with someone they are familiar with, whether or not recognition is still available.

I attended the Alzheimer's Association International Research Conference in Paris this July, learning about the disease process and lifestyle factors that may aide in prevention. My prior education included a B.S. in Psychology and graduate classes in Adult Education and Counseling. Prior to my care taking journey, I was (and still am) a Certified Alcohol and Drug Counselor. I have had a few brief classes in Pharmacology and Neurology, but nothing that fully addresses the mechanisms of Alzheimer's and other dementia diseases.

When I heard that a national advisory council was forming, I relayed feedback via e-mail. However, it seemed so little with such a huge problem / concern looming for the nation. I wish to be involved and helpful in other ways. I am willing to go back to school, move from my current residence -- anything to really make a solid difference in this complex, multi-faceted issue.

Do you have any advice as to a course of action that I can take? Does the National Advisory Council or any other organization involved with Alzheimer's need help that I am qualified to do? I sincerely wish to make a difference.

Thank you,

Annette Guidry, B.S., CADC

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DATE:  September 29, 2011

SUBJECT:  Compulsory national service to all students in USA

I am a retired primary care physician who worked in Long Term Care for over 35 years.

With aging society and growing rate of Dementia, we need the entire society to involve.

Specially we need the our young people to involve and to participate for the care of this enormous medical and global problems.

Even for the few weeks of special human service by the students, probably will make a big difference in national awareness of this problems.

Jhin J. Cynn MD, CMD, FAAFP

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DATE:  September 27, 2011

SUBJECT:  A National Strategy on Alzheimer's

I read the article in the New York Times today about the upcoming committee that will tackle the job of Alzheimer's and our governmentsrole and responsibility. I am a daughter of my 82 year old mother who has been living with this disease for the past seven years. My father, who is 88 years, has been amazing through this entire journey. In February, my mother fell down and broke her hip and my father finally agreed to let me bring someone in to help them 24/7.

This is not an easy task nor an inexpensive one. We are able to manage to have them home right now but the financial and emotional burden that is put upon us by this disease is difficult to describe in words. It is a shame that our government and our health care system does not allow for this type of help to be covered under medical plans. Yes, you can purchase long term care, but really, how many people really ever think about this type of insurance at an early age, before any disease kicks in and you don't qualify. My hope and dream is that this task force can develop a plan that will tackle not only government's role in funding medical research to wipe out this horrific disease, but also will look at the financial burden caregiving places on individual families and our nation. If we could find a cure for Alzheimer's, our nation would flourish. I know I am one small voice in a very big, big picture. I do my part to help every day. I actively fundraise for the Alzheimer's Association and support all causes that can lead to a cure. I am scared not only for my mom, but also for myself and my children. I don't want to go through what my mom is going through now and I certainly can't imagine passing this on to my children. It truly breaks my heart.

But I hope you will listen to my voice and if you ever need information from a person deep in the trenches, I would be happy to share my knowledge on to the committee. As I tell my friends and love ones, I fight for my mom's present and for all of our future!

Thank you.

Diane KounalakisHillsborough, CA

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  September 27, 2011

SUBJECT:  Suggestion

I have been conducting training for health care professionals for over 20 years, including physicians on Alzheimer's disease. It is a fact the thephysicians are not prepared to assess for symptoms of the disease nor able to cooperate with the community health and social agencies on coordinating services that are needed. There needs to be much more education at the basic level through the tele-health programs, especially in the rural areas, on basic skills in assessing for Alzheimer's

The other issue is the importance in establishing a base line for possible early signs of dementia -- i.e. MCI. About 80% of early assessments of MCI usually end up within 10 years or so being "diagnosed" as Alzheimer's.

Suggestion is that a baseline, as one does for blood pressure, using a modified mini mental status test be made for the population starting at 50.

Redo it every year when visiting the doctors office -- and compare the changes. If there are changes then further investigation is needed with possibly early intervention using Aricept or Memantine. These have been shown to be effective together the earlier they are administered.

Thank you for the link to express my ideas and concerns

Ron Lucchino, PhD

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  September 27, 2011

SUBJECT:  Help, Direction for Alzheimer's Caregivers

As you undertake this crucial work, please consider the nearly 14.9 million unpaid Alzheimer's caregivers, many of whom are overwhelmed by their caregiving role. This number will grow year by year as will the number of those diagnosed with Alzheimer's.

In more than 20 readings and discussions which I have conducted this year, I inevitably find a thirst among caregivers for honest, lived, true stories of caregiving. Tonight I will address this issue at a meeting in St. Louis. The issue was framed for me this way: What happens when you have to parent your parents? How do the parents react who are now in the role of care recipient? The FAQs from my meetings represent a document of the profound and thoughtful concerns of audiences from Michigan to Washington state to Missouri. I urge you to consider this aspect of the Alzheimer's "dilemma."

The literature of lived Alzheimer's experiences is invaluable as a tool for caregivers. It complements the excellent medical and advice literature in its human and humane perspective. Please consider its role as part of an outreach to the millions of caregivers who feel as if they are swimming solo in their duties.

Sincerely,

Susan Rava, Ph.D.Author of SWIMMING SOLO: A Daughter's Memoir of Her Parents, His Parents, and Alzheimer's Disease (Sewanee, TN: Plateau Books, 2011).

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  September 27, 2011

SUBJECT:  National Plan for Alzheimer's Disease

I am a practicing geriatric medicine specialist who devotes a large amount of my practice to diagnosing and treating persons with Alzheimer's disease. I would very much like to discuss some recommendations with a staff member of the Advisory Committee.

While a large number of researchers are focused on using new imaging techniques to diagnose this disease earlier, I find in my practice that many people who have had this disease for years are going undiagnosed. I believe that this is because primary care physicians are intimidated by this diagnosis and many psychiatrist and neurologists just not interested in making this diagnosis. I lecture frequently to professional groups on just this topic and in that talk I try to demystify the diagnosis.

I would be very happy to discuss my views with a staff member if you are interested.

Thank you for your time.

James P. Richardson, M.D., M.P.H.Chief, Geriatric MedicineSt. Agnes HospitalBaltimore, MD

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DATE:  September 26, 2011

SUBJECT:  Comments for NAPA advisory council meeting on Sept 27th.

Attached is a copy of my testimony/comments for tomorrow's Council meeting. Would appreciate if copies could be made for each Council member.

Thanks.

Matthew P. Janicki, Ph.D.

Associate Research Professor and Director for Technical Assistance

Rehabilitation Research and Training Center in Aging and Developmental Disabilities -- Lifespan Health and Function

Department of Disability and Human Development

University of Illinois at Chicago

Chicago, IL

ATTACHMENT:

National Task Group on Intellectual Disabilities and Dementia Practices
http://www.aadmd.org/ntg

Comments to the Advisory Council on Alzheimer's Research, Care, and Services
September 27, 2011

By Matthew P. Janicki, Ph.D. on behalf of the National Task Group on Intellectual Disabilities and Dementia Practices

I am the co-chair, along with Dr. Seth M. Keller, the President of the American Academy of Developmental Medicine and Dentistry, of the National Task Group on Intellectual Disabilities and Dementia Practices. The National Task Group was created in 2010 by the American Association on Intellectual and Developmental Disabilities (AAIDD), the American Academy of Developmental Medicine and Dentistry (AADMD), and my university center, the Rehabilitation Research and Training Center on Aging and Developmental Disabilities (Lifespan Health and Function) at the University of Illinois at Chicago. Our charge was to examine the state of practices related to dementia and people with lifelong intellectual disabilities, their families and caregivers, and the organizations that support them, and provide commentary on what needs to be done to further services and practices in the United States related to this population. Our charge also was to provide information and recommendations to the Advisory Council formed under the National Alzheimer’s Project Act.

To this end, the National Task Group, composed of some 100 administrators, academics, providers, clinicians, families, and advocates, have coalesced with a number of national disability and family based organizations, federal agencies, and provider representatives to create a report on our findings and recommendations. The report, “‘My Thinker’s Not Working’: A National Strategy for Enabling Adults with Intellectual Disabilities Affected By Dementia to Remain In Their Community and Receive Quality Supports “, is currently in development and we anticipate having it launched at our next National Task Group meeting in November.

In advance of the release of our Report, it is timely to provide the Advisory Council with some key points from the Report for its use. We have prepared these comments, which I trust the Council members will find informative and helpful:

