Many women having a heart attack don't have chest pain

23 feb 2012--Two out of five women having a heart attack do not experience chest pain, according to a new study.

Instead, they may have harder-to-recognize symptoms, such as pain in the jaw, neck, shoulders or back; stomach discomfort; or sudden trouble breathing, researchers said.

That may be one reason why women also have a higher risk of dying from a heart attack when they're in the hospital compared to men, the study found.

"The hallmark symptoms of a heart attack are chest pain and discomfort. But, women are more likely to have a different attack presentation," said study lead author Dr. John Canto, director of cardiovascular prevention, research and education at the Watson Clinic and director of the Chest Pain Center at Lakeland Regional Medical Center in Fla.

Men and women who have risk factors for heart disease, such as obesity, diabetes, high blood pressure, high cholesterol or a family history of heart disease, should be particularly concerned if they experience these symptoms.

"The reality is that most people who have chest pain and discomfort aren't having a heart attack. But, you can't wait to find out. Time is heart muscle. If you delay seeking treatment, you may be outside the window where you can get the most effective treatment," he said.

The study is in the Feb. 22/29 issue of the Journal of the American Medical Association.

Researchers analyzed data on more than 1.1 million patients seen at U.S. hospitals for heart attacks from 1994 to 2006. About 42 percent were women, who were also on average older than men when they had their heart attack.

Among both men and women, just over 35 percent -- or about one in three -- did not have chest pain.

However, women were more likely to experience an attack without chest pain compared to men, at 42 percent and 31 percent, respectively.

In-hospital deaths from heart attack were also more common among women: 14.6 percent of women died while still in the hospital, compared to just over 10 percent of men.

Dr. Suzanne Steinbaum, director of women and heart disease at Lenox Hill Hospital in New York City and a spokeswoman for the American Heart Association, said other heart attack symptoms women may experience include sweating, nausea and flu-like symptoms.

Though it can be hard to connect those symptoms to a heart attack, if "all of a sudden your daily activities become daunting, and you feel like you just can't function, you have to get checked out. If it's not your heart, so what? It's better to be safe than sorry," she said.

She also advised women to be assertive about their worries with doctors. Say, "I think I'm having a heart attack," she recommended.

Men may need to heed this advice as well, because they too may not have classic chest pain symptoms, she added.

The study found that for men and women -- but particularly for young women -- heart attacks without chest pain were associated with a greater risk of death. One of the main reasons, said Canto, is that people may delay going to the ER, and once they do call for help or go to the hospital, they may downplay their symptoms, leading to less urgent action from health care providers.

In the case of women, said Canto, the higher mortality rates may also be linked to biological differences in heart disease between men and women. When the researchers compared women without chest pain and men without chest pain, they still found a higher risk of death for women.

Cognitive stimulation beneficial in dementia

Cognitive stimulation therapies have beneficial effects on memory and thinking in people with dementia, according to a systematic review by Cochrane researchers. Despite concerns that cognitive improvements may not be matched by improvements in quality of life, the review also found positive effects for well-being.

22 feb 2012--There is a general belief that activities that stimulate the mind help to slow its decline in people with dementia. Cognitive stimulation provides people with dementia with activities intended to stimulate thinking, memory and social interaction, in order to delay the worsening of dementia symptoms. In 2011, the World Alzheimer's Report recommended that cognitive stimulation should be routinely offered to people with early stage dementia. However, increased interest in its use in dementia in recent years has provoked concern about its effectiveness and potential negative effects on well-being.

The review, published in The Cochrane Library, included 15 randomised controlled trials involving 718 people with mild to moderate dementia, mainly in the form of Alzheimer's disease or vascular dementia. Participants were treated in small groups and involved in different activities, from discussions and word games to music and baking. All activities were designed to stimulate thinking and memory. Improvements were weighed against those seen without treatment, with "standard treatments", which could include medicine, day care or visits from community mental health workers, or in some cases alternative activities such as watching TV and physical therapy.

"The most striking findings in this review are those related to the positive effects of cognitive stimulation on performance in cognitive tests," said lead author, Bob Woods, of the Dementia Services Development Centre Wales, at Bangor University in Bangor, UK. "These findings are perhaps the most consistent yet for psychological interventions in people with dementia."

Those who received cognitive stimulation interventions scored significantly higher in cognitive function tests, which measure improvements in memory and thinking. These benefits were still being seen one to three months after treatment. In addition, positive effects on social interaction, communication and quality of life or well-being were observed in a smaller number of the trials, based on self-reported or carer-reported measures.

In one trial, family members were trained to deliver cognitive stimulation on a one-to-one basis, with no additional strain on burden on caregivers reported. "Involving family caregivers in the delivery of cognitive stimulation is an interesting development and deserving of further attention," said Woods.

Provided by Wiley

Cellular aging increases risk of heart attack and early death

This is Clinical Professor of Genetic Epidemiology Borge Nordestgaard from the University of Copenhagen. Professor Nordestgaard is also a chief physician at Copenhagen University Hospital, where he and colleagues conduct large scale studies of groups of tens of thousands of Danes over several decades. Credit: University of Copenhagen

Every cell in the body has chromosomes with so-called telomeres, which are shortened over time and also through lifestyle choices such as smoking and obesity. Researchers have long speculated that the shortening of telomeres increases the risk of heart attack and early death. Now a large-scale population study in Denmark involving nearly 20,000 people shows that there is in fact a direct link, and has also given physicians a future way to test the actual cellular health of a person.

