National Alzheimer's Project Act: Public Comments on Advisory Council Meeting, July 2017

• S. Blumrosen  |  07-27-2017
• J. Dorey  |  07-21-2017
• S. Fournier  |  07-22-2017
• M. Hogan  |  07-23-2017
• M. Janicki  |  07-19-2017
• I. Kremer  |  07-21-2017
• C. Laxton  |  07-21-2017

My father had a stroke in 2011, experienced a sharp decline in 2013, and passed away July 23, 2015. His death certificate lists Alzheimer's Disease (AD) as a cause of death, although there was no brain autopsy to make that determination.

I am not an officer or director of any organization focused on matters concerning AD. While taking care of my father, I did found a company to promote a product I, and other caregivers, found useful. The website is still available at http://www.247caregivingproducts.com.

My father, Alfred W. Blumrosen, the Thomas A. Cowan Distinguished Professor of Law, taught at Rutgers School of Law -- Newark for 46 years, 1955-2002.

He met and married my mother, Ruth Gerber Blumrosen, when they were students at the University of Michigan School of Law. She was one of five women students in their class, one of ten women students in the law school.

They graduated in 1953 and practiced law in the same office where Sol Blumrosen, my father's father, had practiced. Sol graduated from the University of Michigan Law School in 1913.

Following is a brief chronology to inform you about his life and work. Since my father and mother worked on many projects together, I will use their first names (Al and/or Ruth) for clarity:

1960 (approx.), Al was granted tenure and became a full professor.

1961, Al was a visiting professor at LSU, in Baton Rouge, Louisiana.

1963 (approx.), at the request of Sid Reitman, a Newark attorney appointed to the NJ Civil Rights Commission, Al's class studied and made recommendations concerning that agency.

1965, June (approx.), Al and Ruth were each early hires at the Equal Employment Opportunity Commission (EEOC). Eventually, Al became the EEOC's first Director of Federal State Relations and first Chief of Conciliations, for purposes of conciliating cases in which the Commission found reasonable cause to believe several employers in Alabama had violated Title VII, he was based in the Federal Building in Birmingham; Ruth was Acting Chief for Advice and Analysis and Acting Director of Compliance at the EEOC, and became Lecturer of Law and Assistant to the Dean of Howard University School of Law, Clyde Ferguson.

1968, Al was Special Attorney in the Civil Rights Division of the U.S. Department of Justice.

1969-71, Al was a Consultant to Assistant Secretary of Labor for Employment Standards, Arthur Fletcher, where he advised on regulations and procedures including OFCCP-Order No. 4 and a national program concerning the construction trades, the Philadelphia Plan.

1970, Al and Ruth were each a participant in the first International Labor Organization (ILO) conference behind the Iron Curtain, the 5th International Conference of Labor Law and Social Security. By that time, the ILO was part of the United Nations.

1970, Al published "Administrative Creativity: The First Year of the Equal Employment Opportunity Commission" in the George Washington Law Review.

1971, Al published Black Employment and the Law (Rutgers University Press).

1972-73, Al was Acting Director of the Michigan Department of Civil Rights.

1972, Al published "Strangers in Paradise: Griggs v. Duke Power Co. and the Concept of Employment Discrimination" in the Michigan Law Review. This article was cited in a U.S. Supreme Court decision handed down June 25, 2015, Texas Department of Housing and Community Affairs, et al. v. Inclusive Communities Project, Inc., et al (https://www.supremecourt.gov/opinions/14pdf/13-1371_m64o.pdf).

1977-79, Al was Consultant to EEOC Chair Eleanor Holmes Norton in connection with EEOC Reorganization, Uniform Guidelines on Employee Selection Procedures, Affirmative Action Guidelines, and procedures for processing individual and systemic cases. He resigned so Ruth could be Consultant to EEOC Chair Eleanor Holmes Norton on issues raised by workforce reductions and gender-based income inequality.

At that time, Al and Ruth started thinking about why Richard Henry Lee and Thomas Jefferson would want to revolt against Great Britain and began research on a book that was published 25 years later, Slave Nation: How Slavery United the Colonies and Sparked the American Revolution (Sourcebooks, 2005). The first chapter is about James Somerset and the Somerset Case.

1979-1982, Al was Of Counsel to the New York law firm, Kaye, Scholer, Fierman, Hays & Handler advising employers on equal opportunity matters; 1980-81, Ruth was Consultant on Equal Employment Opportunity, here at the Department of Health and Human Services.

1982, Al and Ruth were Counsel to mainly white female employees challenging a discriminatory layoff in Chrapliwy v. Uniroyal, 670 F.2d 760 (7th Cir. 1982) cert. denied, 103 S. Ct.2428 (1983).

1983, Al wrote "Six Conditions for Meaningful Self-Regulation" which won the Ross Essay Prize awarded by the American Bar Association. Later, Al learned that the judge of the competition was Judge Leon Higginbotham.

1985, Al was Counsel to the NAACP in NAACP v. Meese, 615 F. Supp. 200 (D.D.C) seeking an injunction against rescission of consent decrees involving affirmative action.

1986, Al published "Some Thoughts on Affirmative Action Here and in India: Galanter's Competing Equalities," Industrial Relations Law Journal, U.C. Berkeley Law School.

1989, Al was Counsel to the NAACP in Wards Cove Packing Co. v. Atonio, 109 S.Ct. 2115 (D.D.C) concerning the interpretation of Title VII of the Civil Rights Act.

1989, Al and Ruth were Counsel to the mainly white male employees seeking equal pay in Klask v. Northwest Airlines, 57 FEP Cases 1147, 1152 (D. Minn. 1989, 91).

1993, Al and Ruth were each Fulbright Scholars at Stellenbosch University in South Africa where they examined the usefulness of the U.S. experience with equal employment opportunity law in the post-apartheid period and, with Linda Human, published "An Affirmative Action Statute for Employment and Contracting: Some Proposals" in the South Africa industrial Law Journal (1994).

1995, Al was Advisor to the U.S. Department of Labor, which resulted in "How the Courts are Handling Reverse Discrimination Claims," Bureau of National Affairs, Daily Labor Report, March 23.

1995, Al and Ruth were each Resident Scholars at the Rockefeller Institute Conference and Study Center in Bellagio, Italy.

1998: Al and Ruth published "Downsizing and Employee Rights," 50 Rutgers Law Review 943.