  1. Alzheimer’s disease and other dementias affects adults with lifelong intellectual disabilities in similar ways as it does other people, but sometimes has a more profound impact due to particular risk factors -- including genetics, neurological injury, and deprivation. While mostly the disease follows a typical course, at times some adults are profoundly and aggressively affected. Yet all need the typical types of supports and services usually associated with dementia-capable care. We -- the National Task Group -- believe that adults with intellectual disabilities require the same early and periodic diagnostic services, community education, and community-based supports for themselves, their caregivers, and the organizations responsible for them, as do other adults with dementia in the general population.
  2. Many families are the primary lifetime caregivers for adults with intellectual disabilities and when Alzheimer’s disease and dementia occurs, they are particularly affected and need considerable supports. These families not only include parents, but also siblings and other relatives. Many such families are at a loss for providing extensive care at home once dementia becomes progressive and care demands overwhelm them. We -- the National Task Group -- recommend that the nation's providers and state disability authorities invest in increased home-based supports for caregivers who remain the primaries for care for adults affected by dementia.
  3. Many intellectual disabilities provider organizations that are the primary resources for residential and day supports are vexed by the emerging trend of increasing numbers of adults with intellectual disabilities in their services showing signs of early decline and dementia with potentially more demanding care needs. In such cases, staff may be unfamiliar with the signs and symptoms of mild cognitive impairment (MCI) or dementia and may misrepresent or ignore these changes, when early identification could prove beneficial. We -- the National Task Group -- recommend that the nation's providers and state disability authorities invest in increased education and training of personnel with respect to Alzheimer’s disease and other dementias and invest in promoting best practices in models of community care of adults with intellectual disabilities affected by dementia.
  4. As it is important to pick up signs of dementia-related cognitive decline early on , we -- the National Task Group -- recommend that the nation's providers and health authorities undertake a program of early identification screening - beginning at age 50 for adults with intellectual disabilities and at age 40 for adults with Down syndrome and others at early risk. We recognize that the Advisory Council may be debating the issue of early identification and screening in the general population. In this regard, the National Task Group has identified a screening instrument, applicable particularly to adults with an intellectual disability, which seems to work as a first-instance screen and recommends adoption of such an instrument by providers and regulatory authorities to begin to identify those adults at risk due to early signs of mild cognitive impairment (MCI) or dementia.
  5. Most adults with a lifelong intellectual disability live in community settings with support from families, friends and service providers. Research has shown that community-based models of care for adults with intellectual disabilities and dementia include community-based options, such as support for living at home or in small group homes, are viable and gaining preference for all individuals affected by Alzheimer’s disease and other dementia. Institutionalization of adults with intellectual disabilities and dementia is anathema to the core beliefs and commitments to care practices in the intellectual disabilities field and such institutionalization (via use of long-term care facilities) has been shown to have an adverse affect on lifespan and quality of life. The group home model, where a handful of adults with intellectual disabilities and dementia live in a specialized care home, is becoming more prominent across the world. We -- the National Task Group -- recommend that these models be expanded and an investment be made into enabling provider organizations to develop and maintain such care efforts, including developing more small community-based specialized 'dementia capable' group homes.
  6. Dementia has a devastating impact on all people one way or another -- including people with intellectual disabilities and the many families, friends, and staff involved as parents, siblings, advocates, and caregivers. We -- the National Task Group -- wish to give emphasis to this point and ask the Advisory Council on Alzheimer's Research, Care, and Services to include concerns and considerations for people with lifelong intellectual disabilities in any and all documents, plans, and recommendations to Congress that are part of the work of the Council. The National Task Group stands ready to assist and contribute to such efforts and is pleased that this Council recognizes Alzheimer’s disease and other dementias as an ultimate public health issue and a problem to which we collectively need to attend.

Thank you.

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  September 23, 2011

SUBJECT:  Latino Alzheimer's Alliance

Thank you so much for returning my call. As I mentioned to you during the last 4 years the Latino Alzheimer's and Memory Disorders Alliance is working very hard on the Alzheimer's Awareness in the Latino community in the most important cities of the US as is Los Angeles, New York, Chicago and now DC.

Bilingual and Bi-cultural programs has being offering to more than 15,000 Latino families in the last 2 years, not only by support groups, encourage them to participate in clinical studies, provided the follow up to the individuals who required. The Latino ALzheimer'sAlliance train more than 700 healthcare providers a year on how to be sensitive to cultural and social barriers in the Hispanic community. Sinai Health System, Loyola, Rush Alzheimer's Disease Center, Alivio Clinics, Sinai Health System, Psychology School of Chicago and LA, UCLA, are some of the institutions that received our trainings.

The Chicago Tribune, LA Times,,Univision TV/Radio, La Opinion and Washington Post articles about LAMDA are increasing the number of individuals who are asking to attend our programs. Is for this reason it is very important to represent the Latino/Hispanic Community in the US by participate as a member on the Advisory Council on Alzheimer's Research, Care, and Services meeting held on Tuesday, September 27, 2011.

We appreciate your efforts and consideration on this important journey.

Please see attachments

Best regards,

Constantina MizisCEOThe Latino Alzheimer's and Memory Disorders Alliance

ATTACHMENT:   Chicago PSA.wmv   La Opinion LA.docx

Available as separate links:
Para reflexionar sofre la memoria Para reflexionar sobre la memoria
Chicago PSA (Spanish-speaking video file) http://aspe.hhs.gov/daltcp/napa/Comments/cmtach14.wmv

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DATE:  September 10, 2011

SUBJECT:  the prevention and treatment of Alzheimer's disease

My name is Lane Simonian. I am an historian. Seven years ago when my aunt and cousin were in the late stages of Alzheimer's disease and my mother was in the early stages of Alzheimer's disease, I began searching for ways to prevent and treat the disease. As an historian, I began to collect a mass of abstracts and articles in an attempt to tell the story of Alzheimer's disease. At first with a limited background in biology, I made very slow progress in understanding Alzheimer's. Now, though, I can explain almost every new finding in regards to the disease with the attached hypothesis. What used to take me months to figure out now usually only takes a matter of minutes.

The critical finding in regards to Alzheimer's disease was made by Mark Smith and his colleagues in 1997: Peroxynitrite-mediated damage is widespread in Alzheimer's disease. This damage includes the oxidation (loss of electrons and hydrogen) of glucose transport systems, choline transport systems, the enzyme cholineacetyltransferase, g protein-coupled receptors (muscarinic, serotonin, dopamine, olfactory, adrenergic), the nitration of tau proteins, lipid peroxidation, and the influx of calcium. This damage results in a lack of focus and energy, impaired short-term memory due to a shortage of acetylcholine, disturbed sleep and mood, lack of awareness, impaired smell, behavioral problems (in some instances), disrupted neurotransmission, damage to cellular membranes, and neuronal cell death.

The factors that lead to peroxynitriteformation include (but again are not limited to) high glucose levels, high blood pressure, the APOE4 gene, presenilin gene mutations, bisphosphonate osteoporosis drugs, late estrogen replacment therapy, mercury, aluminum fluoride, and stress. Most or all of the factors that lead to peroxynitrite formation also lead to Alzheimer's disease (the connection has not been made as of yet between bisphosphonateosteoporosis drugs and Alzheimer's disease, but the fact that the numbers of cases of Alzheimer's disease has skyrocketed since the introduction of these drugs is perhaps concerning).

Phenolic compounds in various fruits, vegetables, spices, and essential oils and polyunsatured fats inhibit peroxynitrite formation and thus inhibit the development of Alzheimer's disease. The most direct and concentrated way to deliver phenolic compounds to the brain is through aromatherapy with essential oils high in phenoliccompounds.

An impressive number of animal studies, case studies, and clinical trials indicate that Alzheimer's disease can be treated effectively with peroxynitrite scavengers (compounds that are hydrogen donors convert peroxynitrites into a nitrogen dioxide anion and water). These scavengers partially reverse or prevent all of the damage done by peroxynitrites listed above (for example, they add hydrogen back to muscarinicreceptors allowing more choline to enter cells). In the reference section of the attached hypothesis you will find a partial list of peroxynitrite scavengers (most of them are phenolic compounds) which have helped correct cognitive deficits in animal models of Alzheimer's disease. These include rosmarinic acid, grape seed extract, cinnamon extract, eugenol in Cinnamomum zeylanicum essential oil, and thymol and carvacrolin Zataria multiflora Boiss. essential oil. In addition, Jimbo and colleagues in Japan were able to improve cognitive function in dementia patients after giving them rosemary and lemon to smell in the morning and lavender and orange to smell in the evening for 28 days. Akhondzadeh and his colleagues achieved similar results using tinctures of sage and lemon balm essential oils for four months. One reviewer looking at this (and perhaps other clinical trials) concluded "excellent results have been obtained with peroxynitrite scavengers, with reversals of Alzheimer's disease in human clinical trials being repeatedly demonstrated."

Several case studies add further validity to the findings from animal studies and clinical trials. Dramatic improvements in alertness and awareness and modest improvements in short-term memory have been noted. In my mother's case she recognizes her home again, feels comfortable around her brother who she used to think was an impostor, sleeps through the night, can recall her name and sometimes spell it, can sometimes remember the order of days and months, can complete phrases such as I scream, you scream, we all scream for...ice cream and April showers...bring May flowers, and is much more alert and aware than she was four years ago before we began aromatherapy.

Essential oils high in methoxyphenols (such as rosemary, sage, thyme, oregano, clove, and cinnamon leaf) and citrus based essential oils appear to work the best. The patient can smell them under each nostril for a few seconds. It takes about a month to begin seeing some improvement (perhaps because it takes time to reverse the damage that peroxynitrtes do to smell).

Let me highlight the critical points:

Peroxynitrite-mediated damage is widespread in Alzheimer's disease and directly or indirectly causes all the features of the disease.

Most or all of the factors that lead to peroxynitrite formation can cause Alzheimer's disease.

Compound which inhibit peroxynitriteformation inhibit the onset of Alzheimer's disease.

In animal studies, clinical trials, and case studies, peroxynitrite scavengers have lead to improvements in cognitive function.

Phenolic compounds can be used both to prevent and treat Alzheimer's disease. In both cases, aromatherapy is likely the most effective way to deliver these compounds to the brain.

This disease can be treated effectively immediately with few side effects.

I wish you good luck in your work. If the opportunity arises, I would like to meet each of you in person. In the meantime, please feel free to contact me. Nothing pleases me more when I receive questions from people interested in my research.