20 feb 2012--In an ongoing study of almost 20,000 Danes, a team of researchers from the University of Copenhagen have isolated each individual's DNA to analyse their specific telomere length – a measurement of cellular aging.

"The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age," says Clinical Professor of Genetic Epidemiology Borge Nordestgaard from the Faculty of Health and Medical Sciences at the University of Copenhagen. Professor Nordestgaard is also a chief physician at Copenhagen University Hospital, where he and colleagues conduct large scale studies of groups of tens of thousands of Danes over several decades.

In an ongoing study of almost 20,000 Danes, a team of researchers from the University of Copenhagen have isolated each individual’s DNA to analyze their specific telomere length - a measurement of cellular aging. The conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 percent, respectively. Professor Borge Nordestgaard explains the study and the breakthrough results. Read the full University of Copenhagen press release: http://news.ku.dk/all_news/2012/2012.2/cellular-aging-increases-risk-of-heart-attack/ Credit: Credits: Speak: Henrietta von Schilling. Camera: Carl Hagman and Tue Nielsen. Production: Tue Nielsen and Lasse Foghsgaard, Experimentarium.

Lifestyle can affect cellular aging

The recent "Copenhagen General Population Study" involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively.

"That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres - so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time," says Borge Nordestgaard.

One in four Danes has short telomeres

The study also revealed that one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent.

"Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks," says Borge Nordestgaard, and asks, "Does one cause the other or is the telomere length and the coronary event both indicative of a third - yet unknown - mechanism?"

Another possible prospect of the study is that general practitioners could conduct simple blood tests to reveal a person's telomere length and thereby the cellular wear and age.

More information: The study "Short Telomere Length, Myocardial Infarction, Ischemic Heart Disease, and Early Death" is scheduled for the March issue of the journal Arteriosclerosis, Thrombosis and Vascular Biology published by the American Heart Association.

Provided by University of Copenhagen

Aging studies suggest older people are happier

Lab manager Julia Harris (right) places glasses with a mobile tracking device on Derek Isaacowitz, associate professor of psychology, in the Lifespan Emotional Development Lab (LEDlab). Credit: Mary Knox Merrill.

19 feb 2011-- We get wrinkles. Our hair turns gray, or we lose it altogether. Our job prospects diminish and our chances of incurring disease increase. Researchers across the globe focus their efforts on increasing our life span because so many of us believe getting old stinks.

But that may not be so, according to Derek Isaacowitz a newly appointed associate professor of psychology in the College of Science. Contrary to popular opinion, he says, older people are happier than their younger counterparts.

“Self-report studies of happiness typically find that older people are happier,” Isaacowitz explains. But for the psychologist, who joined the Northeastern faculty after spending a decade at Brandeis, self-reporting is not enough. He wants to know why older people are happier.

To tackle this question, he employs a state-of-the-art testing method not typically used in aging research: eye tracking.

Eye tracking, he says, follows a participant’s eye movements by taking 60 snapshots of his or her pupils each second. Isaacowitz couples self-reports of mood with eye tracking data to pinpoint exactly what a person is looking at while rating his or her mood.

“We can analyze data in a moment to say, ‘how does what you’re looking at relate to what you feel?’” Isaacowitz says.

Results revealed that older and younger participants might regulate their emotions in vastly different ways. As Isaacowitz puts it, “One way of regulating emotion is to change your thinking about something, to see something upsetting and say ‘no’.” This seems to be the strategy of most younger test subjects.

On the other hand, older people tend to look at negative images less often, possibly indicating that they regulate emotion by distracting themselves from negative stimuli.

Isaacowitz says this makes sense, since the elderly tend to have fewer resources than the young: “If I made you really tired or gave you something else to do, it would be easier to distract instead of reappraise.”

While Isaacowitz’ research has already confirmed a cognitive difference between older and younger people, many questions remain about how this difference may relate to the role of age in regulating day-to-day emotion.

Isaacowitz was eager to join the Affective Science Institute at Northeastern and help advance the university’s strength in aging research. He says his lab on campus will conduct a number of new studies, including an analysis of subjects in a more natural environment. “We’ll be nicely set up to do that in the lab here,” he says.

Provided by Northeastern University

Psychiatry debates whether the pain of loss is really depression

The pain of losing a loved one can be a searing, gut-wrenching hurt and a long-lasting blow to a person's mood, concentration and ability to function. But is grief the same as depression?

18 feb 2012--That's a lively debate right now, as the psychiatric profession considers a key change in the forthcoming rewrite of its diagnostic "Bible." That proposed modification - one of many - would allow mental health providers to label the psychic pain of bereavement a mood disorder and act quickly to treat it, in some cases, with medication. With the Diagnostic and Statistical Manual's fifth edition set for completion by the end of this year, the editors of the British journal The Lancet have come out in strong opposition to the new language, calling grief a natural and healthy response to loss, not a pathological state.

"Grief is not an illness. It is more usefully thought of as part of being human, and a normal response to the death of a loved one," writes the editor of The Lancet. "Most people who experience the death of someone they love do not need treatment by a psychiatrist or indeed by any doctor. For those who are grieving, doctors would do better to offer time, compassion, remembrance, and empathy, than pills."