1998-2004: Al and Ruth, with the benefit of a Ford Foundation grant administered by Rutgers, published "The Realities of Intentional Job Discrimination in Metropolitan America, 1999." 40 state reports and a national report compare, with statistical precision, the standard deviations of the workforce of each employer-establishment, by occupation, with the workforces of similar establishments in the same Metropolitan Statistical Area and industry, by occupation. Statisticians Don and Stacy Dale worked on the reports. Available at http://www.eeo1.com. My brother, Alex, and I worked with Al and Ruth on this project.

2004, Ruth died suddenly and unexpectedly in an auto accident.

2005, Slave Nation: How Slavery United the Colonies and Sparked the American Revolution was published by Sourcebooks. Alex and I worked with Al and Ruth on this project.

2005, Al and Alex published "Using Statistics to Measure Diversity Compliance by Establishing Deviations from Labor Market Practices -- A Model for Effective and Economic Regulation in the Global Computer Age."

2011, Al and I published "Restoring the Congressional Duty to Declare War," Rutgers Law Review.

2011, Al had a stroke which left him with "expressive aphasia," which meant that, as intellectual and articulate as he used to be, with great dedication to speech, physical and occupational therapy, he was unable to find all the words he wanted, when he wanted to use them. He could take in information through his senses and process that new information with his mind, but he could no longer express himself as fluently as before.

Even so, we began work on our next project, a book about Edward Coles. We wrote about Coles in one of the last chapters of Slave Nation, because it is noted by many historians that he challenged then former-President Thomas Jefferson to free their slaves together. Jefferson refused. Coles proceeded with his plan of emancipation and may have been the first plantation owner to free his slaves while he could have profited from them. We were into the fourth volume of Robert Caro's biography of LBJ when my father was no longer able to concentrate enough on the material to communicate, in any way, about it.

That project was shelved and I focused on being my father's 24/7 caregiver. I got to be so good at taking vitals, giving meds, and keeping my patient safe, germ and rash-free that the home health care professionals suggested I challenge the CNA exam.

Since my father passed away, I have been administering his estate and developing a plan to outline our book about Edward Coles. Recently, I found your website (https://aspe.hhs.gov/national-alzheimers-project-act) and found out about your quarterly meetings.

I am grateful that our nation is taking a comprehensive interest in all of the elements concerning issues related to Alzheimer's Disease and I am especially appreciative of your concern for the needs of caregivers, whether professional or family-volunteer.

Thank you for letting me "pay it forward" by sharing the following top-of-mind comments. Perhaps they will be useful to you and others who are working to efficiently marshal and focus our limited resources on matters concerning AD.

My father chose to "age-in-place" and asked me to take care of him at home in Bonita Springs, Lee County, Florida, as long as I was able. I agreed.

Home Health Care

The greatest help to me, and to my father, were the home health-care workers -- nurses, CNAs and therapists (speech, occupational, and physical).

Under Medicare, they were available only after a hospital stay of at least three days, and only as long as there was opportunity for improvement. I hope this national effort will spend some time and expend some resources:

1. Figuring out ways to provide the connection and services of home health care -- without the pre-requisite of a hospital stay and, in appropriate situations, without the requirement that there be room for improvement, perhaps with the removal of speech, physical and occupational therapy and the retention of nursing and CNA services, and
2. Improving and standardizing the best practices of professionals providing home health care. In our experience, some excelled -- both at the technical aspects of their job and also in approaching people with Alzheimer's Disease -- and some did not do their jobs well. Medicare pays the same to the home health care agencies (I think) but it matters who comes to the house. Therapists, CNAs and nurses are not, yet, fungible in the basic performance of their duties.

    

Brain Autopsies

During my father's last days, many people spoke with us -- hospice, doctors, etc. No one said anything about brain autopsies.

I would like to suggest that someone specific in the health care setting be tasked with informing the health care proxy about the availability of brain autopsies.

I have since learned that Medicare considers the payment for brain autopsies to be included in the cost of a hospital stay, and some hospitals disagree. I hope this has been, or will be, clarified.

I know, for my own peace of mind, I would have liked a definitive diagnosis of AD, which -- at that time -- could only be done with a brain autopsy that revealed whether there were plaques and tangles, or there was something else that mimicked the symptoms of AD.

Based on conversations with Dr. Frederick Schaerf in Ft. Myers, principal investigator and founder of the Neuropsychiatric Research Center of Southwest Florida, I assume that it would be helpful to the medical community to have many more brain autopsies that could provide more data-points about the plaque and tangles, amyloid and tau proteins, in the brain.

I would suggest some consideration of ways to ease the flow of information to health care proxies about brain autopsies, as well as clarification to hospitals that they are expected to perform brain autopsies at no additional cost to the family, the caregiver or the taxpayers.

Perhaps hospitals could be required to submit a small portion of their per diem to a national trust which would save and combine such deposits for the designated purpose of performing brain autopsies. This way, the full cost of a brain autopsy would not have to be borne by the last hospital where a decedent happened to be an in-patient. The cost would be spread over every hospital that charged Medicare for treating a patient with AD.

Research

Shortly before my father passed away, I learned there is research being done on the use of sonogram technology to "cure" Alzheimers. See, for example, http://www.sciencealert.com/new-alzheimer-s-treatment-fully-restores-memory-function.

As you know, sonograms and ultra-sound have been approved for other uses in the United States, for many years and, I have been told, that the technology could be used for this purpose if a doctor was courageous enough. Perhaps such courage could be strengthened with laws protecting doctors from liability for the creative use of current technology (1) with patients who are certified to be in the last stages of life and (2) with the health proxy's consent.

My father could not be more dead than he is now, if a doctor had tried a new use of an approved technology on him. And, he would have made one last contribution to society. I am proud of him for the work he did while active, for his courage in fighting to re-learn skills we took for granted like talking, and for his fight for life. He was reaching for his last gasp of air in the hands of an ambulance attendant and did not go gently into the night. It would have extended my reasons to be proud if we could have furthered Alzheimer's research by trying non-invasive non-pharmaceutical ways to deal with his challenges and our situation.

Alternatives or Supplements to Pharmaceuticals

One time my father was in a small well-respected rehabilitation facility after a hospitalization in Naples, Florida. Rehab, there, is short-term and intense. It requires a certain amount of concentration during the day. My father would get anxious at night and receive medication to calm him. But, that resulted in his being sleepy the next day, which interfered with his therapies.