Best Regards,

Lane Simonian

ATTACHMENT:   

Available as separate links:
Effect of Aromatherapy on Patients with Alzheimer's Disease Effect of Aromatherapy on Patients with Alzheimer's Disease
Aromatherapy in the Treatment of Alzheimer's Disease Aromatherapy in the Treatment of Alzheimer's Disease
The Psychopharmacology of European Herbs with Cognition-Enhancing Properties The Psychopharmacology of European Herbs with Cognition-Enhancing Properties
Current Pharmaceutical Design, 2006, Vol. 12, No. 35, pg 4617 Psychopharmacology of European Herbs
Current Pharmaceutical Design, 2006, Vol. 12, No. 35, pg 4619 Psychopharmacology of European Herbs
Evidence Based OTC Treatment of Alzheimer's Disease I Evidence Based ODC Treatment of Alzheimer's Disease I
Alzheimer's Disease and Dementia Message Board Alzheimer's Disease and Dementia Messageboard
ECU Therapist Studies Links Between Scent and Memory ECU Therapist Studies Links Between Scent and Memory
Texas State Research on Aromatherapy Texas State Research on Aromatherapy

Hypothesis for Alzheimer's Disease

The three factors which increase the risk for Alzheimer's disease are high levels of myo-inositol (a precursor to phosphatidylinostiol 4, 5 biphosphate), increased phospholipase C gamma activity (whose substrate is phosphatidylinositol 4, 5 biphosphate) and the inhibition of the phosphatidylinositol 3/AKT pathway (the PI3 kinase converts phosphatidylinostiol 4,5 biphosphate into phosphatidylinositol 3, 4, 5 triphosphate). Factors which increase myo-inositol levels are high glucose levels (due to the conversion of glucose 6-phosphate into myo-inositol), high blood pressure (due to the sodium/myo-inositol cotransporter), and Down syndrome (because people with Down syndrome have an extra chromosome containing the sodium/myo-inositol transporter). Factors which reduce levels of myo-inositol are certain blood pressure medications, certain diabetes medications, estrogen, tamoxifen, lithium, and scyllo-inositol. Factors that increase phospholipase C gamma are glucose, estrogen, and angiotensin II (a cause of high blood pressure). Factors which lower phospholipase C gamma activity are fish oil (and other polyunsaturated fats) and phenols in various fruits, vegetables, spices, and essential oils. Factors that prevent or inhibit the activation of the PI3 kinase/AKT pathway are presenilin gene mutations, APOE4, and bisphosphonate osteoporosis drugs. Insulin, insulin-like growth factor, and drugs which increase high density lipids can to a limited degree stimulate this pathway. These are the main risk factors and preventative measures for Alzheimer's diseas

e Phospholipase C gamma increases the release of calcium from the endoplasmic reticulum (via inositol 1, 4, 5 triphosphate) which in turn stimulates Protein Kinase C. Protein Kinase C processes the amyloid precursor protein and a calcium dependent enzyme cleaves this protein to form amyloid plaques. Phospholipase C gamma exports zinc and zinc and copper are entombed in the amyloid plaques. This results in higher levels of homocysteine and a decline in the superoxidase dismutase which converts the superoxide anion into hydrogen peroxide. Protein kinase C increases choline uptake (and phospholipase C beta) and phospholipase C gamma increasing the number of plaques created. Homocysteine via Protein Kinase C increases the production of the superoxide anion and inducible nitric oxide. The two combine to form peroxynitrites.

The effects of peroxynitrites are as follows:

Peroxynitrites lower levels of intracellular magnesium which allows more calcium into the cells via the now open gate of the NMDA receptor.

Peroxynitrites cause lipid peroxidation (including the final product of lipid peroxidation--HNE)

The combination of peroxynitrites, HNE, and calcium influx leads to neuronal cell death. Peroxynitrites oxidize g-protein coupled receptors and nitrate tyrosine. The result is the hyperphosphorylation of tau proteins. Moreover, peroxynitrites nitrate tau proteins preventing them from being reconstituted for proper neurotransmission.

Peroxynitrites oxidize choline transport systems, muscarinic receptors (a g protein-coupled receptor involved in the uptake of choline), and the enzyme choline acetyltransferase, thus resulting in a critical shortage of acetylcholine which is needed for the retrieval of short-term memories.

Peroxynitrites oxidize a series of other g-protein coupled receptors including olfactory, serotonin, and dopamine receptors. The results respectively are impaired smell, poor sleep and depression, and lethargy and apathy.

Peroxynitrites oxidize glucose transporters resulting in a lack of energy and focus.

Peroxynitrites can be scavenged using phenolic compounds (one or more OH groups). Phenols in essential oils can be breathed directly into the hippocampus via aromatherapy. They accomplish the following conversion (ONOO- + 2H+ + 2 electrons-->NO2- + H2 0). Essential oils add hydrogen back to g-protein coupled receptors and partially reverse the nitration of tyrosine (including tyrosine residues on tau proteins). They thus partially reverse many if not all of the symptoms of Alzheimer's disease.

Bibliography for Alzheimer's Disease

Myo-Inositol and Alzheimer's Disease

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G. Hauser and V.N. Finelli, The biosynthesis of free and phosphatide myo-inositol from glucose by mammalian tissue slices, J of Biol Chem 238 (1963): 3224-8.

W Huang. G.E. Alexander, E.M. Daly, H.U. Shetty, J.S. Krasuski, et al., High brain myo-Inositol levels in the predementia phase of Alzheimer's disease in adults with Down's Syndrome: A 1H MRS study, J Clin Invest 95 (1995): 542-6.

T. Ernst, L. Chang, D. Cooray, C. Salcador, J. Jovichich, I. Walot, et al., The effects of tamoxifen and estrogen on brain metabolism in elderly women, J Natl Cancer Inst 94 (2002): 592-7.

A. J. Harwood, Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited, Mol Psychiat 10 (2005): 117-25.

J.D. Moyer, N. Malinowski, E.A. Napier, J. Strong, Uptake and metabolism of myo-inositol by L1210 leukemia cells, Biochem. J 254 (1988): 95-100.

Phospholipase C gamma [y] and Alzheimer's Disease

Z. Deqing, H. Dhillon, M.R. Prasa, W.R. Markesbery, Regional levels of brain phospholipase C [y] in Alzheimer's disease, Brain Res 811 (1998): 161-5.

Y. Okuda, H.J. Adrogue, T. Nakajima, M. Mizutani, M. Asano, et al., Increased production of PDGF by angiotensin and high glucose in human vascular endothelium, Life Sci 59 (1996): 1455-61.

R. Graber, C. Sumida, G. Vallette, E.A. Nunez, Rapid and long-term effects of 17ß-estradiol on PIP2-phospholipase C-specific activity of MCF-7 cells, Cell Sign 5 (1993): 181-6.

P. Sanderson and P.C. Calder, Dietary fish oil appears to prevent the activation of phospholipase C-y in lymphocytes, Biochem et Biophys, 1392 (1998): 300-08.

S. Godichaud, K. Si-Tayeb, N. Auge, A. Desmouliere, C. Balabaud, et al., The grape-derived polyphenol resveratrol differentially affects epidermal and platelet .derived growth factor signaling in human liver myofibroblasts, Internat J Biochem and Cell Biol 38 (2006): 629-37.

G.M. Cole, G.P. Kim, F. Yang, B. Teter, A. Begum, et al., Prevention of Alzheimer's disease: Omega-3 fatty acid and phenolic anti-oxidant interventions, Neurobiol Aging (2005): 133-6.

M.A. Kang, S.Y. Yun, J. Won, Rosmarinic acid inhibits CA[2+]-dependent pathways of T-cell antigen receptor-mediated signaling by inhibiting the PLC-y1 and Itk activity, Blood 101 (2003): 3534-42.

Inhibition of PI3 kinase/Akt Pathway and Alzheimer's Disease

L. Baki, J. Shioi, P. Wen, Z. Shao, A. Schwarsman, M Gama-Sosa, et al., PS1 activates PI3K inhibiting GSK-3 activity and tau hyperphosphorylation: effect of FAD mutations, EMBO J 23 (2004): 2586-96.

R. Dekroon, J.B.Robineete, A.B. Hjelmenland, E. Wiggins, M. Blackwell, M. Mihovilovic, et al., APOE4-VLDL inhibits the HDL-activated phosphatidylinositol 3-kinase/Akt pathway via the phosphoinositol phosphotase SHIP2, Circ Res 99 (2006): 829.

R. Inoue, N.A. Matsuki, G. Jing, T. Kanematsu, K. Abe, M. Hirata. The inhibitory effect of alendronate, a nitrogen-containing bisphosphonate on the PI3K-Akt-NFkB pathway in osteosarcoma cells, Brit J Pharmacol 146 (2005): 633-41.

The Disease Process

J.D. Buxbaum, A.A. Ruefli, C.A. Parker, A.M. Cypess, P. Greengard, Calcium regulates the processing of the Alzheimer's amyloid protein precursor in a protein kinase C-independent manner, PNAS 91 (1994): 4489-93.

S. Jansen, J. Arning, D. Beyersmann, Zinc homeostasis in C6 glioma cells: phospholipase C activity regulates cellular zinc export, Bio Trace Elem Res 108 (2005): 87-104.

M.A. Carluccio, M.A. Ancora, M. Massaro, M. Carluccio, E. Scoditti, et al., Homocysteine induces VCAM-1 gene expression through NF-kB and NAD(P)H oxidase activation: protective role of Mediterranean diet polyphenolic antioxidants, Am J Physiol Heart Circ Physiol 293 (2007): 2344-54.

Peroxynitrites in Alzheimer's Disease

M.A. Smith, P.L. Richey Harris, L.M. Sayre, J.S. Beckman, G. Perry, Widespread peroxynitrite-mediated damage in Alzheimer's disease, J Neurosci 17 (1997): 2653-7.

J. Li, W. Li, Wi. Liu, B.T. Altura, Peroxynitrite induces apoptosis and decline in intracellular free Mg with concomitant elevation in [Ca2+] in rat aortic smooth muscle cells; possible roles of extracellular and intracellular magnesium ions in peroxynitrite-induced cell death, Drug Metabol Lett 1 (2007): 85-9.

R. Radi, J.S. Beckman, K.H. Bush, B.A. Freeman, Peroxynitrite-induced lipid peroxidation: the cytotoxic potential of superoxide and nitric oxide, Arch Biochem Biophys 288 (1991): 481-7.

H.L. Viera, A.S.Belzacq, D. Haurzi, F. Bernassola, I. Cohen, E. Jacotot, et al., The adenine nucleotide translocator: a target of nitric oxide, peroxnitrite, and 4-hydroxynonenal, Oncogene 20 (2001): 4305-16.

R. Radi, J.S. Beckman, K.H. Bush, B.A. Freeman, Peroxynitrite oxidation of sulfhydryls. The cytotoxic potential of superoxide and nitric oxide. J Biol Chem 266 (1991): 4244-50.

