Alzheimer’s Drug Turns Back Clock in Powerhouse of Cell

(Salk Institute for Biological Studies) Salk researchers identify the molecular target of J147, which is nearing clinical trials to treat Alzheimer’s disease.

The experimental drug J147 is something of a modern elixir of life; it’s been shown to treat Alzheimer’s disease and reverse aging in mice and is almost ready for clinical trials in humans. Now, Salk scientists have solved the puzzle of what, exactly, J147 does. In a paper published January 7, 2018, in the journal Aging Cell, they report that the drug binds to a protein found in mitochondria, the energy-generating powerhouses of cells. In turn, they showed, it makes aging cells, mice and flies appear more youthful.

“This really glues together everything we know about J147 in terms of the link between aging and Alzheimer’s,” says Dave Schubert, head of Salk’s Cellular Neurobiology Laboratory and the senior author on the new paper.

“Finding the target of J147 was also absolutely critical in terms of moving forward with clinical trials.”

Schubert’s group developed J147 in 2011, after screening for compounds from plants with an ability to reverse the cellular and molecular signs of aging in the brain. J147 is a modified version of a molecule found in the curry spice curcumin. In the years since, the researchers have shown that the compound reverses memory deficits, potentiates the production of new brain cells, and slows or reverses Alzheimer’s progression in mice. However, they didn’t know how J147 worked at the molecular level.

In the new work, led by Schubert and Salk Research Associate Josh Goldberg, the team used several approaches to home in on what J147 is doing. They identified the molecular target of J147 as a mitochondrial protein called ATP synthase that helps generate ATP-the cell’s energy currency-within mitochondria. They showed that by manipulating its activity, they could protect neuronal cells from multiple toxicities associated with the aging brain. Moreover, ATP synthase has already been shown to control aging in C. elegans worms and flies.

“We know that age is the single greatest contributing factor to Alzheimer’s, so it is not surprising that we found a drug target that’s also been implicated in aging,” says Goldberg, the paper’s first author.

Further experiments revealed that modulating activity of ATP synthase with J147 changes the levels of a number of other molecules-including levels of ATP itself-and leads to healthier, more stable mitochondria throughout aging and in disease.

“I was very surprised when we started doing experiments with how big of an effect we saw,” says Schubert. “We can give this to old mice and it really elicits profound changes to make these mice look younger at a cellular and molecular level.”

The results, the researchers say, are not only encouraging for moving the drug forward as an Alzheimer’s treatment, but also suggest that J147 may be useful in other age-associated diseases as well.

“People have always thought that you need separate drugs for Alzheimer’s, Parkinson’s and stroke” says Schubert. “But it may be that by targeting aging we can treat or slow down many pathological conditions that are old-age-associated.”

The team is already performing additional studies on the molecules that are altered by J147’s effect on the mitochondrial ATP synthase-which could themselves be new drug targets. J147 has completed the FDA-required toxicology testing in animals, and funds are being sought to initiate phase 1 clinical trials in humans.

Citation
https://www.salk.edu/news-release/alzheimers-drug-turns-back-clock-powerhouse-cell/

 

Journal Reference:

Joshua Goldberg et al. The mitochondrial ATP synthase is a shared drug target for aging and dementiaAging Cell, 2018 DOI: 10.1111/acel.12715

Copyright 2018 Salk Institute for Biological Studies

Anxiety: An Early Indicator of Alzheimer’s Disease?

(Brigham and Women’s Hospital) A new study suggests an association between elevated amyloid beta levels and the worsening of anxiety symptoms.

A new study suggests an association between elevated amyloid beta levels and the worsening of anxiety symptoms. The findings support the hypothesis that neuropsychiatric symptoms could represent the early manifestation of Alzheimer’s disease in older adults.

Alzheimer’s disease is a neurodegenerative condition that causes the decline of cognitive function and the inability to carry out daily life activities. Past studies have suggested depression and other neuropsychiatric symptoms may be predictors of AD’s progression during its “preclinical” phase, during which time brain deposits of fibrillar amyloid and pathological tau accumulate in a patient’s brain. This phase can occur more than a decade before a patient’s onset of mild cognitive impairment. Investigators at Brigham and Women’s Hospital examined the association of brain amyloid beta and longitudinal measures of depression and depressive symptoms in cognitively normal, older adults.