I suggested that the facility try what they talk about in their beautiful four-color brochure and take an alternative holistic approach by using aromatherapy. When I arrived for visiting hours that evening, they had sprayed his pillow with lavender. He slept well that night, needed less attention from the nursing staff, and was more awake the next day.

I wonder whether non-pharmaceutical solutions (which, I imagine are typically lower cost) are receiving attention equal to pharmaceutical solutions.

AD Mimics

After the experience with my advocacy for my father, one of the head nurses talked with me. There was an article in the April 2014 AARP Bulletin by Margery D. Rosen, "Am I Losing My Mind: Conditions that Mimic Dementia," that says over 100 disorders can mimic AD. The article highlights:

• Normal pressure encephalitis (NPE),
• Medications,
• Depression or another mental health disorder,
• Urinary tract infection (UTI), and
• Thyroid.

   

The nurse explained that there can be difficulties in determining exactly what is producing the symptoms of Alzheimer's.

Perhaps there could be further study and the development of programming, best practices and information for the public, including untrained and unlicensed family caregivers, about ways to filter out symptoms that mimic AD.

I showed the article to my father's neurologist, a dedicated doctor. He set up an appointment with someone who gives tests. I, as someone who was not going to be the subject of the test and was the subject's health proxy, inquired about the nature of the test. The tester was opaque; she would tell me nothing more than the doctor would be able to make a definitive diagnosis of AD, which every article I read said was impossible without a brain autopsy.

I suggest that "experts" be trained and required to explain what they are about to do, in plain language that the health care proxy can understand, so the health care proxy can make an informed decision.

Alzheimer's Village

The nurse at the rehab center also told me she had heard on Facebook about an "Alzheimer's Village." I found there is one. It is called Hogewey, a small village in Weesp, the Netherlands, where every resident has severe dementia (https://www.youtube.com/watch?v=LwiOBlyWpko). Hogewey is specially built, with the intention of maintaining strong connections with the interests and thought patterns of people who show symptoms of AD, while providing a safe and supportive place to live.

It is called a village because it has different areas for different interests. Recognizing that people develop circles of friends with similar interests, Hogewey connects someone with a strong interest in sports, for example, with other people who are interested in sports.

In our experience, living in a place that was familiar to my father and focusing on the work of writing about Edward Coles probably kept my father engaged much longer than if he were in an institution with few touchstones to his personal experience and memories, and little intellectual stimulation.

I saw support for this when my father was in another well-respected rehab facility. They sat people with similar interests or backgrounds at the same table for dinner. Our dinner companions were more engaged in conversation and aware of their circumstances than those in facilities where I would have dinner with my father and the dining room staff was not purposeful and intentional about putting people together who had things to talk about.

The rehab nurse thought there could be room on or near the NCH campus for such a village. Perhaps, nationally, there could be incentives for the study and development of such people-oriented living situations that adjust to activities a patient prefers in their daily life rather than expecting a patient to fit into an institution's routine and "blaming" the patient for not carrying on a pre-determined set of activities in their daily life.

Finally, modern technology and last stages of life.

To return to my anecdote about the use of sonogram technology, according to news releases the principal investigators are at the University of Queensland in Brisbane, Australia. They work with several labs in other places of the world. I tried to email with them, but there was not enough time.

Apparently, the work of the researchers continues, using focused ultra-sound in combination with "microbubbles" to temporarily open the blood brain barrier and enhance delivery of anti-amyloidal antibodies directly to the brain (See, http://www.sciencealert.com/ultrasound-with-immunotherapy-could-be-used-to treat-alzheimer-s and http://www.fusfoundation.org).

This year, this technique has been used on humans. Research is progressing quickly. (http://www.medpagetoday.com/neurology/alzheimersdisease/64114).

It would be nice if there were:

1. A central place where untrained family caregivers could find verified information about the progress of research that is not tied to gatekeepers for the research studies. Perhaps the NIH website could be a source of information that has no interest in any particular path of research.
2. Consideration of conducting experimental research on people with less to lose, who are certifiably near the end of their lives. Families would more fully appreciate the miracle. And, if it doesn't work, the researchers will not unduly hasten the demise of the patient.

Thank you for the opportunity to once again address the Council.

For the past 6 years I have attempted to have a presence at and bring a voice to this forum as a representative of individuals with intellectual disabilities and dementia and their families. I have been driven to do so because of my late brother Bill who had DS, developed AD in his mid 40's and died in 2010 of aspiration pneumonia at age 49. Since his death I have remained determined to improve the quality of life for the ID population with AD and for their caregivers.

For 6 years I have been witness to topic specific NAPA Council agendas and detailed testimony from various arenas about the work that has been done to improve quality of life for those in the general population with ADRD and for their caregivers. I continue to request a quarterly session dedicated to the needs of the ID population who were originally included in Section 2H, populations disproportionately affected by AD. Such a session would be most advantageous as you look forward to a transition period and the arrival of a newly selected Advisory Council Leadership and Team who may bring to the table little or no background information about this special population.

In the course of the last seven years I believe that there has been increased awareness of issues related to those with ID and Dementia, especially those with DS and AD. More recently additional research dollars have been earmarked for research on the correlation of these two diseases with a focus on biomarkers that might help the general population as well.

There has been additional material made available for families on aging, ID/DS and dementia, generated by the NTG and NDSS along with the inclusion of info on the Alzheimer's Association website. A companion publication on DS and AD will soon be released by the NDSS. This work has been the result of a collaboration involving the NDSS, the Alzheimer's Association and the NTG. It is a long awaited and much needed resource. The ACL has identified and funded pilot programs in selected communities across the US. These have been designed to increase the knowledge base of agencies, care providers and family members.

Despite these efforts, individuals with ID experiencing further cognitive decline and their families and care providers face continued serious obstacles. These obstacles are voiced from all regions of the country in a monthly online support group for family members hosted by the NTG. These are the same obstacles repeatedly mentioned in public testimony at NAPA Council meetings over the course of the past 6 years.

They include:

• Limited awareness of or misunderstood risk factors for AD in the ID population
• Difficulty obtaining a differential diagnosis or accessing Physicians familiar with the ID population
• Limited access to Agencies with Skilled Direct Support Professionals familiar with ID and ADRD
• Trouble identifying and accessing resources in ID and Aging networks
• Underdeveloped resources that focus on quality of life for a person with ID and ADRD
• Lifelong caregivers who are aging and facing physical decline as family member needs increase
• Sibling/Compound caregivers, caring for parent, spouse or other family member simultaneously
• Decreased support networks as disability increases, especially in small communities and rural areas
• Limited residential alternatives when caregiving resources are depleted
• Lack of coordination of care
• Limited access to palliative and hospice care

As you look ahead to the Research Summit in October of 2017, I am hopeful that you will consider many of the afore-mentioned challenges faced by families.

