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Thursday, January 28, 2016

Slower Mental Decline Linked to Higher Amounts of Growth Factor in the Brain


Dear Readers,

Older people with higher amounts of a key protein in their brains also had slower decline in their memory and thinking abilities than people with lower amounts of protein from the gene called brain-derived neurotrophic factor, or BDNF, according to a study published in the Jan. 27, 2016, online issue of Neurology.

“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said study author Aron S. Buchman, MD, of Rush University Medical Center in Chicago and a member of the American Academy of Neurology. “This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve, for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer’s disease.”

For the study, 535 people with an average age of 81 were followed until death, for an average of six years. They took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and the amount of protein from BDNF gene expression in the brain was then measured. The participants were part of the Rush Memory and Aging Project and the Religious Orders Study.

The rate of cognitive decline was about 50 percent slower for those in the highest 10 percent of protein from BDNF gene expression compared to the lowest 10 percent. The effect of plaques and tangles in the brain on cognitive decline was reduced for people with high levels of BDNF. In the people with the highest amount of Alzheimer’s disease hallmarks in their brains, cognitive decline was about 40 percent slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.

The researchers found that the plaques and tangles in the brain accounted for 27 percent of the variation in cognitive decline, demographics accounted for 3 percent and BDNF accounted for 2 percent.

Michal Schnaider Beeri, PhD, of the Icahn School of Medicine at Mount Sinai in New York, noted in an accompanying editorial that exercise has been shown to increase levels of BDNF in the blood, but that the relationship between BDNF protein levels in the blood and in the brain is not clear.

“More research is needed to confirm these findings, determine how this relationship between protein produced by BDNF gene expression and cognitive decline works and see if any strategies can be used to increase BDNF in the brain to protect or slow the rate of cognitive decline,” said Buchman.

Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.

The study was supported by the National Institutes of Health, Illinois Department of Public Health and the Robert C. Borwell Endowment Fund.

“Higher brain BDNF gene expression is associated with slower cognitive decline in older adults” by Aron S. Buchman, Lei Yu, Patricia A. Boyle, Julie A. Schneider, Philip L. De Jager, and David A. Bennett in Neurology. Published online January 27 2016.


Thanks for reading,

Jeffree Itrich, M.J., M.S.W,
ADCS
UC San Diego
 
Author: Jeffree Itrich at 11:20 AM 0 Comments

Wednesday, January 20, 2016

Is this the key to fighting Alzheimer’s?


Dear Readers,

Every four seconds, somewhere in the world, there is a new case of dementia. Alzheimer’s disease, which was considered rare 50 years ago, has today reached pandemic proportions, affecting some 45 million people globally. The cost of caring for Alzheimer’s has skyrocketed to more than $600 billion (about 1% of global GDP) and – if a breakthrough doesn’t come soon – those costs are projected to exceed $1 trillion by 2025.

Doctors have made significant progress towards understanding the causes of Alzheimer’s. For the first time, brain scans are revealing changes in the brains of living Alzheimer’s patients, allowing scientists to see how the disease develops. A disease in a dish model of Alzheimer’s is helping researchers efficiently and rapidly screen hundreds of drugs. New cognitive assessment tools and blood tests for early detection are in development. Experimental medicines targeting abnormal brain proteins are in clinical trials, and the first stem-cell trial for Alzheimer’s is about to begin in the United States. Meanwhile, a team of leading researchers recently published a roadmap for accelerating the testing phase of novel regenerative therapies. One of the most interesting areas is optogenetics, which uses light to activate brain cells, and has been shown to restore memories in amnesiac mice.

Despite these advances, there are still a lot of things we don’t know about dementia, and still room for research. We need better tools for detecting Alzheimer’s before it becomes full-blown, as well as new interventions that can delay the onset of disease in those at high risk, plus new treatments that can target tiny regions of the brain and boost memory. At a basic scientific level, we still need to gain clearer insight into what causes Alzheimer’s and the role played by proteins (such as amyloid and tau), as well as the immune system. It’s time for that to change, and a scientific competition with a lucrative prize could be just the thing to bring it about.

If there’s one thing stalling progress on Alzheimer’s, it’s a lack of resources. Our current investment levels remain modest: we spend 400 times less on research than the sum of the economic toll of the disease. More than 100 “promising” experimental medicines for Alzheimer’s have failed in clinical trials and no new treatments have come to market in the past decade. This failure rate also highlights the need to move from conventional thinking to new paradigms when it comes to dementia research.

The good news, however, is that today we are living in an extraordinary time, when technology is allowing small teams of individuals to accomplish what was once the province of only governments and the largest corporations. Empowered by machine learning, artificial intelligence, ubiquitous networks, cloud computing, robotics and digital manufacturing, small teams are building platforms and enterprises that are touching the lives of billions. If these creative and interdisciplinary teams begin to tackle Alzheimer’s, we may have a way forward. The challenge is to motivate them to do so.