M.R. Reynolds, J.F. Reyes, Y. Fu, E. H. Bigio, A.L. Guillozet-Bongaarts, R.W. Berry, et al., Tau nitration occurs at tyrosine 29 in the fibrillar lesions of Alzheimer's disease and other taupathies 26 (2006): 10636-45.

L. Guermonprez, C. Ducrocq, Y.M. Gaudry-Tlarmain, Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrites are differentially prevented by antioxidants, Mol Parmocol 60 (2001): 838-46.

The Treatment of Alzheimer's Disease

T. Alkam, A. Nitta, H. Mozguchi, A. Itoh, T. Nabeshima, A natural scavenger of peroxynitrites, rosmarinic acid protects against impairment of memory induced Aß, Behav Br Res 180 (2007): 139-145.

M.R. al-Sereiti, K.M. Abu-Amer, P. Sen, Pharamacology of rosemary (Rosmarinus officinalis Linn.) and its therapeutic potentials, Indian J Exp Biol, 37 (1999): 124-30.

H.R. Choi, J.S. Choi, Y.N. Han, S.J. Bai, H.Y. Chung, Peroxynitrite scavenging of herb extracts, Phytotherap Res 16 (2002): 364-7.

V. Zilmer, M. Zilmer, K. Zilmer, N. Bogdanovic, E. Karelson, Antioxidant effects of plant polyphenols: from protection of G protein signaling to prevention of age-related pathologies, Ann NY Acad Sci, 1095 (2007): 449-57.

D.W. Peterson, R.C. George, F. Scaramozzinot, N.E. LaPointe, R.A. Anderson, D.J. Graves, J. Lew, Cinnamon extract inhibits tau aggregation associated with Alzheimer's disease in vitro, J Alzheimer's Dis, 17 (2009): 585-97.

A. Frydam-Marom, A. Levin, D. Farfara, T. Benromano, R. Scherzer-Attali. Orally administered cinnamon corrects cognitive impairment in Alzheimer's disease animal models. PLoS One 6 (2011): e16584.

J. Wang, L. Ho, W. Zhao, K. Ono, C. Rosensweig et al., Grape-derived polyphenolics prevent AB oligomerization and attenuate cognitive deterioration in a mouse model of Alzheimer's disease, J Nuerosic 25 )2008): 6388-92.

N. Majlessi, S. Choopan, M. Hamalnejad, Z. Assizi, Amelioration of Amyloid B-Induced cognitive deficits Zataria multiflora Boiss. essential oil in a rat model of Alzheimer's disease, CNS neurosci, online.

S.C. Ho, T.H. Tsai, P.J. Tsai, C. C. Lin, Protective capacities of certain spices against peroxynitrite-mediated biomolecular damage, Food and Chem Toxicol 46 (2008): 920-8.

Y. Irie, Effects of eugenol on the Central Nervous System: Its possible application to treatment of Alzheimer's disease, depression, and Parkinson's disease, Curr. Bioactive Compunds 2 (2008): 57-68.

S. Chericoni, J.M. Prieto, P. Iacopini, P. Cioni, I. Morelli, In vitro activity of the essential oil of Cinnamomum zeylanicum and eugenol in peroxynitrite-induced oxidative processes, J. Agric Food Chem 53 (2005): 4762-5.

J.M. Prieto, P. Iacopini, P. Cioni, S. Chericoni, In vitro activity of the essential oils of Origanum vulgare, Satureja montana and their main constituents in peroxynitrite-induced oxidative processes, Food Chem 104 (2007): 889-905.

Y. Choi, H.S. Kim, K.Y. Shin, E.M. Kim, M. Kim, et al. Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models, Neuropyschopharm 32 (2007): 2393-404.

S. Schildknecht, R. Pape, N. Muller, M. Robotta, a. Marquardt, et al., Neuroprotection by minocycline caused by direct and specific scavenging of peroxynitrite, J Biol Chem 7 (2011): 4991-5002.

D.O. Kennedy and A.B. Scholey, The psychopharmacology of European herbs with cognition-enhancing properties, Curr Pharm Des 35 (2006): 4613-23.

D. Jimbo, Y. Kimura, M. Taniguchi, M. Inoue, K. Urakami, The effect of aromatherapy on patients with Alzheimer's disease, Psychogeriatrics 9 (2009): 173-9.

 

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  September 7, 2011

SUBJECT:  public input

Thank you for the opportunity to give suggestions regarding areas for inclusion into the National Plan for Alzheimer's Disease. I am a Board Certified Family Nurse Practitioner working in a Primary Care Internal Medicine practice and also the daughter of a person with Alzheimer's (late stage, diagnosed in 2000 with symptoms for at least 3 years prior to diagnosis).

  • I would like to see changes in the current care delivery when it is not possible for people affected by the disease to be primarily cared for by family members in their private homes. I believe the current wide spread choices of secured Assisted Living facilities or Long term Intermediate Care in Nursing Facilities are not the best solutions and we need to do a major overhaul in our traditional way of thinking about this type of housing and care. It is not cost effective and certainly does not result in high levels of satisfaction among persons with the disease or their loved ones.

  • Secondly I believe it is a travesty that we have allowed the federal funding of this illness to be so grossly inadequate that we have no significant answers about how we can prevent this illness and no hope of being able to offer treatments that will change the course of this disease. This illness is sapping a huge amount of funding from federal, state and private resources and yet our legislators can't commit to setting aside more than a pittance as compared to funding for other major illnesses. Please imagine the devastation of being diagnosed with AD and having no hope for cure or even remission of symptoms for any period of time but knowing the illness is progressive and fatal. When you look at the history of how concentrated and dedicated effort to research and development changed the outlook for those with HIV/AIDS you have to believe it IS possible to change how a person diagnosed with Alzheimer's could expect the rest of their life to unfold.

  • In this time of advanced electronic communication we should be able to conduct research without burdening people and their families with the need to travel long distances to be seen in major research centers. With the use of (and low intensity training of) qualified people in areas remote to research centers patients could easily undergo periodic evaluations and assessments using tools such as Skype and other Internet communications.

  • Continue to involve mass media resources such as newspapers, television and e-communications to inform and update the public of the realities of Alzheimer's. There has been too long a stigma attached to this illness that keeps even intelligent and otherwise forward thinking people and families from allowing any common knowledge of being diagnosed or affected with the illness. These same people would not hesitate to inform others if they were diagnosed with cancer or heart disease but act as if the diagnosis of Alzheimer's is shameful or an indicator of a personality weakness. It is time for AD to come "out of the closet"!

Thank you for the work you are undertaking and for being dedicated to providing real change for those Americans affected by Alzheimer's either personally or by witness of the illness with anger, sadness and hopelessness. We MUST change the impact of this disease for the millions of Americans who live it daily.

Jana PowellLutheran Medical GroupFort Wayne, IN

[Return to Public Comment Index or This Year's Table of Contents]

AUGUST 2011 COMMENTS

DATE:  August 29, 2011

SUBJECT:  Stopping Alzheimer's Completely

Alzheimer's has a very simple and avoidable cause: steam-refined polyunsaturated vegetable oils. I have been working this out since 1990.

The unsuspected vitamin E deficiency in these widely consumed food oils leads to brain cell membrane oxidation, that impairs the function of important enzymes that normally degrade the beta-amyloid protein. This protein therefore accumulates, incredibly slowly, in the brain of a regular consumer of deodorized vegetable seed oils.

After the age of 65 or so, accumulated beta-amyloidmay release highly toxic soluble aggregates (called oligomers), that are the immediate cause of synaptic toxicity and neuronal death.

That is exactly how over 5 million Americans have ended up with Alzheimer's disease.

My suggestion to your Government, is simply to legislate a requirement for all refined seed oils in your country to have any vitamin E deficit (usually 30%) corrected before distribution and sale. This simple step will also prevent ADHD occurring during pregnancy.

Already, this basic preventive step is under consideration by the Australian Government's Food Standards Authority, and we may be the first nation in the world to eliminate the twin brain epidemics of Alzheimer's and its prenatal partner, ADHD.

The USA--where vacuum steam-refining of seed oils was invented, in 1899 (David Wesson, Savannah)--has no shortage of brain power. What you lack is a safe level of vitamin E in your brain-oxidizing vegetable oils.

Can you fix the problem, and catch up with Australia?

When your Norfolk, Virginia shipyards were mass-producing Liberty ships for WW2 Atlantic convoys, a large banner was hung across the docks, saying:

IT CAN AND WILL BE DONE!!

Can you make vegetable oils safe? Can you do this too?

I attach a draft hypothesis for your inspection: I shall be trimming it down shortly, for submission to The Lancet, in London.

Here, at long last, is the direct cause of the disease: knowing this, we can easily prevent it.

Best To All,

Dr Robert Peers MBBS (Unimelb)General, Preventive & Nutritional Medical PractitionerNorth Carlton. Vic. Australia

ATTACHMENT:

Alzheimer's Disease And Attention Deficit Disorder May Share A Single Cause: Refined Vegetable Oil

By Dr Robert Peers, General Practitioner, North Carlton, MELBOURNE

In 1990 I identified a potential cause of typical late-onset Alzheimer's disease (AD), reporting my findings (a small case/control study) in a letter to the New Zealand Medical Journal [Ref 1] in 1993 (letter: "Alzheimer's Disease And Vegetable Oils"). I found that 12 cases of diagnosed AD had all consumed refined polyunsaturated seed oils for many years, contrasting with 20 age-matched control subjects with good memories, none of whom used such oils.

The reason for seeking a dietary cause was simple and compelling: AD had been seen to sometimes affect only one of a pair of identical twins [Ref 2], a striking finding that points strongly to some toxic or dietary cause. In addition, it was very unlikely to be caused by ageing itself, since the other twin was the same age, but remained unaffected in the long term; and because most older people do not in fact get the disease. I reasoned that those who were affected were somehow getting it from their diet, but how?