Their findings, published today by The American Journal of Psychiatry, suggest that higher levels of amyloid beta may be associated with increasing symptoms of anxiety in these individuals. These results support the theory that neuropsychiatric symptoms could be an early indicator of AD.

“Rather than just looking at depression as a total score, we looked at specific symptoms such as anxiety. When compared to other symptoms of depression such as sadness or loss of interest, anxiety symptoms increased over time in those with higher amyloid beta levels in the brain,” said first author Nancy Donovan, MD, a geriatric psychiatrist at Brigham and Women’s Hospital.

“This suggests that anxiety symptoms could be a manifestation of Alzheimer’s disease prior to the onset of cognitive impairment. If further research substantiates anxiety as an early indicator, it would be important for not only identifying people early on with the disease, but also, treating it and potentially slowing or preventing the disease process early on.”

As anxiety is common in older people, rising anxiety symptoms may prove to be most useful as a risk marker in older adults with other genetic, biological or clinical indicators of high AD risk.

Researchers derived data from the Harvard Aging Brain Study, an observational study of older adult volunteers aimed at defining neurobiological and clinical changes in early Alzheimer’s disease. The participants included 270 community dwelling, cognitively normal men and women, between 62 and 90 years old, with no active psychiatric disorders. Individuals also underwent baseline imaging scans commonly used in studies of Alzheimer’s disease, and annual assessments with the 30-item Geriatric Depression Scale (GDS), an assessment used to detect depression in older adults.

The team calculated total GDS scores as well as scores for three clusters symptoms of depression: apathy-anhedonia, dysphoria, and anxiety. These scores were looked at over a span of five years.

From their research, the team found that higher brain amyloid beta burden was associated with increasing anxiety symptoms over time in cognitively normal older adults. The results suggest that worsening anxious-depressive symptoms may be an early predictor of elevated amyloid beta levels – and, in turn AD — and provide support for the hypothesis that emerging neuropsychiatric symptoms represent an early manifestation of preclinical Alzheimer’s disease.

Donovan notes further longitudinal follow-up is needed to determine whether these escalating depressive symptoms give rise to clinical depression and dementia stages of Alzheimer’s disease over time.

Citation

https://www.eurekalert.org/pub_releases/2018-01/bawh-aa011118.php

Journal Reference:

Nancy J. Donovan, Joseph J. Locascio, Gad A. Marshall, Jennifer Gatchel, Bernard J. Hanseeuw, Dorene M. Rentz, Keith A. Johnson, Reisa A. Sperling. Longitudinal Association of Amyloid Beta and Anxious-Depressive Symptoms in Cognitively Normal Older AdultsAmerican Journal of Psychiatry, 2018; appi.ajp.2017.1 DOI: 10.1176/appi.ajp.2017.17040442

https://www.eurekalert.org/pub_releases/2018-01/bawh-aa011118.php

Copyright © 2018 by the American Association for the Advancement of Science (AAAS)

 

Walk 4,000 Steps Every Day to Boost Brain Function

(MedicalNewsToday) Recent research led by the University of California, Los Angeles shows that taking a short walk each day can help to keep the brain healthy, supporting the overall resilience of cognitive functioning.

As we grow older, memory problems can begin to set in. These could be a natural part of aging and a minor annoyance, but in some cases, the issues may indicate mild cognitive impairment and could even develop into dementia.

Regardless of how mild or severe these memory problems may be, they are definitely distressing and can affect an individual’s quality of life.

New research from the Semel Institute for Neuroscience and Human Behavior at the University of California, Los Angeles suggests that there is a relatively easy way of keeping your brain in top shape as you grow older: take a moderately long walk every day.

This could boost your attention, the efficiency with which you process information, and other cognitive skills, say first study author Prabha Siddarth and colleagues.

The research findings were recently published the Journal of Alzheimer’s Disease.