The change under consideration would expunge any reference to the passage of time since a loved one's death before a diagnosis of depression could be considered. The current edition of the diagnostic manual states that if a patient's low mood and energy, sleep difficulties and appetite changes persist for more than two months following bereavement, a diagnosis of depression might be considered. An earlier edition of the manual had established a year as the period during which mourning should not be confused with depression.

"Putting a time frame on grief is inappropriate," The Lancet's lead editorial states simply. And in a "Perspectives" essay also published Thursday in Lancet, Harvard University medical anthropologist Dr. Arthur Kleinman agrees, eloquently exploring what's at stake.

"Is grief something we can or should no longer tolerate?" asks Kleinman, who describes his own grief after his wife of 46 years died last March from Alzheimer's Disease. "Is this existential source of suffering like any dental or back pain unwanted and unneeded?"

Kleinman calls the current two-month time period allowed for grief a "shockingly short expectation" that no religion or society would support. To allow grief to be redefined as depression with no allowance at all for the passage of time not only spells "the loss of grief": it risks redefining vast numbers of Americans who are taking their time to adjust to the loss of a loved one as sick, he writes. And it powerfully rewrites cultural values about how we understand and mark the loss of a fellow human being.

Proponents of the change have argued that it would allow the bereaved to seek help for their suffering. And they add that it would not define all who grieve as depressed. They argue there is often no difference, but for the recent death of a loved one, between the behaviors that define depression and those that define grief.

The Lancet's editors note there is no evidence that antidepressant medications improve the moods of people who are healthy to begin with. Citing fellow critics of the proposed move, Kleinman suggests that it might have been inevitable once the financial interests of pharmaceutical manufacturers collided with psychiatry's loose definitions of mental illness and the profession's tendency to expand its patient base.

"Its ubiquity makes grief a potential profit centre for the business of psychiatry," writes Kleinman.

Study: Weight training improves Parkinson's symptoms

New research suggests weight training for two years significantly improves the motor symptoms of Parkinson's disease compared to other forms of exercise such as stretching and balance exercises. The clinical trial, which compared two forms of exercise for Parkinson's disease, was released today and will be presented at the American Academy of Neurology's 64th Annual Meeting in New Orleans April 21 to April 28, 2012.

17 feb 2012--"While we have known that many different types of exercise can benefit Parkinson's patients over short time periods, we did not know whether exercise improves the motor symptoms of Parkinson's over the long term," said study author Daniel Corcos, PhD, with the University of Illinois at Chicago.

For the study, 48 people with Parkinson's disease were randomized to progressive resistance exercise, known as weight training, or they were assigned to the exercise known as fitness counts, which includes flexibility, balance and strengthening exercises. The groups exercised for one hour, twice a week for two years.

The severity of motor symptoms, including tremors, was measured using the Unified Parkinson's Disease Rating Scale (UPDRS) after six, 12, 18 and 24 months of exercise. Scores were taken when the participants were not taking their medication.

While both forms of exercise reduced motor symptoms at six months of exercise, participants who did weight training saw a 7.3 point improvement in their UPRDS score after two years while the fitness counts group returned to the same scores they had at the start of the study.

"Our results suggest that long-term weight training could be considered by patients and doctors as an important component in managing Parkinson's disease," said Corcos.

Provided by American Academy of Neurology

Stem cell treatments improve heart function after heart attack

Stem cell therapy moderately improves heart function after a heart attack, according to a systematic review published in The Cochrane Library. But the researchers behind the review say larger clinical trials are needed to establish whether this benefit translates to a longer life.

16 feb 2012--In a heart attack, the blood supply to parts of the heart is cut off by a blocked artery, causing damage to the heart tissue. The cells in the affected area start to die. This is called necrosis and in the days and weeks that follow, the necrotic area may grow, eventually leaving a large part of the heart unable to contract and increasing the risk of further heart problems. Stem cell therapy uses cells from the patient's own bone marrow to try to repair and reduce this damage. Currently, the treatment is only available in facilities with links to scientific research.

The authors of the review drew together all the available evidence to ask whether adult bone marrow stem cells can effectively prevent and repair the damage caused by a heart attack. In 2008, a Cochrane review of 13 stem cell therapy clinical trials addressed the same question, but the new review adds 20 more recent trials, drawing its conclusions from all 33. By incorporating longer follow up, the later trials provide a better indication of the effects of the therapy several years after treatment.

The total number of patients involved in trials was 1,765. All had already undergone angioplasty, a conventional treatment that uses a balloon to open the blocked artery and reintroduce the blood supply. The review's findings suggest that stem cell therapy using bone marrow-derived stem cells (BMSCs) can produce a moderate long-term improvement in heart function, which is sustained for up to five years. However, there was not enough data to reach firm conclusions about improvements in survival rates.

"This new treatment may lead to moderate improvement in heart function over standard treatments," said lead author of the study, Enca Martin-Rendon, of the Stem Cell Research laboratory, NHS Blood and Transplant at the John Radcliffe Hospital in Oxford, UK. "Stem cell therapy may also reduce the number of patients who later die or suffer from heart failure, but currently there is a lack of statistically significant evidence based on the small number of patients treated so far."

It is still too early to formulate guidelines for standard practice, according to the review. The authors say further work is required to establish standard methods, including cell dosage, timing of cell transplantation and methods to measure heart function. "The studies were hard to compare because they used so many different methods," said Martin-Rendon. "Larger trials with standardised treatment procedures would help us to know whether this treatment is really effective.