My initial reading even disclosed a likely dietary suspect: Professor Scott Henderson, an Australian research psychiatrist, cites in his 1988 AD review/hypothesis paper [Ref 3] a remarkable study [Ref 4] done by Professor Denham Harman in 1976, in Nebraska. Harman had a free radical theory of ageing, and knowing that both seed oils and the brain are rich in oxidizable polyunsaturated fatty acids, he wondered whether feeding safflower oil to his rats might cause free radical damage to the brain: it certainly did, as his rats soon lost their way in a maze. Furthermore, giving vitamin E to a new group of rats, fed the same oil, prevented these cognitive deficits--a finding that suggests that his oil, and perhaps other seed oils too, were low in vitamin E.

This work made me very curious about common vegetable seed oils, which were well known to reduce cholesterol and heart disease risk, but nobody had previously suspected them of actually causing a disease, and here they were evidently oxidizing the brain!

Soon after setting out on my library search for a dietary factor in 1990, I discovered that deodorized seed oils lose about a third of their antioxidant vitamin E during refining [Ref 5]--a potentially serious deficiency not seen in the soft margarines made from the same oils, which suffer polyunsaturate losses during hydrogenation, restoring the vitamin E/polyunsaturate balance. I realized immediately how important this deficiency would be in the brain, whose nerve cell membranes are very rich in highly oxidizable long-chain polyunsaturated fatty acids.

Since the main function of vitamin E is to protect these vulnerable essential fatty acids against oxidation, a low level of vitamin E in the nerve cell membrane would invite cerebral "lipid peroxidation". Oxidation of polyunsaturated fatty acids breaks up the fatty acid chain, and among the fragments are neurotoxic aldehyde molecules.

Oxidized Omega-6 fatty acids, in particular, release the highly reactive aldehyde 4-hydroxy nonenal (4-HNE), whose toxic effects on nerve synapses may account for the faulty memory seen in "Seed Oil Syndrome", described below. But 4-HNE does more than that: it activates a key enzyme involved in AD development, and may also--more importantly--mediate the impaired beta-amyloid clearance caused by cerebral lipid peroxidation.

Elena Tamagno, in Turin, has shown [Ref 6], in recent years, that 4- HNE indirectly activates the pivotal AD enzyme beta-secretase (BACE 1), a small rise in the activity of which causes a sharp increase in betaamyloid formation [S Cole, Ref 7]. Beta-amyloid is a peptide--a small protein fragment--that is the molecular cause of AD, as in rare genetic cases, where a gene mutation increases the production of a more toxic form of this peptide (the longer form, with 42 aminoacids, rather than the 40 residues seen in the much less toxic and more abundant form).

Although small amounts of this important protein fragment are produced in the normal brain, it is easily cleared away by degrading enzymes, and it can also exit the brain through the blood-brain barrier. However, people consuming refined vegetable oil will be forming increased beta-amyloid in abnormal oxidizing conditions, that may damage the clearance mechanism, resulting in progressive betapeptide accumulation and, ultimately, Alzheimer's disease.

One possibility is that lipid peroxidation products, like the same 4-HNE, might inhibit a key clearance enzyme, called Insulin-Degrading Enzyme (which also degrades beta-amyloid). In fact, an amyloid clearance problem is all that is required to cause AD, since even a mild over-production of beta-amyloid--as I postulate above--may still be successfully cleared.

So my theory does require a clearance defect, whether or not amyloid production is increased. And now, in 2009, Dr Y Nishida in Japan has shown [Ref 8] that by blocking vitamin E transport to mouse brain, lipid membrane peroxidation ensues, which impairs beta-amyloid clearance, by somehow reducing the expression of the gene coding for the above Insulin-Degrading Enzyme. Vitamin E-depleted seed oils, likewise, lower vitamin E levels in most tissues, causing lipid peroxidation [Y H Wang, Ref 9], which must include the brain, as shown by the early cognitive deficits seen in Harman's pioneering work (above), and their notable prevention with vitamin E.

Common Omega-6 seed oils, which are usually steam-deodorized, have been linked to cognitive decline in Holland [S Kalmijn, Ref 10], and also in Greece [D Psaltopoulou, Ref 11]), and to over double the risk of incident dementia (70% being AD) in the prospective "Three Cities Study" in France [P Barberger-Gateau, Ref 12]. Processed safflower oil, as discussed above, was shown many years ago (1976!) to cause memory faults in rats, which could be prevented with vitamin E. For some reason, Dr Harman did not alert the US food safety authorities to this alarming discovery.

Low vitamin E levels in corn, soya and safflower oils were first demonstrated by Dr David Herting in Rochester, New York State (Ref 5--see "herting d and 1963" on http://www.pubmed.gov, to find and download his free Journal of Nutrition paper). He concluded that widespread vitamin E deficiency would occur in populations consuming processed polyunsaturated seed oils. However, he did not realize the extreme peroxidation vulnerability of the brain and retina, where reduced vitamin E levels mean rapid lipid peroxidation of long-chain Omega-3 and Omega-6 fatty acids, in synapses and in retinal rod cell disc membranes. Had he known this, he could have predicted a new disease of the brain, with the further possibility of a new childhood brain disorder, arising in the fetal brain during pregnancy.

It was precisely these most vulnerable tissues that were tragically ignored in the landmark nutritional study, completed in 1960 in Illinois, on which current recommended daily intake of vitamin E is based [Ref 13]. Although lead investigator Dr Max Horwitt should have been aware of the brain's rich concentration of polyunsaturated fatty acids (mentioned, for example, in 1950s biochemistry texts), he judged vitamin E requirement exclusively by testing the fragility of red blood cell membranes in vitamin E-deprived human subjects, finding even greater fragility when the subjects were given vitamin E-stripped corn oil.

It did not occur to Horwitt to ask his vitamin E-deprived subjects about higher mental functions like memory or mood. Memory difficulties (and glare sensitivity and night-blindness from retinal damage) are likely to occur long before the red cell test becomes positive in response to gradual dietary vitamin E depletion, because the oxidizable polyunsaturated fatty acids are much less concentrated in the red cell membrane, than in retina and brain. Lipid peroxidation is a very rapid chain-reaction, that proceeds much faster in a vitamin E-depleted cell membrane containing a high concentration of polyunsaturated fatty acids, especially when those fatty acids--as in brain and retina--are of the long-chain variety, full of oxidizable double bonds.

To his credit, Horwitt did realize that the main function of vitamin E is to protect polyunsaturated fatty acids, so he based the recommended daily intake on the ratio of vitamin E to the intake of these fatty acids. He assumed that higher polyunsaturate intake, for example seed oil, would automatically mean higher vitamin E intake, but neglected the possibility that processed seed oils might lose some of this vitamin E during refining, and so cause some new disease specifically involving tissues prone to lipid peroxidation.

Indeed, he failed to pursue this possibility, even when he found that some members of staff at the Elgin Mental Hospital, who were not on the vitamin E deficient test diet, also had an abnormal red cell test. He did not ask himself how that could have happened, but could have taken a dietary history, and might have discovered that they were consumers of common vegetable oils, which could therefore have had something in common with his experimental stripped corn oil: low content of vitamin E. He may then have gone on to investigate the vitamin E content of such oils, and found it to be low--as David Herting found three years later, in 1963. Had Horwitt detected mild memory faults in consumers of refined seed oils, and set himself to do a little thinking, he could have nipped Alzheimer's in the bud, in 1960.

Any child, young person or adult consuming refined seed oils will report, if asked, memory problems, poor dark adaptation and glare sensitivity (photophobia--which is irreversible). I discovered this syndrome in general practice, and I call it Seed Oil Syndrome, and it probably reflects 4-HNE neurotoxicity in the synapses. Lipid peroxidation, which in the long term causes impaired beta-amyloid clearance, has early clinical effects due to synaptic damage: 4-HNE impairs neuronal glucose uptake, among other effects.

I have seen this hitherto undescribed syndrome in 100s of oil-using patients in family practice, over many years. The memory responds well to vitamin E (I sometimes add fish oil, for a faster response), except after the age of 50 or so, when subjects report long-term stability of memory, without actual improvement.

I am hoping that these cases, who, after some 20-30 years of refined oil exposure, may have a significant brain amyloid load, will not progress to AD, once off seed oils, and using olive oil, vitamin E and fish oil supplement. I also have some of them on Inositol, a seed sugar known to neutralize toxic Abeta oligomers [Ref 14] and improve language and orientation in established AD [Ref 15].

This simple glucose isomer, which is easily obtained in the diet (from grains, nuts, legumes, soymilk, cantaloupe and citrus), may prove to be a powerful weapon--along with cessation of refined-oil exposure-- in preventing Seed Oil Syndrome progressing slowly to Mild Cognitive Impairment and, ultimately, diagnosed AD. Given the extensive neuronal damage already evident in these two later stages, ultra-early prevention is now thought to be the only way to stop this disease, and nutrition--if it can do the job--is far preferable to preventive drugs.

From the public health angle, all cases of Seed Oil Syndrome--which is easily identified by symptoms and diet history--should change to olive oil (or any cold-pressed oil), eat a high.Inositol diet (even citrus juice is very rich in Inositol), and preferably take fish-oil capsules as well.

Saturated fat intake from butter, cream, cheese, fatty meat, pastries etc., must also be reduced, for it commonly causes co-morbid vascular dementia in the Alzheimer victim.

Inositol, given as a higher dose (5 gm/day) via supplement, also reverses anxiety disorder and depression [Ref 16], which affect perhaps 40% of AD cases. Anxiety alone doubles the risk of progressing from Mild Cognitive Impairment to AD [Ref 17], possibly because of cortisol-induced hippocampal damage, low Brain-Derived Neurotrophic Factor levels and poor hippocampal neurogenesis. Depression, often resulting from anxiety plus fatty diet, may increase inflammation--pro-inflammatory cytokines like Interleukin 1-beta may aggravate neuronal damage and increase stress axis activation even further. Anti-anxiety doses of Inositol also have a place here, by greatly decreasing stress-induced comfort-eating of fatty foods like chocolate, cheese, cakes and pastries [author's clinical observations].