Throughout history, our indomitable spirit of competition has brought about breakthroughs and solutions that once seemed unimaginable and impossible. In 1714, the British government’s Longitude rewards inspired a solution to the great scientific challenge of pinpointing a ship’s location at sea. The Apollo Project, to land a man on the moon, was spurred by intense competition between the US and USSR.

More recently, in 2004, a $10 million competition dubbed the Ansari XPRIZE challenged private entrepreneurs to build a spacecraft. The award spurred the advent of the private space industry and ushered in a new era of scientific prizes. Unlike awards given decades after a discovery, and often to an individual or small academic group (such as the Nobel or Lasker award) competition-based XPRIZEs offer a fast payout (two to seven years depending on the challenge) and revolve around narrowly defined, preset goals. Since the Ansari challenge began, XPRIZEs have led to the development of new oil-spill clean-up methods and a portable, real-life Star Trek Tricoder to diagnose disease. Prior XPRIZES have ranged from $2 million to $30 million.

Ken Dychtwald of Age Wave, a leading think tank on ageing, has co-conceived an Alzheimer’s XPRIZE. By offering a large monetary award, he hopes to inspire brilliant innovators who wouldn’t otherwise study Alzheimer’s to delve into the challenge. Whether they come from academia, industry or the general public, the hope is that new teams will look at dementia with fresh eyes and be able to see things that have been missed. A sponsor is now being sought to create the prize.



P. Murali Doraiswamy,MD,MBBS, FRCP, is Professor of Psychiatry and Medicine at Duke University and a leading researcher at the Duke Institute for Brain Sciences. He chairs the World Economic Forum’s Global Agenda Council for Brain Research and is a co-author of The Alzheimer’s Action Plan.

Peter H. Diamandis, MD, is the Chairman and Founder of the Xprize Foundation, which designs and launches large incentive prizes to drive radical breakthroughs for the benefit of humanity. He is Co-founder and Chairman of the Singularity University, which counsels the world’s top enterprises on how to utilize exponential technologies. He is the coauthor of BOLD: How to Go Big, Create Wealth and Impact the World.

Originally published in World Economic Forum.
 
Author: Guest at 9:41 AM 0 Comments

Friday, January 15, 2016

New Study Shows Connection Between Traumatic Brain Injury & Neurodegenerative Diseases Like AD


Dear Readers,

Researchers at the University of Texas in Galveston separated a toxic form of the tau protein in mice that had suffered a traumatic brain injury (TBI) and injected it into a group of healthy mice to see if they would develop dementia symptoms.

In previous research the same group found that this toxic form of tau, which traditionally increases after brain injury, could be why those who suffer TBIs develop chronic traumatic encephalopathy (CTE), a condition seen in many professional athletes and military personnel. They set out to test their theory that the toxic form of tau could be behind the condition.

In the second study the healthy animals that received the injections of toxic tau in the hippocampus, an area of the brain essential to memory, went on to develop the same cognitive impairments as seen in Alzheimer’s disease. The results suggest that the increased incidence of acquiring CTE and Alzheimer’s disease many years after the traumatic brain injury could be due to the seeding and dispersal of toxic tau following the brain injury. This has important implications for both TBI treatment and the prevention of brain degeneration in later life.

The group’s findings were published online in the January 5th, 2016 issue of Journal Neurotrauma. The study was headed up by Rakez Kayed in the department of neurology and the Mitchell Center for Neurodegenerative Diseases and Bridget Hawkins in the department of anesthesiology.


Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Manager, Recruitment & Communications
Alzheimer's Disease Cooperative Study
University of California San Diego
 
Author: Jeffree Itrich at 12:14 PM 0 Comments

Thursday, January 07, 2016

2015: The Year in AD Research


It is estimated that 5.3 million Americans and nearly 47 million worldwide have Alzheimer’s (AD). In the absence of a definitive treatment, the disease is pervasive and insidious, killing more people than breast cancer and prostate cancer combined. Due to the intense care that late-stage patients require, it’s also one of the most expensive—costing the U.S. $226 billion in 2015 alone. That figure is due to rise to $1.1 trillion (in 2015 dollars) by 2050. The sixth-leading cause of death, it’s the only one in the top 10 that cannot be cured, slowed, stopped, or prevented. Researchers are dutifully investigating every possible avenue to locate the underlying cause and find a possible treatment or prevention. Below are some of the more unconventional, non-drug studies that both made the news and provided a glimmer of hope in 2015.

MIND

In 2015 researchers presented additional evidence to support the ongoing theory that a Mediterranean style diet featuring olive oil may help protect the brain from Alzheimer’s disease. A nutritional epidemiologist at Rush University in Chicago, Martha Clare Morris, PhD, and colleagues developed the "Mediterranean-DASH Intervention for Neurodegenerative Delay" (MIND) diet. Study results were published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association in March.