Recently, the task force of the European Society of Cardiology for Stem Cells and Cardiac Repair received funding from the European Union Seventh Framework Programme for Research and Innovation (EU FP7-BAMI) to start such a trial. Principal Investigator for the BAMI trial, and co-author of this Cochrane review, Anthony Mathur, said, ''The BAMI trial will be the largest stem cell therapy trial in patients who have suffered heart attacks and will test whether this treatment prolongs the life of these patients."

More information: Clifford DM, Fisher SA, Brunskill SJ, Doree C, Mathur A, Watt S, Martin-Rendon E. Stem cell treatment for acute myocardial infarction. Cochrane Database of Systematic Reviews 2012, Issue 2. Art. No.: CD006536. DOI: 10.1002/14651858.CD006536.pub3

Cognitive impairment in older adults often unrecognized in the primary care setting

A new study published in the Journal of the American Geriatrics Society reveals that brief cognitive screenings combined with offering further evaluation increased new diagnoses of cognitive impairment in older veterans two to three fold.

15 feb 2012--Led by J. Riley McCarten, MD, of the Minneapolis VA Health Care System and the University of Minnesota, researchers assessed the effect of screening on diagnosing cognitive impairment in patients who were seen in VA primary care clinics and had no indiction of memory loss. Veterans aged 70 and older who failed the brief cognitive screen at a routine primary care visit were offered a further, comprehensive evaluation.

Of the 8,342 Veterans offered screening, 8,063 (97%) accepted, 2,081 (26%) failed the screen, and 580 (28%) agreed to further evaluation.

Among those accepting further evaluation, 93% were documented to have cognitive impairment, including 75% with dementia.

Additionally, 118 patients who passed the initial screen still requested further evaluation, and 87% were found to have cognitive impairment, including 70% with dementia.

"Our study demonstrates that proactive strategies such as routine screening are well-accepted and effective in diagnosing cognitive impairment, and that primary care providers value the diagnostic and management services involved," McCarten notes. "This project has implications for strategies that seek to improve care and contain costs in dementia."

The findings of this study run counter to the current standard recommendations by the American College of Physicians, U.S. Preventive Health Task Force, and Alzheimer's Association, which discourage routine cognitive impairment/dementia screening on all older patients at a certain age. Screening is only recommended if a person comes to a provider with some type of complaint that could be due to dementia.

Provided by Wiley

Overeating may double risk of memory loss

New research suggests that consuming between 2,100 and 6,000 calories per day may double the risk of memory loss, or mild cognitive impairment (MCI), among people age 70 and older. The study was released today and will be presented at the American Academy of Neurology's 64th Annual Meeting in New Orleans April 21 to April 28, 2012. MCI is the stage between normal memory loss that comes with aging and early Alzheimer's disease.

14 feb 2012--"We observed a dose-response pattern which simply means; the higher the amount of calories consumed each day, the higher the risk of MCI," said study author Yonas E. Geda, MD, MSc, with the Mayo Clinic in Scottsdale, Arizona and a member of the American Academy of Neurology.

The study involved 1,233 people between the ages of 70 and 89 and free of dementia residing in Olmsted County, Minn. Of those, 163 had MCI. Participants reported the amount of calories they ate or drank in a food questionnaire and were divided into three equal groups based on their daily caloric consumption. One-third of the participants consumed between 600 and 1,526 calories per day, one-third between 1,526 and 2,143 and one-third consumed between 2,143 and 6,000 calories per day.

The odds of having MCI more than doubled for those in the highest calorie-consuming group compared to those in the lowest calorie-consuming group. The results were the same after adjusting for history of stroke, diabetes, amount of education, and other factors that can affect risk of memory loss. There was no significant difference in risk for the middle group.

"Cutting calories and eating foods that make up a healthy diet may be a simpler way to prevent memory loss as we age," said Geda.

Provided by American Academy of Neurology

Exercise triggers stem cells in muscle

University of Illinois researchers determined that an adult stem cell present in muscle is responsive to exercise, a discovery that may provide a link between exercise and muscle health. The findings could lead to new therapeutic techniques using these cells to rehabilitate injured muscle and prevent or restore muscle loss with age.

13 feb 2012--Mesenchymal stem cells (MSCs) in skeletal muscle have been known to be important for muscle repair in response to non-physiological injury, predominantly in response to chemical injections that significantly damage muscle tissue and induce inflammation. The researchers, led by kinesiology and community health professor Marni Boppart, investigated whether MSCs also responded to strain during exercise, and if so, how.

"Since exercise can induce some injury as part of the remodeling process following mechanical strain, we wondered if MSC accumulation was a natural response to exercise and whether these cells contributed to the beneficial regeneration and growth process that occurs post-exercise," said Boppart, who also is affiliated with the Beckman Institute for Advanced Science and Technology at the U. of I.

The researchers found that MSCs in muscle are very responsive to mechanical strain. They witnessed MSC accumulation in muscle of mice after vigorous exercise. Then, they determined that although MSCs don't directly contribute to building new muscle fibers, they release growth factors that spur other cells in muscle to fuse and generate new muscle, providing the cellular basis for enhanced muscle health following exercise.

A key element to the Illinois team's method was in exercising the mice before isolating the cells to trigger secretion of beneficial growth factors. Then, they dyed the cells with a fluorescent marker and injected them into other mice to6 see how MSCs coordinated with other muscle-building cells.