However, as a lay person, my greatest fear is that there will be added lag time as areas of research are identified, studies conducted and the findings translated into actions that may possibly improve the quality of life for all people with ADRD and their caregivers.

Change cannot come soon enough for individuals with ID and ADRD and their families scattered around the US in both rural and urban settings. Each month when we meet on line or share an email, I hear in their many voices the same sense of desperation that I experienced more the 10 years ago. Their voiced desperation reinforces the fact that we have not come far enough, fast enough and need to be more action oriented in the immediate future. This is a population of individuals and most often lifetime caregivers that cannot be forgotten.

Thank you for the opportunity to address the Council today.

Seven Hills RI and the Project Partners involved with our project funded through would like to express appreciation to the Administration for Community Living or for the funding opportunity that Seven Hills RI received to address efforts to create a more dementia capable system of care for individuals with intellectual and developmental disabilities and dementia. We would also like to express our appreciation for the support of Erin Long and Sari Shuman, and to make available the newly published document Intellectual Disability and Dementia: A Caregiver's Resource Guide for Rhode Islanders.

Seven Hills also extends thanks to the collaborative partners of the National Task Group on Intellectual Disabilities and Dementia Practices (NTG), Alzheimer's Association of Rhode Island (AARI), Lt. Governor, Dan McKee and his staff, the RI Geriatric Education Center (RIGEC) at the University of RI (URI), and the families and agency personnel who served as focus group members and who provided their comments prior to the Resource Guide's publication. Without the help of each of these groups, this guide, and its dissemination, would not have been possible.

Our hope is that this Resource Guide will provide the foundation that caregivers need to begin the conversation in planning supports for the individuals you support. Additionally, we hope this Resource Guide will serve as a reference tool for other states to develop their state specific Guides and include them in their state plans that address Alzheimer's Disease and related dementias.

Intellectual Disability and Dementia: A Caregiver's Resource Guide for Rhode Islanders [Available as a separate link: https://aspe.hhs.gov/sites/default/files/private/pdf/257486/cmtach-SF1.pdf]

I am submitting herewith as a public comment to be read at the next meeting of the "Advisory Council on Alzheimer's Research, Care and Services" a manuscript entitled "Alzheimer's Hypothesis" as copied below and also attached hereto in pdf format.

The manuscript outlines a pathological hypothesis which offers a complete explanation for the development of Alzheimer's disease, compressed into a one page submission that can be read at the meeting within the allotted two minute limit for such public comments.

I have also attached two other items as supporting documentation which will allow you to better evaluate the validity of the hypothesis. in accordance with your procedure for public submissions this supporting documentation is not intended to be considered as a submission to the meeting.

I do not propose to attend the meeting, please confirm my understanding that the submission can be read to the meeting in my absence.

I am a retired professional engineer and have no organizational affiliation. On reading the submission you will realize that the pathology for Alzheimer's disease bears a resemblance to an engineered system and my hypothesis was developed on the basis of a system engineering study that correlated apparently unrelated findings in numerous published manuscripts.

Alzheimer's Hypothesis

This presentation offers a complete explanation for the development of Alzheimer's disease and identifies a possible way to reduce the incidence of Alzheimer's disease in future.

In a catechol-o-methyl transferase reaction norepinephrine released in the cortex of the brain breaks down elastic polymers in the walls of the arteries resulting in a gradual build-up of atherosclerosis in those arteries. The extent of atherosclerosis that has built up over many years significantly restricts the flow of blood through the arteries causing Alzheimer's brains shrink from a lack of nourishment in support of neuron activity and the beta amyloid deposits that form in Alzheimer's brains are the misfolded protein remnants of broken down polymers from the walls of the damaged arteries. Mental, physical and chemical types of stress all tend to promote the release of norepinephrine thus accelerating the build up of atherosclerosis for an increased risk of developing Alzheimer's disease during a person's lifetime.

Cerebrospinal fluid (CSF) is pumped through aquaporins wound in a covering spiral over the arteries in the brain and the pulsating elastic expansion and contraction of healthy arteries pressing against the covering of aquaporinins provides the pumping mechanism for the flow of CSF through the aquaporins and its circulation throughout the individual areas of the brain served by each artery. As atherosclerosis builds up in the arteries their walls harden and cause the pumping action for circulation of CSF to become reduced due to a loss of pulsating arterial expansion and contraction. The build-up of beta amyloid deposits in the brain also tends to obstruct the circulation of CSF; therefore, the circulation of CSF becomes compromised both by the build-up of beta amyloid deposits and by a steadily decreasing pumped volume of CSF through the aquaporins.

At the start of each activity cycle, neurons in the brain emit a K+ ion and thus acquire an internal negative electrical charge. During recovery from activation a neuron which still retains its negative internal electrical charge before achieving electrical equilibrium will undergo a seizure and be destroyed if it happens to capture a nearby K+ ion which has not been washed far enough away by the circulation of CSF. The circulation of CSF in healthy brains establishes a virtually negligible probability for the capture of K+ ions but the statistical probability for capture of K+ ions during recovery from activation increases exponentially in areas of the brain where the circulation of CSF becomes compromised. A compromised inadequate circulation of cerebrospinal fluid and the resulting destruction of neurons is the direct cause of Alzheimer's disease. The tau tangles that form in Alzheimer's brains are the remnants of destroyed neurons.

Brain plasticity is so effective in programming repairs which bypass destroyed neurons that the first symptoms of cognitive impairment only become apparent after too much extensive vascular damage and resulting neuron destruction has already taken place, making it impossible to effect a cure for the disease. However, the incidence of Alzheimer's disease could be greatly reduced in future by the development of a daily prophylactic therapy which would restrict the release of norepinephrine in the brain and slow down the build up of atherosclerosis in the intracranial arteries. Ideally, such a therapy should be commenced at an early age, typically before age 30. A small daily dosage of alpha blocker medication with supplements of vitamins D, B6, B12 and folic acid might possibly serve as such a prophylactic therapy. (Adding a beta blocker could possibly extend scope of the therapy to also reduce the incidence of type 2 diabetes and vascular disease.)