One extra benefit from Inositol in brain disease is its unexpected antiageing effect [Ref 18], a possible example of which is the NIH 31 grain-rich mouse diet, that prolongs the median lifespan of female mice by 25% [Ref 19]. By altering the same genes that are altered by caloric restriction--including the key mitochondrial biogenesis gene PGC 1 alpha--Inositol is clearly a caloric restriction mimetic, with the same potential as dietary restriction to provide neurotrophic, antioxidant and energizing benefits in brain, as described by nutritional neuroscientist Mark Mattson [Ref 20]. Already, a multiple sclerosis animal model has been found to respond well to caloric restriction [Ref 21]: Inositol is a more practical intervention.

Variations in AD incidence around the world (low in West Africa, very high in Wadi Ara Arabs in Israel, 4 times higher in Pittsburgh than in Ballabgarh, Northern India) probably reflect local patterns of refined seed oil consumption. In Northern India, unrefined traditional oils are still very popular (eg. pungent mustard oil, crude peanut oil), and in the South there is mostly coconut oil and crude peanut oil--and possibly an even lower AD rate.

Refined oils are, however, encroaching on these traditional markets. Palm oil is the main cooking oil in Malaysia and Indonesia, where AD rates may be low, but in the US and Europe--and the Middle East too-- refined oils are the rule, apart from those people lucky enough to still use mainly olive oil. A study in Bari, Italy, some years ago, showed cognitive decline in older subjects not using olive oil [Ref 22]; they were apparently using common refined supermarket seed oils, which are widely used in Italy for frying.

An oil that causes a serious brain disease in adult life might also be expected to affect the fetal brain: when asking many oil-using patients about symptoms of Seed Oil Syndrome, I have noticed--as a family doctor--that young adults with the syndrome frequently have children with Attention Deficit Hyperactivity Disorder (ADHD). I proceeded to do a pilot case/control study on retrospective pregnancy diet, in 80 cases versus 80 controls.

Almost all (78) of the mothers of ADHD cases gave a history of regular consumption of refined seed oils during all or part of the pregnancy, often from fried takeaway food. All of these mothers had permanent glare sensitivity (most carried sunglasses, usually perched conveniently on their head), and those who still consumed these oils had ongoing memory difficulties and impaired night vision.

Similarly, I have met young adults with residual ADHD, who report that their mother, if still using such oils, and now in her mid- to lateforties, has an obvious memory problem. The Scottish breath-analysis scientist Brian Ross has found evidence of lipid peroxidation (increased breath ethane gas) in some children with ADHD [Ref 23], probably due to ongoing childhood exposure to the same refined seed oils that caused their condition during gestation.

In my child patients, such further exposure significantly worsens the ADHD, by increasing cognitive problems, mood issues, aggression and impulsivity--all of which improve rapidly by stopping the exposure and recommending fish oil, to assist synaptic recovery and plasticity. Not only does fish oil work faster when refined oils are first excluded from the diet (to prevent peroxidative destruction of the fish oil fatty acids in vitamin E-depleted synapses), but the synaptic benefits of fish oil may be greatly enhanced by adding two more "synaptic building blocksh--uridine and choline--as proposed for Alzheimer's, by nutritional neuroscientist Dr Richard Wurtman, at the Massachusets Institute of Technology [Ref 24]. Uridine sources include brewer's yeast, broccoli and beetroot, while choline is found in egg, chicken, lecithin and wheat germ. Wurtman's "Souvenaid" synapse-restoring mixture, which increases synaptic density and cognitive function in gerbil rats, does improve Alzheimer symptoms, and may work even better in the developing ADHD brain of a young child, to the extent that usual medications for the latter disorder may become obsolete, due to advances in brain nutrition.

I believe there is enough evidence available to conclude that deodorized seed oils are a major public health hazard, being directly responsible for ADHD, widespread Seed Oil Syndrome, and Alzheimer's disease. I notice in my clinic that Seed Oil Syndrome causes depression and irritability in anxious subjects, and aggravates ADHD in children and adolescents, promoting delinquency, serious aggression, antisocial behaviour, and substance abuse. These problems are now endemic in Western cities, and increasing world-wide.

Correction of all such brain peroxidation problems is very simple: to protect their citizens, while at the same time keeping these heartfriendly oils available, governments must be persuaded to pass laws requiring that all deodorized seed oils be rendered safe, with respect to their vitamin E content, before being sold. Natural vitamin E can 8 easily be recovered from the steam distillate at the food oil refinery, and replaced in the deodorized oil: or synthetic vitamin E could be used instead. Urgent action is required.

The highly desirable result of fixing this seed oil catastrophe would be to eliminate the twin epidemics of Alzheimer's and ADHD, along with the alarming antisocial effects of refined seed oils, as specified above.

REFERENCES

  1. Peers R. Alzheimer's disease and vegetable oils (letter). NZ Med J. 1993 Nov 10; 106(967): 481
  2. Davidson EA, Robertson EE. Alzheimer's disease with acne rosacea in one of identical twins. J Neurol Neurosurg Psychiatry. 1955 Feb; 18(1): 72-7
  3. . Henderson AS. The risk factors for Alzheimer's disease: a review and a hypothesis. Acta Psychiatr Scand. 1988 Sept; 78(3):257-75
  4. Harman D, Hendricks S, Eddy DE, Seibold J. Free radical theory of aging: effect of dietary fat on central nervous system function. J Amer Geriat Soc. 1976 Jul; 24(7): 301-7
  5. . Herting DC, Drury EJ. Vitamin E content of vegetable oils and fats. J Nutr. 1963 Dec; 81: 335-42
  6. Tamagno E, Parola M, Bardini P et al.. Beta-site APP cleaving enzyme up-regulation induced by 4-hydroxynonenal is mediated by stress-activated protein kinases. J Neurochem. 2005 Feb; 92(3): 628-36
  7. Cole SL, Vassar R. The Alzheimer's disease beta-secretase enzyme, BACE 1. Mol Neurodegener. 2007 Nov 15; 2: 22
  8. Nishida Y, Ito S, Ohtsuki S et al.. Depletion of vitamin E increases amyloid beta accumulation by decreasing its clearances from brain and blood in a mouse model of Alzheimer's disease. J Biol Chem. 2009 Nov 27; 284(48): 33400-8
  9. Wang YH, Leibholz J, Bryden WL, Fraser DR. Lipid peroxidation status as an index to evaluate the influence of dietary fats on vitamin E requirements of growing pigs. Br J Nutr. 1996 Jan; 75(1): 81-95
  10. Kalmijn S, Feskens EJ, Launer LJ, Kromhout D. Polyunsaturated fatty acids, antioxidants, and cognitive function in very old men. Am J Epidemiol. 1997 Jan 1; 145(1): 33-41
  11. Psaltopoulou T, Kyrozis A, Stathopoulos P et al.. Diet, physical activity and cognitive impairment among elders: the EPIC-Greece cohort (European Prospective 9 Investigation into Cancer and Nutrition). Public Health Nutr. 2008 Oct; 11(10): 1054-62
  12. Barberger-Gateau P, Raffaitin C, Letenneur L et al.. Dietary patterns and risk of dementia: the Three-Cities cohort study. Neurology. 2007 Nov 13; 69(20): 1921-30
  13. Horwitt MK. Vitamin E and lipid metabolism in man. Am J Clin Nutr. 1960 Jul- Aug; 8: 451-61
  14. McLaurin J, Golomb R, Jurewicz A et al.. Inositol stereoisomers stabilize an oligomeric aggregate of Alzheimer amyloid beta peptide and inhibit abeta-induced toxicity. J Biol Chem. 2000 Jun 16; 275(24): 18495-502
  15. Barak Y, Levine J, Glasman A et al.. Inositol treatment of Alzheimer's disease: a double-blind, crossover placebo-controlled trial. Prog Neuropsychopharmacol Biol Psychiatry. 1996 May; 20(4): 729-35
  16. Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol. 1997 May; 7(2): 147-55
  17. Palmer K, Berger AK, Monastero R et al.. Predictors of progression from mild cognitive impairment to Alzheimer's disease. Neurology. 2007 May 8; 68(19): 1596- 602
  18. Barger JL, Kayo T, Pugh TD et al.. Short-term consumption of a resveratrol- containing nutraceutical mixture mimics gene expression of long-term caloric restriction in mouse heart. PLoS One. 2008 Jun 4; 3(6): e2264
  19. Turturro A, Witt WW, Lewis S et al.. Growth curves and survival characteristics of the animals used in the biomarkers of aging program. J Gerontol. 1999; 54A: B492-B501
  20. Mattson MP. The impact of dietary energy on cognitive aging. Front Aging Neuroscience. 2010 Mar 8; 2:5
  21. Piccio L, Stark JL, Cross AH. Chronic caloric restriction attenuates experimental autoimmune encephalomyelitis. J Leukoc Biol. 2008 Oct; 84(4): 940-8
  22. Solfrizzi V, Panza F, Torres F et al.. High monounsaturated fatty acids intake protects against age-related cognitive decline. Neurology. 1999 May 12; 52(8): 1563-9
  23. Ross BM, McKenzie I, Glen I, Bennett CP. Increased levels of ethane, a non- invasive marker of n-3 fatty acid oxidation, in breath of children with Attention Deficit Hyperactivity Disorder. Nutr Neurosci. 2003 Oct; 6(5): 277-81
  24. Wurtman RJ, Cansev M, Ulus IH. Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phophatides. J Nutr Health Aging. 2009 Mar; 13(3): 189-97

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  August 29, 2011

SUBJECT:  Suggestion for Alzheimer research

I think that the most urgent problem in Alzheimer's research is the need for a soul-searching by policymakers for a correct perception of the disease.

Alzheimer research has been misled by hypes and illusions for too long. We believe that the ultimate strategy to delay it and ameliorate its social impact will take two basic approaches. First, motivate society as a whole to supports the elderly for better social connections and healthy lifestyles; and second, develop medications to extend the lifespan of old neurons by activating their lifeline metabolisms, rather than "inhibiting" the farfetched "causal" factors as widely believed today.