In addition to examining the cells in vivo, the researchers studied the cells' response to strain on different substrates. They found that MSC response is very sensitive to the mechanical environment, indicating that conditions of muscle strain affect the cells' activity.

"These findings are important because we've identified an adult stem cell in muscle that may provide the basis for muscle health with exercise and enhanced muscle healing with rehabilitation/movement therapy," Boppart said. "The fact that MSCs in muscle have the potential to release high concentrations of growth factor into the circulatory system during exercise also makes us wonder if they provide a critical link between enhanced whole-body health and participation in routine physical activity."

Next, the group hopes to determine whether these cells contribute to the decline in muscle mass over a person's lifetime. Preliminary data suggest MSCs become deficient in muscle with age. The team hopes to develop a combinatorial therapy that utilizes molecular and stem-cell-based strategies to prevent age-related muscle loss.

"Although exercise is the best strategy for preserving muscle as we age, some individuals are just not able to effectively engage in physical activity," Boppart said. "Disabilities can limit opportunities for muscle growth. We're working hard to understand how we can best utilize these cells effectively to preserve muscle mass in the face of atrophy."

The team published its findings in the journal PLoS One. The Illinois Regenerative Medicine Institute, the Ellison Medical Foundation and the Mary Jane Neer Foundation supported this work.

More information: The paper, "Eccentric Exercise Facilitates Mesenchymal Stem Cell Appearance in Skeletal Muscle," is available online on PLoS ONE site.

Provided by University of Illinois at Urbana-Champaign

Cognitive problems common among non-demented elderly

Both subjective and objective cognitive impairment are highly common among non-demented elderly Swedes, with an overall prevalence of 39 percent and 25 percent respectively, according to a nationwide twin study by researchers at the Aging Research Center of Karolinska Institutet, Sweden. The study confirms higher education as a major protective factor and stresses the importance of environmental aspects over genes in mild cognitive disorders in old age.

12 feb 2012--In the current study, which is published in the Journal of Alzheimer's Disease, the researchers investigated the distribution and heritability of subjective and objective cognitive impairment in the population by using data from 11,926 twins aged 65 and above in the Swedish Twin Registry. Objective cognitive impairment involves a reduced performance on tests measuring different cognitive abilities, such as memory and attention, while subjective cognitive impairment involves the same type of problems but experienced only at the subjective level. The researchers then found, that together subjective and objective cognitive impairment affect the majority of non-demented Swedish elderly (joint prevalence 64 percent), suggesting that mild cognitive disorders may represent a major public health concern even in the absence of dementia.

The study also highlights that subjective and objective cognitive impairment has distinct socio-demographic profiles. Specifically, when compared with people with objective cognitive impairment, elderly with subjective complaints only were more educated, more likely to be married, and to have higher socio-economic status – pointing to a possible protective effect of this favorable life conditions. Co-twin control analysis showed that the detrimental effect of lower educational level on cognitive functioning is largely independent by genetic background and early life environment.

"This underlies the relevance of adult life educational achievements for preserved cognitive functioning in older life", says Dr Barbara Caracciolo, who led the study at the Aging Research Center in Stockholm.

Regarding the heritability of subjective and objective cognitive impairment, the researchers observed concordance rates of 63 percent and 52 percent in monozygotic twins, 63 percent and 50 percent in dizygotic same-sex twins, and 42 percent and 29 percent in dizygotic unlike-sex twins. The lack of substantial differences in concordance rates between genetically identical (monozygotic) and or non-identical (dizygotic) twins suggests that environmental influences rather than genetic background play the major role in the occurrence of mild cognitive disorders in non-demented elderly.

More information: 'Differential Distribution of Subjective and Objective Cognitive Impairment in the Population: A Nation-Wide Twin-Study', Caracciolo B, Gatz M, Xu W, Pedersen NL, Fratiglioni L., Journal of Alzheimer's Disease, epub ahead of print 10 January 2012, doi:10.3233/JAD-2011-111904

Provided by Karolinska Institutet

News of plaque-clearing drug tops week of major advances against Alzheimer's disease

In the last eight days, scientists have delivered a powerful one-two punch in the fight to defeat Alzheimer's disease. At the same time, the White House and members of Congress are proposing increases in Alzheimer's research funding. This has been a big week for all who seek to end this disease, says the CEO of the American Health Assistance Foundation.

11 feb 2012--"In the last eight days, scientists have delivered a powerful one-two punch in the fight to defeat Alzheimer's disease," said Stacy Pagos Haller, President and CEO of the American Health Assistance Foundation (AHAF), a nonprofit that identifies and funds exceptionally high-impact research worldwide through its Alzheimer's Disease Research program.

"We are excited about today's announcement by Case Western University researchers that a cancer drug, used in mice studies, appears to help clear out the excess plaque found in the Alzheimer's-disease brain and it does this by enhancing the body's natural defense mechanisms," noted Haller. "This follows last week's announced discovery of how Alzheimer's disease spreads in the brain. The timing of these findings coincides with new proposals in Congress and the White House to increase federal funding for Alzheimer's research. This has been a big week for all who seek to end this disease."

In a study of mice, a research team headed by Case Western University scientist Gary Landreth, Ph.D., found that bexarotene—a drug currently used to combat T cell lymphoma— helped the body clear out amyloid beta proteins. Alzheimer's disease arises in large part from the body's inability to clear these naturally occurring proteins. As amyloid beta levels increase they tend to aggregate and contribute to the so-called brain "plaques" found in Alzheimer's disease.