Cortical Thickness to Assess Cognitive Health

Siddarth and team initially recruited 29 adults aged 60 and over, of which 26 completed the study over a 2-year period. The participants were split into two distinct groups:

  • a low physical activity group, comprising people who walked 4,000 or fewer steps each day
  • a high physical activity group, made up of people who walked more than 4,000 steps per day

All the participants reported a degree of memory complaints at baseline, but none of them had a dementia diagnosis.

In order to explore the potential effect of physical activity on cognitive ability, the researchers used MRI to determine the volume and thickness of the hippocampus, which is a brain region associated with memory formation and storage, and spatial orientation.

Previous research suggested that the size and volume of this brain region can tell us something about cognitive health. For instance, a higher hippocampal volume has been shown to indicate more effective memory consolidation.

“Few studies have looked at how physical activity affects the thickness of brain structures,” says Siddarth.

“Brain thickness,” she notes, “a more sensitive measure than volume, can track subtle changes in the brain earlier than volume and can independently predict cognition, so this is an important question.”

Walk More Every Day for a Resilient Brain

In addition to the MRI scans, the participants also underwent a set of neuropsychological tests, to consolidate the assessment of their cognitive capacity.

It was found that those in the high physical activity group — who walked more than 4,000 steps (approximately 3 kilometers) each day — had thicker hippocampi, as well as thicker associated brain regions, when compared with that of the those falling under the low physical activity category.

The highly active group was also found to have better attention, speedier information processing abilities, and more efficient executive function, which includes working memory. Working memory is the resource that we tap into on a daily basis when we need to make spontaneous decisions.

However, Siddarth and colleagues reported no significant differences between the high activity and low activity groups when it came to memory recall.

The next step from here, the researchers suggest, should be to undertake a longitudinal analysis in order to test the relationship between physical activity and cognitive ability over time.

They also note the need to better understand the mechanisms behind cognitive decline in relation to hippocampal atrophy.

Citation

https://www.medicalnewstoday.com/articles/320463.php

By Maria Cohut

© 2004-2018 All rights reserved. MNT is the registered trade mark of Healthline Media.

 

Alzheimer’s Is Accelerating Across the U.S.

(AARP) The Alzheimer’s Association says, “Someone in the United States develops Alzheimer’s dementia every 66 seconds.”

Degenerative brain disease and dementia are on the rise across all 50 U.S. states, according to the Alzheimer’s Association. As the rate of Alzheimer’s continues to escalate, more financial stress will be placed on health care programs. The trend will also increase the need for caregivers nationwide.

An estimated 5.5 million Americans are living with Alzheimer’s disease, according to the Alzheimer’s Association. The statistics are broken down by age and ethnicity and are listed as follows on their site.

  • One in 10 people age 65 and older (10 percent) has Alzheimer’s dementia.
  • Almost two-thirds of Americans with Alzheimer’s are women.
  • African Americans are about twice as likely to have Alzheimer’s or other dementia as whites.
  • Hispanics are about one and one-half times as likely to have Alzheimer’s or other dementia as whites.

Another startling figure exposed by the Alzheimer’s Association (AA) is that “Someone in the United States develops Alzheimer’s dementia every 66 seconds.”

The state with the highest rate of Alzheimer’s is Alaska. Cases of the disease are projected to increase from 7,100 in 2017 to 11,000 in 2025 — an increase of 54.9 percent, reports AA.

Why are rates so high there? It’s most likely due to the projected growth of Alaska’s elderly population. The older population is expected to increase to 35.6 percent by 2025; an estimated 70,900 to 110,000 people will be 65 and over.

Below is a list of the 10 states that are predicted to have the highest rate increases of Alzheimer’s by 2025.

1. Alaska

Alzheimer’s Increase, 2017-2025: 54.9 percent

Alaska may have the highest rate of Alzheimer’s, but it also has the lowest mortality rate from the disease. For Alaska, the rate is 9.2 deaths per 100,000 people. The U.S. rate is 29 deaths per 100,000, which is more than triple the mortality projected for Alaska.

2. Arizona

Alzheimer’s Increase, 2017-2025: 53.8 percent

According to the Centers for Disease Control and Prevention, Alzheimer’s disease was the eighth-leading cause of death in Arizona. Arizona’s older population, one of the largest of all states, is estimated to grow by approximately 29.1 percent by 2025.