The level of plasma total homocysteine in the blood and of normetanephrine in the urine are biomarkers for the release of norepinephrine and also for a resulting increased risk of developing Alzheimer's disease in future. The development of a reasonably priced capability for monitoring such a biomarker would allow people to assess the effectiveness of the prophylactic therapy and to adjust their diet, lifestyle and medication etc to minimize the risk of developing Alzheimer's disease in future.

There are medications which promote the release of norepinephrine that should be identified and either shown on the label to have an associated Alzheimer's risk or removed from the market if their benefit does not justify the risk.

Pumping of CSF Through Aquaporins of the Brain

A study contribution by John D. Dorey

Results of a study by Maiken Nedergaard and Jeffrey Iliff as outlined in the following two pages describe the glyampic system of aquaporins that delivers cerebrospinal fluid (CSF) which circulates throughout the brain. The additional information provided below describes the pumping mechanism which promotes the flow of CSF through the aquaporins and how that pumping mechanism and the circulation of CSF becomes inhibited in areas of the brain where atherosclerosis develops in the walls of the intracranial arteries.

The CSF circulating to the brain is delivered through aquaporin pipes which form a sheath over the outer surface of the intracranial arteries that distribute blood within the brain. In healthy brains the arteries have elastic walls and are continuously undergoing cycles of expansion and contraction as spurts of blood pass through them under pressure from the pulsating pumping action of the heart and when the arteries expand they compress against the surrounding aquaporin pipes forcing spurts of the contained CSF to flow through the aquaporin pipes ahead of the advancing spurts of blood in the arteries, much like the process of squeezing toothpaste out of a tube. This mechanism is what circulates CSF throughout the brain.

Atherosclerosis is a condition where the walls of the intracranial arteries gradually harden and lose their elasticity and ability to expand and contract as necessary to circulate CSF through the brain. One purpose of CFS circulation is to cleanse waste matter from the brain however the absolutely vital purpose is that a good flow of CFS is required to maintain the statistical probability for excitotoxic destruction of neurons as a negligibly rare occurrence that the brain's plasticity can work around.

The study referenced below in bold type indicates that the statistical probability of excitotoxic neuron destruction increases enormously in areas of the brain where the circulation of CSF is significantly reduced. This would explain why atherosclerosis from damage to arteries by dopamine produced in the substantia nigra area of the brain results in Parkinson's disease and from damage to arteries by norepinephrine produced in the cortex of the brain results in Alzheimer's disease or dementia.

Delayed K+clearance associated with aquaporin-4 mislocation:
Phenotypic defects in brains of á-syntrophin-null mice.
Nov 11, 2003 - by Mahmood Amiry-Moghaddam, Professor of Medicine, University of Oslo
Proceedings of the National Academy of Sciences Vol. 100 No. 23
(The text of this study can be viewed on the Internet.)

Two possible secondary consequences of atherosclerosis in the intracranial arteries are:

The flow of blood through healthy arteries is facilitated by their elastic expansion and contraction and when the walls of the intracranial arteries lose their elasticity the flow of blood to provide oxygen and glucose in support of neuron activity becomes significantly reduced.

A healthy human brain continually produces about 20 Watts of heat within the close confines of the skull and the circulation of blood and CSF throughout the brain provides liquid cooling that removes heat from inside the skull and ensures that all parts of the brain are maintained at about the same ideal operating temperature. When the circulation of blood and CSF is curtailed there is a possibility of impaired operation if part of the brain is not maintained at its optimum operating temperature.

Scientists Discover Previously Unknown Cleansing System in Brain -- The Glymphatic System

Wednesday, August 15, 2012

A previously unrecognized system that drains waste from the brain at a rapid clip has been discovered by neuroscientists at the University of Rochester Medical Center. The findings were published online August 15 in Science Translational Medicine [http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.3003748].

The highly organized system acts like a series of pipes that piggyback on the brain's blood vessels, sort of a shadow plumbing system that seems to serve much the same function in the brain as the lymph system does in the rest of the body -- to drain away waste products.

"Waste clearance is of central importance to every organ, and there have been long-standing questions about how the brain gets rid of its waste," said Maiken Nedergaard, M.D., D.M.Sc. [http://www.urmc.rochester.edu/people/23788299-maiken-nedergaard], senior author of the paper and codirector of the University's Center for Translational Neuromedicine [http://www.urmc.rochester.edu/ctn/]. "This work shows that the brain is cleansing itself in a more organized way and on a much larger scale than has been realized previously.

"We're hopeful that these findings have implications for many conditions that involve the brain, such as traumatic brain injury, Alzheimer's disease, stroke, and Parkinson's disease," she added.

Nedergaard's team has dubbed the new system "the glymphatic system," since it acts much like the lymphatic system but is managed by brain cells known as glial cells. The team made the findings in mice, whose brains are remarkably similar to the human brain.

Scientists have known that cerebrospinal fluid or CSF plays an important role cleansing brain tissue, carrying away waste products and carrying nutrients to brain tissue through a process known as diffusion. The newly discovered system circulates CSF to every corner of the brain much more efficiently, through what scientists call bulk flow or convection.

"It's as if the brain has two garbage haulers -- a slow one that we've known about, and a fast one that we've just met," said Nedergaard. "Given the high rate of metabolism in the brain, and its exquisite sensitivity, it's not surprising that its mechanisms to rid itself of waste are more specialized and extensive than previously realized."

While the previously discovered system works more like a trickle, percolating CSF through brain tissue, the new system is under pressure, pushing large volumes of CSF through the brain each day to carry waste away more forcefully.

The glymphatic system is like a layer of piping that surrounds the brain's existing blood vessels. The team found that glial cells called astrocytes use projections known as "end feet" to form a network of conduits around the outsides of arteries and veins inside the brain -- similar to the way a canopy of tree branches along a well-wooded street might create a sort of channel above the roadway. Those end feet are filled with structures known as water channels or aquaporins, which move CSF through the brain. The team found that CSF is pumped into the brain along the channels that surround arteries, then washes through brain tissue before collecting in channels around veins and draining from the brain.

How has this system eluded the notice of scientists up to now?

The scientists say the system operates only when it's intact and operating in the living brain, making it very difficult to study for earlier scientists who could not directly visualize CSF flow in a live animal, and often had to study sections of brain tissue that had already died. To study the living, whole brain, the team used a technology known as two-photon microscopy, which allows scientists to look at the flow of blood, CSF and other substances in the brain of a living animal.