Bexarotene appeared to improve brain function in these mice. Study results were published in the journal Science.

"Although this is a mouse study, the results are encouraging, and the drug did its job with unprecedented speed, by targeting ApoE, the primary genetic risk factor for Alzheimer's disease," said AHAF Vice President for Scientific Affairs Guy Eakin, Ph.D.

"This announcement is particularly exciting because bexarotene achieved regulatory approval by the U.S. Food and Drug Administration more than a decade ago for the treatment of cancer. That earlier approval could speed up the prospects for human clinical trials of the drug as an Alzheimer's treatment."

AHAF, which had also supported Landreth earlier in his career, started funding the preliminary work leading to this line of research in 2007. Currently, AHAF is funding follow-up studies in which the Landreth team is testing the latest findings on other "mouse models" that may better represent the human form of Alzheimer's disease. Positive findings could help pave the way towards human clinical studies.

"While it is still too early to make predictions, if these findings can be replicated in additional preclinical studies, and then later in human clinical trials, we may have a powerful new weapon in the battle to halt this disease," noted Eakin.

This latest news comes only one week after an AHAF-funded research team in Boston and another team in New York announced a major breakthrough in understanding how Alzheimer's disease spreads in the brain. By learning that toxic "tau" proteins jump from nerve cell to nerve cell, scientists can now focus on ways to target and stop this cell-to-cell spread.

Although these reports are coming in rapid succession, the overall progress of Alzheimer's disease research has been slower than that of other major diseases, due in part to comparatively meager financial support for Alzheimer's disease research. "We hope this funding scenario will improve, as promising study results stimulate our national resolve to defeat this disease," said Haller.

This week the Obama Administration announced it will provide an additional $130 million in Alzheimer's research funding over the next two years. Last week a bipartisan group in Congress unveiled the Spending Reductions through Innovations in Therapies (SPRINT) Agenda Act of 2012. The legislation, introduced by Senators Barbara Mikulski (D-MD) and Susan Collins (R-ME) and Representatives Chris Smith (R-NJ) and Ed Markey (D-MA), would spur public and private research funding and streamline the regulatory review of treatments.

More information: http://www.science … ence.1217697

Provided by AHAF-American Health Assistance Foundation

FDA-approved drug rapidly clears amyloid from the brain, reverses Alzheimer's symptoms in mice

Neuroscientists at Case Western Reserve University School of Medicine have made a dramatic breakthrough in their efforts to find a cure for Alzheimer's disease. The researchers' findings, published in the journal Science, show that use of a drug in mice appears to quickly reverse the pathological, cognitive and memory deficits caused by the onset of Alzheimer's. The results point to the significant potential that the medication, bexarotene, has to help the roughly 5.4 million Americans suffering from the progressive brain disease.

10 feb 2012--Bexarotene has been approved for the treatment of cancer by the U.S. Food and Drug Administration for more than a decade. These experiments explored whether the medication might also be used to help patients with Alzheimer's disease, and the results were more than promising.

Alzheimer's disease arises in large part from the body's inability to clear naturally-occurring amyloid beta from the brain. In 2008 Case Western Reserve researcher Gary Landreth, PhD, professor of neurosciences, discovered that the main cholesterol carrier in the brain, Apolipoprotein E (ApoE), facilitated the clearance of the amyloid beta proteins. Landreth, a professor of neurosciences in the university's medical school, is the senior author of this study as well.

Landreth and his colleagues chose to explore the effectiveness of bexarotene for increasing ApoE expression. The elevation of brain ApoE levels, in turn, speeds the clearance of amyloid beta from the brain. Bexarotene acts by stimulating retinoid X receptors (RXR), which control how much ApoE is produced.

In particular, the researchers were struck by the speed with which bexarotene improved memory deficits and behavior even as it also acted to reverse the pathology of Alzheimer's disease. The present view of the scientific community is that small soluble forms of amyloid beta cause the memory impairments seen in animal models and humans with the disease. Within six hours of administering bexarotene, however, soluble amyloid levels fell by 25 percent; even more impressive, the effect lasted as long as three days. Finally, this shift was correlated with rapid improvement in a broad range of behaviors in three different mouse models of Alzheimer's.

One example of the improved behaviors involved the typical nesting instinct of the mice. When Alzheimer's-diseased mice encountered material suited for nesting – in this case, tissue paper – they did nothing to create a space to nest. This reaction demonstrated that they had lost the ability to associate the tissue paper with the opportunity to nest. Just 72 hours after the bexarotene treatment, however, the mice began to use the paper to make nests. Administration of the drug also improved the ability of the mice to sense and respond to odors.

Bexarotene treatment also worked quickly to stimulate the removal of amyloid plaques from the brain. The plaques are compacted aggregates of amyloid that form in the brain and are the pathological hallmark of Alzheimer's disease. Researchers found that more than half of the plaques had been cleared within 72 hours. Ultimately, the reduction totaled 75 percent. It appears that the bexarotene reprogrammed the brain's immune cells to "eat" or phagocytose the amyloid deposits. This observation demonstrated that the drug addresses the amount of both soluble and deposited forms of amyloid beta within the brain and reverses the pathological features of the disease in mice.