3. Nevada

Alzheimer’s Increase, 2017-2025: 48.8 percent

The expected increase in the older population in Nevada is 32.3 percent, which is a much higher rate than the anticipated growth of the entire country.

4. Vermont

Alzheimer’s Increase, 2017-2025: 41.7 percent

Vermont’s older residents encompass 7.2 percent of Vermont’s population, the sixth highest among all states. The sharp increase in Alzheimer’s in Vermont is due to the large portion of people who are 75 and over.

5. Utah

Alzheimer’s Increase, 2017-2025: 40.0 percent

It’s estimated that older residents are just 10.3 percent of the population, but are expected to increase to 33 percent by 2025.

6. New Mexico

Alzheimer’s Increase, 2017-2025: 39.5 percent

Although lower than the national average, the estimated increase in New Mexico’s older population is 24.6 percent.

7. South Carolina

Alzheimer’s Increase, 2017-2025: 39.5 percent

The death rate from Alzheimer’s in South Carolina is the eighth highest in the U.S. — 40.1 deaths among every 100,000 people. Medicaid cost for Alzheimer’s patients in South Carolina reached $544 million in 2017 and is estimated to climb to $793 million by 2025.

8. Florida

Alzheimer’s Increase, 2017-2025: 38.5 percent

Florida’s older population is above average. Approximately 1 in 5 residents are 65 and older and the older population is expected to grow by 25 percent by 2025.

9. Wyoming

Alzheimer’s Increase, 2017-2025: 38.3 percent

The older population will grow from 83,000 to an estimated 116,800 in 2025.

10. Idaho

Alzheimer’s Increase, 2017-2025: 37.5 percent

The Medicaid cost of care for the disease is expected to soar to 47.8 percent from 2017 to 2025 in Idaho.

Where does your state rank on the list? See the full report.

Citation

https://www.aarp.org/health/conditions-treatments/info-2017/alzheimers-rates-rise-fd.html

Copyright 2018 AARP

 

Best Diets Overall: U.S. News Rankings for 2018

(U.S. News and World Report) U.S. News evaluated 40 of the most popular diets and identified the best. Find which top-rated diet is best for your health and fitness goals.

Best Diets Overall 

See the full rankings list »


Best Weight-Loss Diets

See the full rankings list »


Best Commercial Diet Plans

See the full rankings list »


Best Diabetes Diets

See the full rankings list »


Best Diets for Healthy Eating

See the full rankings list »


Best Fast Weight-Loss Diets

See the full rankings list »


Best Heart-Healthy Diets

See the full rankings list »


Best Plant-Based Diets

See the full rankings list »


Easiest Diets to Follow

See the full rankings list »

Citation
https://health.usnews.com/best-diet

Copyright 2017 © U.S. News & World Report L.P.

 

Diabetes Drug ‘Significantly Reverses Memory Loss’ in Mice with Alzheimer’s

(Lancaster University) A drug developed for diabetes could be used to treat Alzheimer’s after scientists found it “significantly reversed memory loss” in mice through a triple method of action.

The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer’s disease through the use of a drug originally created to treat type 2 diabetes.

Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment “holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer’s disease.”

Alzheimer’s disease is the most common cause of dementia and the numbers are expected to rise to two million people in the UK by 2051 according to Alzheimer’s Society, who part- funded the research.

Dr Doug Brown, Director of Research and Development at Alzheimer’s Society, said:

“With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer’s. It’s imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer’s and other forms of dementia. This approach to research could make it much quicker to get promising new drugs to the people who need them.”

Although the benefits of these ‘triple agonist’ drugs have so far only been found in mice, other studies with existing diabetes drugs such as liraglutide have shown real promise for people with Alzheimer’s, so further development of this work is crucial.”

This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines GLP-1, GIP and Glucagon which are all growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer’s patients.

The study used APP/PS1 mice, which are transgenic mice that express human mutated genes that cause Alzheimer’s. Those genes have been found in people who have a form of Alzheimer’s that can be inherited. Aged transgenic mice in the advanced stages of neurodegeneration were treated.