While a few scientists two or three decades ago hypothesized that CSF flow in the brain is more extensive than has been realized, they were unable to prove it because the technology to look at the system in a living animal did not exist at that time. "It's a hydraulic system," said Nedergaard. "Once you open it, you break the connections, and it cannot be studied. We are lucky enough to have technology now that allows us to study the system intact, to see it in operation."

First author Jeffrey Iliff, Ph.D. [http://www.linkedin.com/pub/jeffrey-iliff/47/856/a52], a research assistant professor in the Nedergaard lab, took an in-depth look at amyloid beta, the protein that accumulates in the brain of patients with Alzheimer's disease. He found that more than half the amyloid removed from the brain of a mouse under normal conditions is removed via the glymphatic system.

"Understanding how the brain copes with waste is critical. In every organ, waste clearance is as basic an issue as how nutrients are delivered. In the brain, it's an especially interesting subject, because in essentially all neurodegenerative diseases, including Alzheimer's disease, protein waste accumulates and eventually suffocates and kills the neuronal network of the brain," said Iliff.

"If the glymphatic system fails to cleanse the brain as it is meant to, either as a consequence of normal aging, or in response to brain injury, waste may begin to accumulate in the brain. This may be what is happening with amyloid deposits in Alzheimer's disease," said Iliff. "Perhaps increasing the activity of the glymphatic system might help prevent amyloid deposition from building up or could offer a new way to clean out buildups of the material in established Alzheimer's disease," he added.

In addition to Iliff and Nedergaard, other authors from Rochester include Minghuan Wang, Yonghong Liao, Benjamin Plogg, Weiguo Peng, Edward Vates, Rashid Deane, and Steven Goldman. Also contributing were Erlend Nagelhus and Georg Gundersen of the University of Oslo, and Helene Benveniste of the Health Science Center at Stony Brook University.

The work was funded by the National Institutes of Health (grant numbers R01NS078304 and R01NS078167), the U.S. Department of Defense, and the Harold and Leila Y. Mathers Charitable Foundation.

How to optimise your brain's waste disposal system

Aug 22, 2015

New research suggests that body posture during sleep may affect the efficiency of the brain's self-cleaning process

The human brain can be compared to something like a big, bustling city. It has workers, the neurons and glial cells which co-operate with each other to process information; it has offices, the clusters of cells that work together to achieve specific tasks; it has highways, the fibre bundles that transfer information across long distances; and it has centralised hubs, the densely interconnected nodes that integrate information from its distributed networks. Like any big city, the brain also produces large amounts of waste products, which have to be cleared away so that they do not clog up its delicate moving parts. Until very recently, though, we knew very little about how this happens. The brain's waste disposal system has now been identified. We now know that it operates while we sleep at night, just like the waste collectors in most big cities, and the latest research suggests that certain sleeping positions might make it more efficient.

Waste from the rest of the body is cleared away by the lymphatic system [http://www.cancerresearchuk.org/about-cancer/what-is-cancer/body-systems-and-cancer/the-lymphatic-system-and-cancer], which makes and transports a fluid called lymph. The lymphatic system is an important component of the immune system. Lymph contains white blood cells that can kill microbes and mop up their remains and other cellular debris. It is carried in branching vessels to every organ and body part, and passes through them, via the spaces between their cells, picking up waste materials. It is then drained, filtered, and recirculated.

The brain was thought to lack lymphatic vessels altogether, and so its waste disposal system proved to be far more elusive. Several years ago, however, Maiken Nedergaard [https://www.urmc.rochester.edu/labs/nedergaard-lab/] of the University of Rochester Medical Center and colleagues identified a system of hydraulic "pipes" [https://www.newscientist.com/article/dn22183-waste-disposal-network-discovered-in-the-brain/] running alongside blood vessels in the mouse brain. Using in vivo two-photon imaging to trace the movements of fluorescent markers, they showed that these vessels carry cerebrospinal fluid around the brain, and that the fluid enters inter-cellular spaces in the brain tissue, picking up waste [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551275/] on its way.

Nedergaard and her colleagues also discovered that proper function of these vessels depends on movements of water around the brain, which are carried out by glial cells called astrocytes, [https://www.theguardian.com/science/neurophilosophy/2013/mar/07/human-brain-cells-boost-mouse-memory] and therefore named them the glymphatic system. They went on to show that inter-cellular spaces expand by up to 60% in the brains of naturally sleeping and anaesthetised mice, and that this expansion drives the clearance of waste from the brain [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/] by facilitating the movements of lymph and water.

Last month, researchers from the University of Virginia reported the identification of lymphatic vessels in the central nervous system [https://www.nature.com/articles/nature14432.epdf?referrer_access_token= 73VNMajh-YctNTGco_XUj9RgN0jAjWel9jnR3ZoTv0PP9svrp_06Oir1YyDWe7ejvVLL2VbrH_EwNtYJfrQFs0e9-52wHfwKPwFmFnLP6V31OlM0nnYEmBXU_cERvmChguYSd02A9zDIMThkJLhI_iVl4f1FJO IZ7PnYDwSJ0ANlqQQ0LnUd3e_CFRU0mcDKYsPUDBoHrQFYKAyuXzHBsJfzRxH0ZsJuk50cmJ-Z0S2GOBquBoA09XaF-yZQO-PmnSWBFlT7TBPGHTyzhkDq_w==&tracking_referrer=www.theguardian.com]. They demonstrated that the lymphatic system extends into the dura mater, the thickest and outer-most of the three meningeal membranes that envelope the brain and spinal cord. These vessels run parallel to the major veins and arteries, and split to send branches deep into the brain's crevices. The researchers believe that they could be linked to the glymphatic system, and may be the second stage of the disposal mechanism, which would transport waste out of the brain and spinal cord altogether.

The latest study from Nedergaard's group, published [http://www.jneurosci.org/content/35/31/11034] in the Journal of Neuroscience earlier this month, shows that body posture affects the efficiency of the glymphatic system's waste clearance. Using fluorescence microscopy and radioactive tracing once again, they showed that drainage of the cerebrospinal fluid worked best in mice lying on their sides [http://www.jneurosci.org/content/35/31/11034] compared to those lying on their back or standing up.