Please see our recent article (attached) in which the rationale for this strategy is discussed.

Thank you for sharing this letter to the members of the NAPA Advisory Council

Respectfully,

Ming Chen, Ph.D.Associate Professor and director of Aging Research LaboratoryBay Pines VA Medical Center and University of South Florida

ATTACHMENT:   Alzheimer Truth.pdf

Available as separate links:
Scientific Truth or False Hope? Understanding Alzheimer's Disease from an Aging Perspective Perspective: Scientific Truth or False Hope? Understanding Alzheimer’s Disease from an Aging Perspective

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  August 25, 2011

SUBJECT:  Alzheimer's advisory committee questions and information

I have two questions: will there be public comment at any or all of the advisory council meetings and what would be the best way to communicate with members of the committee?

Based on animal model studies, clinical trials, and case studies (including my mother), I know how to treat this disease and likely how to delay its onset. In the hypothesis, you will find references that show that peroxynitrite-mediated damage is widespread in Alzheimer's disease and that this damage can partially be corrected with peroxynitrite scavengers. Some of the most effective scavengers are methoxyphenols (eugenol,thymol, and carvacrol) in various essential oils (such as cinnamon leaf, clove, oregano, thyme, rosemary, and sage) in part because they can be inhaled directly into to the part of the brain affected by Alzheimer's disease: the hippocampus.

With some help from this committee, it is likely that Alzheimer's disease could be effectively treated within this next year.

Best Regards,

Lane Simonian

ATTACHMENT:     img005.jpg   img007.jpg

Available as separate links:
Effect of Aromatherapy on Patients with Alzheimer's Disease Effect of Aromatherapy on Patients with Alzheimer's Disease
Aromatherapy in the Treatment of Alzheimer's Disease Aromatherapy in the Treatment of Alzheimer's Disease

Hypothesis for Alzheimer's Disease

The three factors which increase the risk for Alzheimer's disease are high levels of myo-inositol (a precursor to phosphatidylinostiol 4, 5 biphosphate), increased phospholipase C gamma activity (whose substrate is phosphatidylinositol 4, 5 biphosphate) and the inhibition of the phosphatidylinositol 3/AKT pathway (the PI3 kinase converts phosphatidylinostiol 4,5 biphosphate into phosphatidylinositol 3, 4, 5 triphosphate). Factors which increase myo-inositol levels are high glucose levels (due to the conversion of glucose 6-phosphate into myo-inositol), high blood pressure (due to the sodium/myo-inositol cotransporter), and Down syndrome (because people with Down syndrome have an extra chromosome containing the sodium/myo-inositol transporter). Factors which reduce levels of myo-inositol are certain blood pressure medications, certain diabetes medications, estrogen, tamoxifen, lithium, and scyllo-inositol. Factors that increase phospholipase C gamma are glucose, estrogen, and angiotensin II (a cause of high blood pressure). Factors which lower phospholipase C gamma activity are fish oil (and other polyunsaturated fats) and phenols in various fruits, vegetables, spices, and essential oils. Factors that prevent or inhibit the activation of the PI3 kinase/AKT pathway are presenilin gene mutations, APOE4, and bisphosphonate osteoporosis drugs. Insulin, insulin-like growth factor, and drugs which increase high density lipids can to a limited degree stimulate this pathway. These are the main risk factors and preventative measures for Alzheimer's diseas

e Phospholipase C gamma increases the release of calcium from the endoplasmic reticulum (via inositol 1, 4, 5 triphosphate) which in turn stimulates Protein Kinase C. Protein Kinase C processes the amyloid precursor protein and a calcium dependent enzyme cleaves this protein to form amyloid plaques. Phospholipase C gamma exports zinc and zinc and copper are entombed in the amyloid plaques. This results in higher levels of homocysteine and a decline in the superoxidase dismutase which converts the superoxide anion into hydrogen peroxide. Protein kinase C increases choline uptake (and phospholipase C beta) and phospholipase C gamma increasing the number of plaques created. Homocysteine via Protein Kinase C increases the production of the superoxide anion and inducible nitric oxide. The two combine to form peroxynitrites.

The effects of peroxynitrites are as follows:

Peroxynitrites lower levels of intracellular magnesium which allows more calcium into the cells via the now open gate of the NMDA receptor.

Peroxynitrites cause lipid peroxidation (including the final product of lipid peroxidation--HNE)

The combination of peroxynitrites, HNE, and calcium influx leads to neuronal cell death. Peroxynitrites oxidize g-protein coupled receptors and nitrate tyrosine. The result is the hyperphosphorylation of tau proteins. Moreover, peroxynitrites nitrate tau proteins preventing them from being reconstituted for proper neurotransmission.

Peroxynitrites oxidize choline transport systems, muscarinic receptors (a g protein-coupled receptor involved in the uptake of choline), and the enzyme choline acetyltransferase, thus resulting in a critical shortage of acetylcholine which is needed for the retrieval of short-term memories.

Peroxynitrites oxidize a series of other g-protein coupled receptors including olfactory, serotonin, and dopamine receptors. The results respectively are impaired smell, poor sleep and depression, and lethargy and apathy.

Peroxynitrites oxidize glucose transporters resulting in a lack of energy and focus.

Peroxynitrites can be scavenged using phenolic compounds (one or more OH groups). Phenols in essential oils can be breathed directly into the hippocampus via aromatherapy. They accomplish the following conversion (ONOO- + 2H+ + 2 electrons-->NO2- + H2 0). Essential oils add hydrogen back to g-protein coupled receptors and partially reverse the nitration of tyrosine (including tyrosine residues on tau proteins). They thus partially reverse many if not all of the symptoms of Alzheimer's disease.

Bibliography for Alzheimer's Disease

Myo-Inositol and Alzheimer's Disease

M. Catani, P. Mecocci, R. Tarducci, R. Howard, G.P. Pelliccioli, E. Mariani, et al. Proton magnetic resonance spectroscopy reveals similar white matter biochemical changes in patients with chronic hypertension and early Alzheimer's disease, J Am Geriatr Soc 50 (2002): 1707-10.

G. Hauser and V.N. Finelli, The biosynthesis of free and phosphatide myo-inositol from glucose by mammalian tissue slices, J of Biol Chem 238 (1963): 3224-8.

W Huang. G.E. Alexander, E.M. Daly, H.U. Shetty, J.S. Krasuski, et al., High brain myo-Inositol levels in the predementia phase of Alzheimer's disease in adults with Down's Syndrome: A 1H MRS study, J Clin Invest 95 (1995): 542-6.

T. Ernst, L. Chang, D. Cooray, C. Salcador, J. Jovichich, I. Walot, et al., The effects of tamoxifen and estrogen on brain metabolism in elderly women, J Natl Cancer Inst 94 (2002): 592-7.

A. J. Harwood, Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited, Mol Psychiat 10 (2005): 117-25.

J.D. Moyer, N. Malinowski, E.A. Napier, J. Strong, Uptake and metabolism of myo-inositol by L1210 leukemia cells, Biochem. J 254 (1988): 95-100.

Phospholipase C gamma [y] and Alzheimer's Disease

Z. Deqing, H. Dhillon, M.R. Prasa, W.R. Markesbery, Regional levels of brain phospholipase C [y] in Alzheimer's disease, Brain Res 811 (1998): 161-5.

Y. Okuda, H.J. Adrogue, T. Nakajima, M. Mizutani, M. Asano, et al., Increased production of PDGF by angiotensin and high glucose in human vascular endothelium, Life Sci 59 (1996): 1455-61.

R. Graber, C. Sumida, G. Vallette, E.A. Nunez, Rapid and long-term effects of 17ß-estradiol on PIP2-phospholipase C-specific activity of MCF-7 cells, Cell Sign 5 (1993): 181-6.

P. Sanderson and P.C. Calder, Dietary fish oil appears to prevent the activation of phospholipase C-y in lymphocytes, Biochem et Biophys, 1392 (1998): 300-08.

S. Godichaud, K. Si-Tayeb, N. Auge, A. Desmouliere, C. Balabaud, et al., The grape-derived polyphenol resveratrol differentially affects epidermal and platelet .derived growth factor signaling in human liver myofibroblasts, Internat J Biochem and Cell Biol 38 (2006): 629-37.

G.M. Cole, G.P. Kim, F. Yang, B. Teter, A. Begum, et al., Prevention of Alzheimer's disease: Omega-3 fatty acid and phenolic anti-oxidant interventions, Neurobiol Aging (2005): 133-6.

M.A. Kang, S.Y. Yun, J. Won, Rosmarinic acid inhibits CA[2+]-dependent pathways of T-cell antigen receptor-mediated signaling by inhibiting the PLC-y1 and Itk activity, Blood 101 (2003): 3534-42.

Inhibition of PI3 kinase/Akt Pathway and Alzheimer's Disease

L. Baki, J. Shioi, P. Wen, Z. Shao, A. Schwarsman, M Gama-Sosa, et al., PS1 activates PI3K inhibiting GSK-3 activity and tau hyperphosphorylation: effect of FAD mutations, EMBO J 23 (2004): 2586-96.

R. Dekroon, J.B.Robineete, A.B. Hjelmenland, E. Wiggins, M. Blackwell, M. Mihovilovic, et al., APOE4-VLDL inhibits the HDL-activated phosphatidylinositol 3-kinase/Akt pathway via the phosphoinositol phosphotase SHIP2, Circ Res 99 (2006): 829.

R. Inoue, N.A. Matsuki, G. Jing, T. Kanematsu, K. Abe, M. Hirata. The inhibitory effect of alendronate, a nitrogen-containing bisphosphonate on the PI3K-Akt-NFkB pathway in osteosarcoma cells, Brit J Pharmacol 146 (2005): 633-41.

The Disease Process

J.D. Buxbaum, A.A. Ruefli, C.A. Parker, A.M. Cypess, P. Greengard, Calcium regulates the processing of the Alzheimer's amyloid protein precursor in a protein kinase C-independent manner, PNAS 91 (1994): 4489-93.