In a maze test, learning and memory formation were much improved by the drug which also:-

  • enhanced levels of a brain growth factor which protects nerve cell functioning
  • reduced the amount of amyloid plaques in the brain linked with Alzheimer’s
  • reduced both chronic inflammation and oxidative stress
  • slowed down the rate of nerve cell loss

Professor Holscher said:

“These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes but have shown consistent neuro- protective effects in several studies.”

“Clinical studies with an older version of this drug type already showed very promising results in people with Alzheimer’s disease or with mood disorders”

“Here we show that a novel triple receptor drug shows promise as a potential treatment for Alzheimer’s but further dose-response tests and direct comparisons with other drugs have to be conducted in order to evaluate if this new drugs is superior to previous ones.”

Citation

https://www.eurekalert.org/pub_releases/2017-12/lu-dd122017.php

Journal Reference:

Jingjing Tai, Weizhen Liu, Yanwei Li, Lin Li, Christian Hölscher. Neuroprotective effects of a triple GLP-1/GIP/glucagon receptor agonist in the APP/PS1 transgenic mouse model of Alzheimer’s disease. Brain Research, 2018; 1678: 64 DOI: 10.1016/j.brainres.2017.10.012

Copyright © 2018 by the American Association for the Advancement of Science (AAAS)

 

Alzheimer’s Association: Prevention and Risk of Alzheimer’s and Dementia

(Alzheimer’s Association) Can Alzheimer’s be prevented? It’s a question that continues to intrigue researchers and fuel new investigations. There are no clear-cut answers yet — partially due to the need for more large-scale studies — but promising research is under way. The Alzheimer’s Association continues to fund studies exploring the influence of exercise, diet, social and mental stimulation, and other factors in the development of Alzheimer’s.

What Causes Alzheimer’s?

Experts agree that in the vast majority of cases, Alzheimer’s, like other common chronic conditions, probably develops as a result of complex interactions among multiple factors, including age, genetics, environment, lifestyle, and coexisting medical conditions. Although some risk factors — such as age or genes — cannot be changed, other risk factors — such as high blood pressure and lack of exercise — usually can be changed to help reduce risk. Research in these areas may lead to new ways to detect those at highest risk.

Prevention Studies

A small percentage of people with Alzheimer’s disease (less than 1 percent) have an early-onset type associated with genetic mutations. Individuals who have these genetic mutations are guaranteed to develop the disease. An ongoing clinical trial conducted by the Dominantly Inherited Alzheimer Network (DIAN), is testing whether antibodies to beta-amyloid can reduce the accumulation of beta-amyloid plaque in the brains of people with such genetic mutations and thereby reduce, delay or prevent symptoms. Participants in the trial are receiving antibodies (or placebo) before they develop symptoms, and the development of beta-amyloid plaques is being monitored by brain scans and other tests.

Another clinical trial, known as the A4 trial (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s), is testing whether antibodies to beta-amyloid can reduce the risk of Alzheimer’s disease in older people (ages 65 to 85) at high risk for the disease. The A4 trial is being conducted by the Alzheimer’s Disease Cooperative Study.

Catalyst to Progress

In 2014, the Alzheimer’s Association awarded $8 million to researchers in Massachusetts to conduct a companion study to the A4 trial known as LEARN (Longitudinal Evaluation of Amyloid Risk and Neurodegeneration). The LEARN study will follow over time older people who do not have beta-amyloid plaques in the brain to determine what brain changes are associated with cognitive decline. Learn more about the drug treatment horizon

Heart–Head Connection

Several conditions known to increase the risk of cardiovascular disease — such as high blood pressure, diabetes and high cholesterol — also increase the risk of developing Alzheimer’s. Some autopsy studies show that as many as 80 percent of individuals with Alzheimer’s disease also have cardiovascular disease.

A longstanding question is why some people develop hallmark Alzheimer’s plaques and tangles but do not develop the symptoms of Alzheimer’s. Vascular disease may help researchers eventually find an answer. Some autopsy studies suggest that plaques and tangles may be present in the brain without causing symptoms of cognitive decline unless the brain also shows evidence of vascular disease. More research is needed to better understand the link between vascular health and Alzheimer’s.