This study identifies a link between the primary genetic risk factor for Alzheimer's disease and a potential therapy to address it. Humans have three forms of ApoE: ApoE2, ApoE3, and ApoE4. Possession of the ApoE4 gene greatly increases the likelihood of developing Alzheimer's disease. Previously, the Landreth laboratory had shown that this form of ApoE was impaired in its ability of clear amyloid. The new work suggests that elevation of ApoE levels in the brain may be an effective therapeutic strategy to clear the forms of amyloid associated with impaired memory and cognition.

"This is an unprecedented finding," says Paige Cramer, PhD candidate at Case Western Reserve School of Medicine and first author of the study. "Previously, the best existing treatment for Alzheimer's disease in mice required several months to reduce plaque in the brain."

Added Professor Landreth: "This is a particularly exciting and rewarding study because of the new science we have discovered and the potential promise of a therapy for Alzheimer's disease. We need to be clear; the drug works quite well in mouse models of the disease. Our next objective is to ascertain if it acts similarly in humans. We are at an early stage in translating this basic science discovery into a treatment."

Daniel Wesson, PhD, assistant professor of neurosciences at Case Western Reserve School of Medicine and co-author of the study agreed.

"Many often think of Alzheimer's as a problem of remembering and learning, but the prevalent reality is this disease spreads throughout the brain, resulting in serious insults to numerous functions," he said. "The results of this study, showing the preservation of behaviors across a wide spectrum, and accompanying brain function, are tremendously exciting and suggest great promise in the utility of this approach in treatment of Alzheimer's disease."

Bexarotene has a good safety and side-effect profile. The Case Western Reserve researchers hope these attributes will help speed the transition to clinical trials of the drug.

Professor Landreth said modest resources funded this self-described "far-fetched idea." Crucial support came from the Blanchette Hooker Rockefeller Foundation, the Thome Foundation, and the National Institutes of Health.

Provided by Case Western Reserve University

Tai Chi program helps Parkinson's disease patients

An Oregon Research Institute (ORI) exercise study conducted in four Oregon cities has shown significant benefits for patients with mild-to-moderate Parkinson's disease. In an original article published in the February 9, 2012 issue of the New England Journal of Medicine (NEJM), ORI scientist Fuzhong Li, Ph.D. and colleagues report that a tailored program of twice-weekly Tai Chi training resulted in improved postural stability and walking ability, and reduced falls in the participants.

09 feb 2012--"These results are clinically significant because they suggest that Tai Chi, a low-to-moderate impact exercise, may be used, as an add-on to current physical therapies, to address some of the key clinical problems in Parkinson's disease, such as postural and gait instability. Since many training features in the program are functionally oriented, the improvements in the balance and gait measures that we demonstrated highlight the potential of Tai Chi-based movements in rehabilitating patients with these types of problems and, consequently, easing cardinal symptoms of Parkinson's disease and improving mobility, flexibility, balance, and range of motion," noted Dr. Li.

In the 4-year project funded by the National Institute of Neurological Disorders and Stroke, the investigators randomly assigned 195 patients to one of three exercise groups: Tai Chi, resistance training, or stretching. The patients participated in 60-minute exercise sessions twice weekly for 24 weeks.

The results of the study showed that the Tai Chi group performed consistently better than the stretching group in how far they could lean in any direction without losing balance as well as demonstrating better levels of directional control of the body and walking ability (i.e., longer stride length). Tai Chi participants also outperformed those in the resistance training group on the balance and stride length measures. Finally, Tai Chi training was shown to significantly lower the incidence of falls compared to stretching and to be as equally effective as resistance training in reducing falls.

Impaired movement, especially the loss of ability to maintain standing balance, adversely affects function and quality of life in patients with Parkinson's disease. With progression of the disease, patients lose stability and have trouble walking, difficulty managing activities of daily living, and experience frequent falls. Exercise is an important part of the management of Parkinson's disease because physical activity has been shown to retard the deterioration of motor function and to prolong functional independence. However, research on alternative forms of exercise, such as Tai Chi, that could improve balance, gait, and function in patients with Parkinson's disease is scarce.

The Tai Chi program developed by Dr. Li consisted of six Tai Chi movements integrated into an eight-form routine that focused on weight-shifting, controlled-displacement of the center of gravity over the base of support, ankle sway, and front-to-back and sideways stepping. Natural breathing was integrated into the training routine.

"There are a number of practical advantages to using Tai Chi to improve motor dysfunction of Parkinson's disease - it is a low cost activity that does not require equipment, it can be done anywhere, at any time, and the movements can be easily learned. It can also be incorporated into a rehabilitation setting as part of existing treatment. Similarly, because of its simplicity, certain aspects of this Tai Chi program can also be prescribed to patients as a self-care/home activity," Dr. Li added.

Provided by Oregon Research Institute

Mild cognitive impairment is associated with disability and neuropsychiatric symptoms

In low- and middle-income countries, mild cognitive impairment—an intermediate state between normal signs of cognitive aging, such as becoming increasingly forgetful, and dementia, which may or may not progress—is consistently associated with higher disability and with neuropsychiatric symptoms but not with most socio-demographic factors, according to a large study published in this week's PLoS Medicine.

08 feb 2012--The established 10/66 Dementia Research Group interviewed approximately 15 000 people over 65 years of age who did not have dementia in eight low- and middle-incomes countries: Cuba, Dominican Republic, Peru, Mexico, Venezuela, Puerto Rico, China, and India.