S. Jansen, J. Arning, D. Beyersmann, Zinc homeostasis in C6 glioma cells: phospholipase C activity regulates cellular zinc export, Bio Trace Elem Res 108 (2005): 87-104.

M.A. Carluccio, M.A. Ancora, M. Massaro, M. Carluccio, E. Scoditti, et al., Homocysteine induces VCAM-1 gene expression through NF-kB and NAD(P)H oxidase activation: protective role of Mediterranean diet polyphenolic antioxidants, Am J Physiol Heart Circ Physiol 293 (2007): 2344-54.

Peroxynitrites in Alzheimer's Disease

M.A. Smith, P.L. Richey Harris, L.M. Sayre, J.S. Beckman, G. Perry, Widespread peroxynitrite-mediated damage in Alzheimer's disease, J Neurosci 17 (1997): 2653-7.

J. Li, W. Li, Wi. Liu, B.T. Altura, Peroxynitrite induces apoptosis and decline in intracellular free Mg with concomitant elevation in [Ca2+] in rat aortic smooth muscle cells; possible roles of extracellular and intracellular magnesium ions in peroxynitrite-induced cell death, Drug Metabol Lett 1 (2007): 85-9.

R. Radi, J.S. Beckman, K.H. Bush, B.A. Freeman, Peroxynitrite-induced lipid peroxidation: the cytotoxic potential of superoxide and nitric oxide, Arch Biochem Biophys 288 (1991): 481-7.

H.L. Viera, A.S.Belzacq, D. Haurzi, F. Bernassola, I. Cohen, E. Jacotot, et al., The adenine nucleotide translocator: a target of nitric oxide, peroxnitrite, and 4-hydroxynonenal, Oncogene 20 (2001): 4305-16.

R. Radi, J.S. Beckman, K.H. Bush, B.A. Freeman, Peroxynitrite oxidation of sulfhydryls. The cytotoxic potential of superoxide and nitric oxide. J Biol Chem 266 (1991): 4244-50.

M.R. Reynolds, J.F. Reyes, Y. Fu, E. H. Bigio, A.L. Guillozet-Bongaarts, R.W. Berry, et al., Tau nitration occurs at tyrosine 29 in the fibrillar lesions of Alzheimer's disease and other taupathies 26 (2006): 10636-45.

L. Guermonprez, C. Ducrocq, Y.M. Gaudry-Tlarmain, Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrites are differentially prevented by antioxidants, Mol Parmocol 60 (2001): 838-46.

The Treatment of Alzheimer's Disease

T. Alkam, A. Nitta, H. Mozguchi, A. Itoh, T. Nabeshima, A natural scavenger of peroxynitrites, rosmarinic acid protects against impairment of memory induced Aß, Behav Br Res 180 (2007): 139-145.

M.R. al-Sereiti, K.M. Abu-Amer, P. Sen, Pharamacology of rosemary (Rosmarinus officinalis Linn.) and its therapeutic potentials, Indian J Exp Biol, 37 (1999): 124-30.

H.R. Choi, J.S. Choi, Y.N. Han, S.J. Bai, H.Y. Chung, Peroxynitrite scavenging of herb extracts, Phytotherap Res 16 (2002): 364-7.

V. Zilmer, M. Zilmer, K. Zilmer, N. Bogdanovic, E. Karelson, Antioxidant effects of plant polyphenols: from protection of G protein signaling to prevention of age-related pathologies, Ann NY Acad Sci, 1095 (2007): 449-57.

D.W. Peterson, R.C. George, F. Scaramozzinot, N.E. LaPointe, R.A. Anderson, D.J. Graves, J. Lew, Cinnamon extract inhibits tau aggregation associated with Alzheimer's disease in vitro, J Alzheimer's Dis, 17 (2009): 585-97.

A. Frydam-Marom, A. Levin, D. Farfara, T. Benromano, R. Scherzer-Attali. Orally administered cinnamon corrects cognitive impairment in Alzheimer's disease animal models. PLoS One 6 (2011): e16584.

J. Wang, L. Ho, W. Zhao, K. Ono, C. Rosensweig et al., Grape-derived polyphenolics prevent AB oligomerization and attenuate cognitive deterioration in a mouse model of Alzheimer's disease, J Nuerosic 25 )2008): 6388-92.

N. Majlessi, S. Choopan, M. Hamalnejad, Z. Assizi, Amelioration of Amyloid B-Induced cognitive deficits Zataria multiflora Boiss. essential oil in a rat model of Alzheimer's disease, CNS neurosci, online.

S.C. Ho, T.H. Tsai, P.J. Tsai, C. C. Lin, Protective capacities of certain spices against peroxynitrite-mediated biomolecular damage, Food and Chem Toxicol 46 (2008): 920-8.

Y. Irie, Effects of eugenol on the Central Nervous System: Its possible application to treatment of Alzheimer's disease, depression, and Parkinson's disease, Curr. Bioactive Compunds 2 (2008): 57-68.

S. Chericoni, J.M. Prieto, P. Iacopini, P. Cioni, I. Morelli, In vitro activity of the essential oil of Cinnamomum zeylanicum and eugenol in peroxynitrite-induced oxidative processes, J. Agric Food Chem 53 (2005): 4762-5.

J.M. Prieto, P. Iacopini, P. Cioni, S. Chericoni, In vitro activity of the essential oils of Origanum vulgare, Satureja montana and their main constituents in peroxynitrite-induced oxidative processes, Food Chem 104 (2007): 889-905.

Y. Choi, H.S. Kim, K.Y. Shin, E.M. Kim, M. Kim, et al. Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models, Neuropyschopharm 32 (2007): 2393-404.

S. Schildknecht, R. Pape, N. Muller, M. Robotta, a. Marquardt, et al., Neuroprotection by minocycline caused by direct and specific scavenging of peroxynitrite, J Biol Chem 7 (2011): 4991-5002.

D.O. Kennedy and A.B. Scholey, The psychopharmacology of European herbs with cognition-enhancing properties, Curr Pharm Des 35 (2006): 4613-23.

D. Jimbo, Y. Kimura, M. Taniguchi, M. Inoue, K. Urakami, The effect of aromatherapy on patients with Alzheimer's disease, Psychogeriatrics 9 (2009): 173-9.

[Return to Public Comment Index or This Year's Table of Contents]

DATE:  August 24, 2011

SUBJECT:  Meeting Agenda: National Alzheimer's Project Advisory Council

I was a caregiver to my mother who recently passed in New York. My years as a caregiver was for the most part stressful and more so due to the everyday care issues that came up in connection with her home-care agency and home health aides.

I do not live in the US anymore but would like to be keep informed as to NAPAC agenda and advocacy goals.

Thank you

Cory Lemos

[Return to Public Comment Index or This Year's Table of Contents]

JUNE 2011 COMMENTS

DATE:  June 9, 2011

SUBJECT:  Advisory Council on Alzheimer's Research, Care, and Services

I am a retired public school principal (age 64) and a caregiver for my wife (age 65), who has Alzheimer's Disease (AD). I have written two articles that have recently been published in American Journal of Alzheimer's Disease & Other Dementias. "Alzheimer's and Baby Boomers" was published in their September, 2010 issue, and "Ten Things You Should Do When the Diagnosis is Alzheimer's" appeared in their March, 2011 issue. I also had a third article published, "Forget the Mental Status Test and Learn to Listen," as a lengthy Letter to the Editor in the May issue of Journal of Family Practice. These three articles were written to help doctors improve their process of diagnosis and treatment of AD patients ... and their caregivers ... based upon my experience to date. I am now writing a fourth article to educate the public on the urgent need to increase federal funding though NIH for research. I have appended a draft of that piece to the end of this email.

I respectfully request that your Advisory Council address the issues raised in my three articles, as well as in the attached draft. Aside from the need to increase AD research funding,

Thank you for your time and consideration.

Alzheimer's ... Our New Cancer?Allan Vann

Cancer is the second leading cause of death in this country. Earlier this year, the Centers for Disease Control reported that between 1971-2007, the number of cancer survivors in the United States grew tremendously due to "earlier detection, improved diagnostic methods, and more effective treatment," among other reasons. Furthermore, according to CDC, "about 1.1 million of the (cancer) survivors had lived with the diagnosis for more than 25 years."

Alzheimer's Disease (AD) is the sixth leading and fastest growing cause of death in this country, and the onlyone of the top ten causes with no means of prevention or cure. Unlike with cancer, CDC cannot report any AD survivors. None. Most people only live for 8-10 years after an AD diagnosis, and between 5-10% of those with Alzheimer's are still in their thirties, forties, and fifties when diagnosed.

Our country faces a huge AD crisis in the years ahead. More than 5 million Americans have already been diagnosed with AD, and with so many baby boomers now turning 65 each day this number is expected to triple in the next 30-40 years.

One politician seeking greater funding for AD research is Maine Senator Susan Collins. She noted that, "We spend one penny on research for every dollar the federal government spends on care for patients with Alzheimer's. That just doesn't make any sense." Care for Alzheimer's patients already costs this country nearly $200 billion a year and, according to Senator Collins, "If nothing is done to slow or stop the disease, Alzheimer's will cost the United States $20 trillion over the next 40 years."

This year, our National Institutes of Health (NIH) will allocate more than $6 billion for cancer research ... but less than $500 million for AD research ... just as was true last year. This doesn't make any sense. Despite the need to reduce overall federal spending, we must increase NIH funding for AD research. Aside from the human cost to AD patients, caregivers, and their families, current research spending is penny wise and dollar foolish. As Senator Collins suggested, without major breakthroughs in treating AD, let alone finding a cure, future long term costs to our Medicare system will be astronomical.

My wife was diagnosed with AD at age 63. No treatment or cure will arrive in time for her. But if our country begins to devote funding for AD research as we have for cancer, then perhaps one day some people will be able to say that they are AD survivors. And perhaps our health care system will be that much further away from bankruptcy.

Allan Vann, Ed.DCommack, NY


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