Physical Exercise and Diet

Regular physical exercise may be a beneficial strategy to lower the risk of Alzheimer’s and vascular dementia. Exercise may directly benefit brain cells by increasing blood and oxygen flow in the brain Because of its known cardiovascular benefits, a medically approved exercise program is a valuable part of any overall wellness plan.

Current evidence suggests that heart-healthy eating may also help protect the brain. Heart-healthy eating includes limiting the intake of sugar and saturated fats and making sure to eat plenty of fruits, vegetables, and whole grains. No one diet is best. Two diets that have been studied and may be beneficial are the DASH (Dietary Approaches to Stop Hypertension) diet and the Mediterranean diet. The DASH diet emphasizes vegetables, fruits and fat-free or low-fat dairy products; includes whole grains, fish, poultry, beans, seeds, nuts, and vegetable oils; and limits sodium, sweets, sugary beverages, and red meats. A Mediterranean diet includes relatively little red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts, olive oil and other healthy fats.

Catalyst to Progress

The Alzheimer’s Association was among the first to encourage investigation of the impact of vascular factors on Alzheimer’s disease. We have funded such studies for more than 20 years and continue to highlight this promising avenue of research into potentially modifiable risk factors. Learn more about our commitment to research.

Social Connections and Intellectual Activity

A number of studies indicate that maintaining strong social connections and keeping mentally active as we age might lower the risk of cognitive decline and Alzheimer’s. Experts are not certain about the reason for this association. It may be due to direct mechanisms through which social and mental stimulation strengthen connections between nerve cells in the brain.

Catalyst to Progress

Animal studies can be especially helpful in increasing our knowledge about direct mechanisms through which physical and mental stimulation may benefit the brain. Orly Lazarov, PhD, received a 2007 Alzheimer’s Association New Investigator Research Grant to explore the impact of physical activity and an enriched environment on mice genetically engineered to carry one of the human genes that causes Alzheimer’s disease. Her results showed that physical and mental stimulation appear to decrease hallmark Alzheimer’s pathologies and support new nerve cell growth and better cell-to-cell communication.

Head Trauma

There appears to be a strong link between future risk of Alzheimer’s and serious head trauma, especially when injury involves loss of consciousness. You can help reduce your risk of Alzheimer’s by protecting your head.

  • Wear a seat belt
  • Use a helmet when participating in sports
  • “Fall-proof” your home

What You Can Do Now

While research is not yet conclusive, certain lifestyle choices, such as physical activity and diet, may help support brain health and prevent Alzheimer’s. Many of these lifestyle changes have been shown to lower the risk of other diseases, like heart disease and diabetes, which have been linked to Alzheimer’s. With few drawbacks and plenty of known benefits, healthy lifestyle choices can improve your health and possibly protect your brain. Learn more about brain health.

You can help increase our knowledge by considering participation in a clinical study. Prevention and risk management studies need healthy participants who are willing to make a long-term commitment to moving the field forward. You can find prevention trials currently recruiting volunteers through TrialMatch®, our free clinical trial matching service.

Understanding Prevention Research

Here are some things to keep in mind about the research underlying much of our current knowledge about possible prevention:

  • Insights about potentially modifiable risk factors apply to large population groups, not to individuals. Studies can show that factor X is associated with outcome Y, but cannot guarantee that any specific person will have that outcome. As a result, you can “do everything right” and still have a serious health problem or “do everything wrong” and live to be 100.
  • Much of our current evidence comes from large epidemiological studiessuch as the Honolulu-Asia Aging Study, the Nurses’ Health Study, the Adult Changes in Thought Study and the Kungsholmen Project. These studies explore pre-existing behaviors and use statistical methods to relate those behaviors to health outcomes. This type of study can show an “association” between a factor and an outcome but cannot “prove” cause and effect. This is why we describe evidence based on these studies with such language as “suggests,” “may show,” “might protect,” and “is associated with.”
  • The gold standard for showing cause and effect is a clinical trial in which participants are randomly assigned to a prevention or risk management strategy or a control group. Researchers follow the two groups over time to see if their outcomes differ significantly.
  • It is unlikely that some prevention or risk management strategies will ever be tested in randomized trials for ethical or practical reasons. One example is exercise. Definitively testing the impact of exercise on Alzheimer’s risk would require a huge trial enrolling thousands of people and following them for many years. The expense and logistics of such a trial would be prohibitive, and it would require some people to go without exercise, a known health benefit.