The function of sleep was once deeply mysterious, but there's plenty of evidence that it is critical for memory consolidation, [https://www.theguardian.com/science/neurophilosophy/2014/jun/09/sleep-dendritic-spines-memory] and it would now seem to be required for the effective removal of waste from the brain, too. Although these studies were performed in mice, preliminary results suggest that lymphatic vessels are also present in the human brain and spinal cord, but further research will be needed to confirm that they actually constitute a working waste disposal system.

Eventually, the link to sleep could have important implications for the treatment of neurodegenerative diseases such as Alzheimer's and Parkinson's, all of which involve the build-up of misfolded proteins within and around nerve cells, because of a defective waste disposal system. Indeed, it is now seems clear that good sleep hygiene has a neuroprotective effect [https://www.theguardian.com/science/neurophilosophy/2014/sep/22/the-neuroprotective-lifestyle] and, in line with this, other research shows that sleep disturbances predict the onset of neurodegeneration. [https://www.theguardian.com/science/neurophilosophy/2013/may/22/dreaming-of-animals-and-other-warning-signs-of-neurodegeneration]

Sleeping on the side just happens to be the most popular sleeping posture for both mice and humans, and so this preference may have evolved to optimise the waste disposal system and thus ensure that the metropolis of the brain runs as effectively as possible.

References

Lee, H. et al. (2015). The Effect of Body Posture on Brain Glymphatic Transport. J. Neurosci, 35: 11034-44. DOI: 10.1523/JNEUROSCI.1625-15.2015. [http://www.jneurosci.org/content/35/31/11034]

Louveau, A., et al. (2015). Structural and functional features of central nervous system lymphatic vessels. Nature, 523: 337-41. DOI: 10.1038/nature14432. [https://www.nature.com/nature/journal/v523/n7560/full/nature14432.html]

Xu, L., et al. (2014). Sleep Drives Metabolite Clearance from the Adult Brain. Science, 342: 373-7. DOI: 10.1126/science.1241224. [Full text http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/]

Iliff, J., et al. (2013). A Paravascular Pathway Facilitates CSF Flow Through the Brain Parenchyma and the Clearance of Interstitial Solutes, Including Amyloid ß. Sci. Trans. Med., 4: 147ra111. DOI: 10.1126/scitranslmed.3003748. [Full text http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551275/]

Delayed K+ clearance associated with aquaporin-4 mislocalization: Phenotypic defects in brains of a-syntrophin-null mice, PNAS, 2003, Vol. 100, No. 23, pg 13615-13620 [Available as a separate link: https://aspe.hhs.gov/sites/default/files/private/pdf/257481/cmtach-JD1.pdf]

In today's meeting, the Advisory Council is focusing on research gaps and dementia prevention strategies. So it is particularly fitting that NIH will present its FY 2019 Bypass Budget for Alzheimer's Disease and Related Dementias. We remain optimistic that NIH laying out an ambitious research agenda and supporting highly meritorious science will continue to inspire bold funding support from Congress -- as has been the pattern in recent years. Our confidence was bolstered earlier this month when the House Appropriations Committee approved the draft FY 2018 Labor, Health and Human Services, and Education (LHHS) bill, which included a $400 million increase for NIA dementia research. As the Advisory Council knows, there has been significant progress in both NIH's bypass budget and its actual grant allocations to better support both social science and bench science so that we improve quality of life for people facing dementia now while seeking breakthroughs to prevent, modify or cure these diseases and disorders.

In the spirit of identifying research gaps, thank you again to the Advisory Council for your deep engagement in, and strong support for, the National Research Summit on Care, Services, and Supports for Persons with Dementia and Their Caregivers [https://aspe.hhs.gov/national-research-summit-care-services-and-supports-persons-dementia-and-their-caregivers]. I serve on the summit steering committee and we look forward to delivering findings and recommendations that will inform your next National Plan Update, and help both the public and private sectors improve research, and ultimately deliver tangible, transformative results for tens of millions people across this country.

I also would offer congratulations to all those who made possible the 2018 Alzheimer's Association International Conference. Each year, AAIC is a crown jewel in advancing both science and the understanding of science by the broader public. This year was no exception. We look forward to a time when science liberates us all from the shadows of dementia.

And to the entire Advisory Council, thank you for your leadership toward the 2017 National Plan Update. We look forward to its publication and welcome the opportunity to participate in its implementation.

My name is Mary Radnofsky. I'm a former college professor and have been living with dementia since 2005. I'm sorry not to be here today to deliver these remarks in person, but the date conflicted with another commitment. Since this is the last NAPA Advisory Council meeting before the National Research Summit in October, I appreciate the opportunity to provide comments.

Having conducted, taught, analyzed, and participated research studies for the past 30 years, I value the convening of a Research Summit. As a person living with dementia (PWD), based upon reading the Background Papers and other pre-Summit materials available online, I am, however, alarmed about the context and direction of this Summit whose focus is on the service, support and care needs of people like me and our care partners. The first Background Paper, "Research on Care Needs and Supportive Approaches for Persons with Dementia," starts with, "As the disease progresses, individuals with dementia become more dependent on others for assistance with daily activities. Ultimately, in advanced dementia, people with the disease need assistance with basic tasks, such as eating. Dementia reduces a person's cognitive function and ability to perform routine activities; it also is often associated with challenging behaviors. The psychosocial aspects of dementia often include depression, anxiety, and strain on family relationships."

Framing dementia in this context reduces the humanity of people with dementia to mere bodily functions and emotional difficulties. Stripped away are many vital and fundamental aspects of being human, including the need to be connected to others, feeling productive and having purpose, doing activities that bring satisfaction and joy, and maintaining self-sufficiency. Without understanding that these are vital aspects of living, is there any wonder emotional outcomes include depression, anxiety and strain on family relationships?

A stated goal of the National Research Summit is to identify what is known and what needs to be known about care, services and support for PWDs and CPs. What needs to be known is to expand the boundaries and horizons of the deficit-oriented, capacity-defined, negative attributes mindset. The barriers to well-being that lie outside these parameters, including the origins and effects of pervasive stigma, misperceptions and low expectations for people living with dementia, and mistaking dementia as one, homogenous condition need exploration. There are many types of dementia, so symptoms vary significantly from person to person, as does the progression. Yet we are not recognized as individuals with unique needs different from those of others.