Over five years the researchers studied more than 900 middle-aged Americans on the MIND diet, which consists of foods like fish, grains, vegetables, and healthy fats. In those participants who followed the MIND diet “rigorously,” the researchers found that participants reduced their risk of developing AD by 53 percent. Those who did not follow it as stringently but still followed it “moderately well” presented a reduced risk of 35 percent.

COFFEE

There was great news for coffee drinkers this past year. Researchers came across evidence that coffee can help reduce the risk of AD. Part of a larger analysis of mortality by the Harvard School of Public Health, the study was published in the journal Circulation.

The researchers analyzed over 90,000 women and 40,000 men, finding that coffee consumption had a “significant inverse association” with death due to neurological diseases such as AD.

Coffee’s ability to possibly lower risk of death from AD wasn’t the only finding —researchers also discovered that regular coffee drinkers were less likely to die from a handful of other conditions as well, ranging from suicide to heart disease. The scientists hypothesized that coffee’s “bioactive compounds” coffee may be responsible, adding that further research should be conducted to verify this finding.

SLEEP

For decades doctors have observed a link between sleep problems and memory disorders. A lack of sleep is common in people with AD. And now, scientists at the University of California, Berkeley, have found convincing evidence that poor sleep, particularly a deficit of deep, restorative sleep, provides a conduit through which the beta-amyloid protein assaults the brain's long-term memories. The study was published in the journal Nature Neuroscience.

Using a combination of brain imaging and other diagnostic tools on 26 older adults without dementia, researchers looked for the link between bad sleep, poor memory and the toxic accumulation of beta-amyloid proteins. A buildup of beta-amyloid has been found in AD patients and, separately, in people reporting sleep disorders. A 2013 University of Rochester study showed that the brain cells of mice would shrink during non-rapid-eye-movement (non-REM) sleep to make space for cerebrospinal fluids to wash out toxic metabolites such as beta-amyloid. In short, sleep washes away toxic beta amyloid at night, preventing them from building up and destroying healthy brain cells. The researchers likened it to a brain power cleanse. The good news about the findings is that poor sleep can be treatable.

EXERCISE

At the Alzheimer’s Association International Conference in July, Laura D. Baker, Ph.D., of Wake Forest School of Medicine, presented study findings suggesting that exercise may be able slow the progression of AD in people at high risk for developing the disease.

Her study demonstrated that after six months, participants who built up to exercising at an elevated heart rate for 30 minutes, four times a week, improved their cognition and had decreased levels of phosphorylated tau protein compared to those in a stretching-only control group. This is tremendous news because currently no approved drug has demonstrated that same effect. Tau protein levels are the measure scientists use to gauge AD disease progression. While the protein naturally increases with age in everyone, in people with AD, it increases significantly more. In Baker’s study, the exercise group saw a slight decrease in their levels after six months. Baker is embarking on a larger, similar study called EXERT that will enroll 300 subjects.

NEGATIVE BELIEFS

Newly published research out of the Yale School of Public Health revealed that people who sustain negative beliefs about aging are more likely to experience brain changes associated with AD. The study proposed that resisting negative beliefs about aging could possibly offer a way to reduce the incidence of AD.

Led by Becca Levy, associate professor of public health and of psychology, the study is the first to link a cultural-based psychosocial risk factor to the AD brain changes. The findings were published online Dec. 7 in the journal Psychology and Aging. Study authors examined healthy, dementia-free subjects from the Baltimore Longitudinal Study of Aging, the nation’s longest-running scientific study of aging. Based on MRIs, the researchers found that participants who held more negative beliefs about aging showed a greater decline in hippocampus volume. Reduced hippocampus volume is an indicator of AD.
Researchers also used brain autopsies to examine two other indicators of AD: amyloid plaques, and neurofibrillary tangles, which are twisted strands of protein that build up within brain cells. Participants holding more negative beliefs about aging had a significantly greater number of plaques and tangles.


Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Manager, Recruitment & Communications
Alzheimer's Disease Cooperative Study
University of California San Diego



 
Author: Jeffree Itrich at 9:45 AM 0 Comments

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The Alzheimer's Disease Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a major initiative for Alzheimer's disease (AD) clinical studies in the Federal government, addressing treatments for both cognitive and behavioral symptoms. This is part of the NIA Division of Neuroscience's effort to facilitate the discovery, development and testing of new drugs for the treatment of AD and also is part of the Alzheimer's Disease Prevention Initiative.

The ADCS was developed in response to a perceived need to advance research in the development of drugs that might be useful for treating patients with Alzheimer's disease (AD), particularly drugs that might not be developed by industry.