Selected Reports and Resources

“Summary of the Evidence on Modifiable Risk Factors for Cognitive Decline and Dementia: A Population-Based Perspective.” Baumgart, Matthew; Snyder, Heather M.; Carrillo, Maria C.; Fazio, Sam; Kim, Hye; Johns, Harry. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, June 2015; Vol. 11(6): 718-726. (9 pages)

In 2014, the World Dementia Council (WDC) requested the Alzheimer’s Association summarize the evidence on the risk factors associated with cognitive decline and dementia. The Association believes there is sufficient evidence to support the link between several risk factors and a reduced risk for cognitive decline and dementia.

Specifically, the Association believes there is sufficiently strong evidence, from a population-based perspective, to conclude that regular physical activity and management of cardiovascular risk factors (diabetes, obesity, smoking, and hypertension) reduce the risk of cognitive decline and may reduce the risk of dementia. The Association also believes there is sufficiently strong evidence to conclude that a healthy diet and lifelong learning/cognitive training may also reduce the risk of cognitive decline.

The Healthy Brain Initiative: The Public Health Road Map for State and National Partnerships, 2013–2018. Alzheimer’s Association and Centers for Disease Control and Prevention. Alzheimer’s Association, 2013. (64 pages)

The Centers for Disease Control, in collaboration with the Alzheimer’s Association and many other partners, released the second in a series of Road Maps in July 2013. This Road Map describes 35 actions that public health officials can implement take to promote cognitive functioning, address cognitive impairment and help meet the needs of caregivers.

“Advances in the Prevention of Alzheimer’s Disease and Dementia.” Solomon, Alina; Mangialasche, Francesca; Edo, Richard; et al. Journal of Internal Medicine, March 2015; Vol. 275(3): 229–250. (30 pages)

This article was written to further the understanding of the diagnostic criteria used to diagnose and ultimately prevent Alzheimer’s disease. The author describes the many different kinds of studies commonly used today, such as brain imaging or long-term observational studies. The author suggests that more public health-based research is needed to ensure prevention strategies are positively impacting people at risk for Alzheimer’s.

“Preventing Alzheimer’s Disease.” Selkoe, Dennis. Science, September 12, 2012; 337(6101): 1488-1492 (5 pages)

Despite tremendous efforts of researchers there is still no treatment to prevent the onset and progression of Alzheimer’s disease. The author argues that to prevent Alzheimer’s disease, studies must begin to uncover biomarkers that might exist even before symptoms are obvious. He reviews current biomarkers (such as Beta-amyloid) and how they correlate to progress in the treatment of Alzheimer’s disease. He offers suggestions for future study designs that integrate multiple approaches while maintaining scientific rigor.

Citation

https://www.alz.org/research/science/alzheimers_prevention_and_risk.asp#

© 2017 Alzheimer’s Association. All rights reserved.

 

Alzheimer’s Semipostal Fundraising Stamp Dedicated

(NIH) Postmaster General Megan J. Brennan dedicated a stamp today to fund research to help find a cure for one of the top 10 leading causes of death — Alzheimer’s.

Alzheimer's first class stamp; older woman, with someone's hand on her shoulder.

The first-day-of-issue dedication ceremony for the Alzheimer’s Semipostal Fundraising stamp took place at Johns Hopkins Bayview Medical Center in Baltimore. Please share the news on social media using the hashtag #AlzheimersStamp.

The price of the stamp includes the First-Class Mail single-piece postage rate in effect at the time of purchase plus an amount to fund Alzheimer’s research. By law, revenue from sales of the Alzheimer’s Semipostal stamp — minus the postage paid and the reimbursement of reasonable costs incurred by the Postal Service — will be distributed to the National Institutes of Health, which is part of the U.S. Department of Health and Human Services.

“The Postal Service is proud to issue this stamp today to help raise public awareness of Alzheimer’s,” said Brennan.

“Proceeds from its sale will help support urgently needed medical research into this incredibly debilitating disease.”