In the 1960's, there was a major breakthrough in psychology with the Rosenthal and Jacobson study. The results of the study, commonly known as the Pgymalion Effect, found that reality can be positively or negatively influenced by the expectations and perspectives of others. Thus, if the focus is on functional deficits and negative attributes of people with dementia, that's what will be found. As an example of such negative perceptions of people with dementia, one of the six Summit sessions is titled, "Challenges in Involving Persons with Dementia as Study Participants." A positive perception would be "What Do Researchers Need to Know about Involving Persons with Dementia as Study Participants?" Such adjustments would go far in alleviating the misunderstandings and social stigma attached to people with dementia.

As a former Board member of the Dementia Alliance International, I have had the opportunity to speak with many PWDs and CPs all over the world, and to speak at the United Nations on the importance of including people with dementia in the conduct of research and policy. We universally need you to enable, rather than further disable, us. That is, we need to be included as equals to learn what is needed to be supported and accommodated.

Like you, I am a complex human being with feelings and emotions, ideas and opinions, social and spiritual needs, and even a sense of humor. These aspects of my life are not irrelevant or secondary to my physical capacity, but are indeed central to who I am. Marcel Proust famously said, "The real voyage of discovery consists not in seeking new landscapes, but in having new eyes." People living with dementia sorely need you to have new eyes and see a wider perspective on what is needed to support, accommodate and enable people living with the many forms of dementia!

I and Dr. Seth Keller are the co-chairs of the National Task Group on Intellectual Disabilities and Dementia Practices (NTG), a group formed in 2010 with a mission to advocate for people with intellectual disability and their families and other caregivers when an adult with intellectual disability is affected by dementia (http://www.aadmd.org/ntg). The NTG is an affiliate of the American Academy of Developmental Medicine and Dentistry and is associated with the Rehabilitation Research and Training Center on Developmental Disabilities and Health at the University of Illinois at Chicago.

NTG Activities on Information Development and Dissemination

What we wish to raise today concerns our efforts to create and disseminate information related to dementia and intellectual disabilities. We recognize, as does the Council, that much of the general public, health care professionals, and even workers in the field of intellectual disability, are relatively uninformed about the nuances of dementia and how it affects adults with intellectual disability, as well as their spouses, friends, and caregivers. In concert with colleagues within the Alzheimer's and other dementias, intellectual disability, and university educational community, the NTG continues to develop materials in various media to inform and disseminate such information.

The basis for this is that many families have experienced in obtaining reliable information on recognizing dementia and how to best provide care and supports, in particular when their relative with intellectual disability is in the late or advanced stage of dementia and needing end-of-life specialized care. Further, we recognize that there are many nuanced issues that at times mirror those affecting adults with dementia in general, but also differ due to factors posed by lifelong intellectual disability. These differences can pose barriers to acceptance into generic services or add to confusion about how to provide specialized services. It is our hope at the NTG, as it is among our international colleagues in the intellectual disability and aging community, that any information produced will provide a basis for increased understanding of how dementia affects people with intellectual disability (as it might among other recognized 'special populations') and constructively influence and affect state and local planning, public policies, and clinical and service practices.

NTG Related Publications

Last February we reported on the International Summit on Intellectual Disability and Dementia that was held in October 2016 in Scotland, which came about from a partnership between the NTG and the University of Stirling. We noted that the participants came from numerous countries within Europe and from the USA and Canada. We also noted that subsequent to that meeting the NTG has spearheaded the development of a series of reports, many of which were pending publication in professional journals. These reports covered select issues and contain recommendations that can help expand knowledge, influence policy, and enhance services affecting adults with dementia and intellectual disability.

Thus, we are pleased to report that since February, a number of these papers have been published. One of the papers, Consensus Statement of the International Summit on Intellectual Disability and Dementia Related to Nomenclature, will appear in the October issue of the American Association on Intellectual and Developmental Disabilities' journal, Intellectual and Developmental Disabilities. Another, Consensus Statement of the International Summit on Intellectual Disability and Dementia Related to End-of-life Care in Advanced Dementia, has been published in the Journal of Applied Research in Intellectual Disability. A third, International Summit Consensus Statement: Intellectual Disability Inclusion in National Dementia Plans, has been published by the American Journal of Alzheimer's Disease and Other Dementias. A fourth, Dying Well with an Intellectual Disability and Dementia, has just been published in the Journal of Dementia Care.

Several other papers are under consideration by various journals. One, Consensus Statement of the International Summit on Intellectual Disability and Dementia Related to Post-Diagnostic Support, is with the journal, Aging & Mental Health, and another, Quality Care for People with Intellectual Disability and Advanced Dementia: Guidance on Service Provision, is with BMJ Supportive & Palliative Care. A paper titled, Consensus Statement of the International Summit on Intellectual Disability and Dementia on Valuing the Perspectives of Persons with Intellectual Disability, is under consideration by the Journal of Intellectual Disabilities, and the paper, a Summative Report of the International Summit on Intellectual Disability and Dementia, is under consideration by The Gerontologist.

Another reports and papers are in various states of preparation. These will address a variety of additional topics, including the needs of family caregivers, quality of life and dementia, and dementia-capable services design for providers. Each of these papers contains a series of recommendations that would address issues raised in the papers. These reports and publications are posted on the NTG website -- http://www.aadmd.org/ntg.

NIH Research Summit on Dementia Care: Building Evidence for Services and Supports

We are pleased to report that the NTG commissioned pre-Summit activity has produced a report titled, "Caregiving and Intellectual Disabilities and Dementia: Report of the Pre-Summit Workgroup on Caregiving and Intellectual and Developmental Disabilities". The members of the workgroup, led by Professor Tamar Heller, the chair of the Department on Human Development and Disability at the University of Illinois at Chicago, have completed their discussions and have provided us with a report with recommendations which will be submitted shortly to the Planning Group for the Summit. Copies will be available on the websites of the NTG (http://www.aadmd.org/ntg), the University, and the Summit.

Caregiver Resource Guide

We are also pleased to report that the NTG has completed the booklet and website media, "Intellectual Disability and Dementia: A Caregiver's Resource Guide for Rhode Islanders." This resource was commissioned by the Foundation for Seven Hills Rhode Island and was designed to provide valuable background information for caregivers, including a listing of relevant Rhode Island resources for helping caregivers. Seven Hills Rhode Island is one of the Administration on Community Living's Alzheimer's Disease Initiative grantees and its project work in currently in its second year. The Guide will be on the agency's website and print copies distributed throughout Rhode Island.

Closing

It is our hope that the Council will give due consideration to the substance and recommendations embedded in these various articles and reports, as well as the resource guide, at future meetings and when constructing next year's update of the National Plan to Address Alzheimer's Disease.