Joining Brennan in the ceremony were National Institute of Health Deputy Director of the National Institute on Aging Dr. Marie A. Bernard and Johns Hopkins Bayview Medical Center President Dr. Richard Bennett. Johns Hopkins Bayview Medical Center Memory and Alzheimer’s Treatment Center Director Dr. Constantine Lyketsos served as master of ceremonies.

“We’re in a new age of Alzheimer’s research with a number of efforts underway,” said Bernard.

“NIA is working to identify new genes that affect Alzheimer’s disease and their role as risk factors or protective factors, to explore imaging techniques and ways to detect development of the disease well before symptoms appear, to develop and test new therapies, and to test and implement new approaches to providing care and supporting caregivers. The new semipostal stamp will both raise awareness of Alzheimer’s research and care, as well as contribute to the search for effective ways to prevent and treat this heart-breaking disease.”

“Johns Hopkins Bayview has a long history of geriatric care and research,” said Bennett.

“We are honored to host the dedication of the United States Postal Service’s Alzheimer’s Semipostal stamp. Proceeds from the sale of this beautiful stamp will benefit the next generation of research at the National Institutes of Health. We hope this research will lead to new answers for our patients and their families who live with the everyday realities of Alzheimer’s disease.”

Also attending was Kathy Siggins of Mount Airy, MD, who followed the discretionary semipostal program criteria for submitting the stamp suggestion. Siggins’ husband succumbed to the disease in 1999.

The artwork is an illustration that first appeared on the 2008 42-cent Alzheimer’s Awareness stamp. It shows an older woman in profile with a hand on her shoulder, the suggestion of sunlight behind her, and clouds in front of and below her. On the 2008 stamp, she was facing left; the artwork for this stamp shows her facing right to help differentiate between the two stamps. Stamp artist Matt Mahurin of Topanga Canyon, CA, worked under the direction of art director Ethel Kessler of Bethesda, MD.

A Heart-Breaking Disease Affecting Millions of Individuals and Caregivers

According to the Centers for Disease Control, Alzheimer’s is one of the top 10 leading causes of death in the United States. It destroys the minds of those affected by it and poses challenges for family members and caregivers. It is the most common form of dementia, but is not a normal part of aging.

The disease is named after Alois Alzheimer, the German physician who in 1906 discovered and described two hallmark signs of the disease in the brain — clumps of amyloid protein fragments and tangles of tau protein fibers — and linked them to observable symptoms.

Symptoms can include:

  • loss of memory;
  • problems with speech and language;
  • inability to perform familiar daily tasks;
  • trouble interpreting visual images, spatial relationships, and other sensory information; and
  • changes in personality and behavior such as depression, apathy and agitation.

While there is not yet a cure for Alzheimer’s or a way to prevent it, public support has intensified the search for ways to treat its symptoms, slow its progression, and care for those who live with the disease. In 2012, the U.S. Department of Health and Human Services released a “National Plan to Address Alzheimer’s Disease” that addresses the many challenges faced by patients, researchers and caregivers. The plan offered a coordinated effort to prevent and effectively treat the disease by the year 2025 and called for improvements in clinical and long-term care.

According to the Alzheimer’s Association, more than 5.3 million Americans age 65 and older are estimated to have Alzheimer’s disease, a number predicted to rise as the population ages. Net proceeds from this stamp will be distributed to the U.S. Department of Health and Human Services, all part of a national effort to find ways to prevent, treat, and someday stop this disease.

The Semipostal Authorization Act, Pub. L. 106–253, grants the Postal Service discretionary authority to issue and sell semipostal fundraising stamps to advance such causes as it considers to be ”in the national public interest and appropriate.”

Under the program, the Postal Service intends to issue five semipostal fundraising stamps over a 10-year period, with each stamp to be sold for no more than two years. The Alzheimer’s Semipostal stamp is the first and will be followed by a Post-Traumatic Stress Disorder (PTSD) semipostal stamp to be issued in 2019. The next three discretionary semipostal stamps have not yet been determined.

Citation

https://www.nia.nih.gov/news/alzheimers-semipostal-fundraising-stamp-dedicated