Participants also completed standardized assessments of their mental and physical health and cognitive function and the researchers also interviewed relatives and carers for further details about any memory loss or other declines in cognitive function or the presence of any neuropsychiatric symptoms.

Then, using a clinical framework and a statistical model, the authors found that mild cognitive impairment with related memory problems was associated with disability, anxiety, apathy, and irritability but not with depression.

Increasing age or former education level did not seem to be linked but the authors found that men had a slightly higher prevalence of mild cognitive impairment than women. Furthermore, the prevalence of this type of mild cognitive impairment ranged from 0.8% in China to 4.3% in India.

The authors say: "This is one of the first studies, to our knowledge, to investigate the prevalence of [mild cognitive impairment with related memory problems] in [low- and middle-income countries], where the large majority of older people and people with dementia currently live."

They continue: "Differences in prevalence between countries were marked and ranged from 0.8% (China) to 4.3% (India), that is, greater than fivefold variation. After direct standardization for age, gender, and education, using the whole population as the reference, these differences were not markedly attenuated."

The authors conclude: "Further evaluation is needed of the associations with disability and neuropsychiatric symptoms since our findings do suggest higher than expected comorbidity and there are large absolute numbers of older people with [mild cognitive impairment with related memory problems] in these rapidly ageing and populous world regions."

More information: Sosa AL, Albanese E, Stephan BCM, Dewey M, Acosta D, et al. (2012) Prevalence, Distribution, and Impact of Mild Cognitive Impairment in Latin America, China, and India: A 10/66 Population-Based Study. PLoS Med 9(2): e1001170. doi:10.1371/journal.pmed.1001170

Provided by Public Library of Science

Revised criteria could reclassify many with mild Alzheimer dementia

Many patients currently diagnosed with very mild or mild Alzheimer disease dementia could potentially be reclassified as having mild cognitive impairment (MCI) under revised criteria for that condition, according to a report published Online First by Archives of Neurology.

07 feb 2012--The National Institute on Aging and the Alzheimer's Association convened a work group to update criteria for MCI, and the revised criteria allow "considerable latitude" as to what represents functional independence, writes the study's sole author, John C. Morris, M.D., of Washington University School of Medicine in St. Louis. For example, "mild problems" performing daily activities such as shopping, paying bills and cooking are permissible, as is dependency on aids or assistance to complete those tasks.

In this study, the functional ratings of patients enrolled at federally funded Alzheimer's Disease Centers with clinical and cognitive data maintained by the National Alzheimer's Coordinating Center were evaluated. A total of 17,535 people with normal cognition, MCI or AD dementia met eligibility requirements. The mean (average) age of the total sample was 74.6 years.

The study suggests that 99.8 percent of patients currently diagnosed with very mild AD dementia and 92.7 percent of those diagnosed with mild AD dementia could be reclassified as having MCI based on the revised criteria.

The difference between MCI and AD dementia in its earliest symptomatic stages has largely been based on whether cognitive impairment disrupts the activities of daily living. The revised criteria "now obscure this distinction," Morris notes.

"The elimination of the functional boundary between MCI and AD dementia means that their distinction will be based solely on the individual judgment of clinicians, resulting in nonstandard and ultimately arbitrary diagnostic approaches to MCI," Morris comments. "This recalibration of MCI moves its focus away from the earliest stages of cognitive decline, confounds clinical trials of individuals with MCI where progression to AD dementia is an outcome, and complicates diagnostic decisions and research comparisons with legacy data."

The author suggests that the revised criteria for MCI "laudably recommend" an etiologic (origins) diagnosis, "MCI due to AD," when the physician's judgment is that AD is responsible for an individual's cognitive dysfunction.

"The diagnostic overlap for MCI with milder cases of AD dementia is considerable and suggests that any distinction is artificial and arbitrary," Morris concludes. "Already, many individuals with MCI are treated with pharmacological agents approved for symptomatic AD, indicating that clinicians often do not distinguish the two conditions when faced with issues of medical management. It now is time to advance AD patient care and research by accepting that 'MCI due to AD' is more appropriately recognized as the earliest symptomatic stage of AD."

More information: Arch Neurol. Published online February 6, 2012. doi:10.1001/archneurol.2011.3152

Provided by JAMA and Archives Journals

New study to assess 3 simple, cost-effective strategies to promote healthy aging

In Europe, the number of seniors aged 70 and over will increase by 40% in the next 20 years, while those aged 80 and over will more than double. Health authorities and the medical community expect a corresponding increase in the number of people suffering costly and debilitating age-related chronic diseases such as osteoporosis, arthritis, heart and lung diseases and dementia. The significant increase in the numbers of people suffering age-related chronic diseases is expected to have serious social and health-economic repercussions across Europe – unless effective prevention strategies are put in place.

06 feb 2012--A new international study announced today by the University of Zurich hopes to provide definitive evidence that three effective, affordable and safe measures can be taken to significantly reduce the burden of chronic diseases in the elderly. The DO-HEALTH study (VitaminD3-Omega3-Home Exercise-Healthy Ageing and Longevity Trial) will be Europe's largest healthy ageing study. It expects to provide solid evidence for the efficacy and safety of three simple preventive interventions: vitamin D, omega-3 fatty acids and a simple home exercise programme.

Professor Heike Bischoff-Ferrari, Director of the Centre on Aging and Mobility of Zurich University and DO-HEALTH Principal Investigator said "Various studies have shown that vitamin D and simple targeted exercise programmes can significantly improve functional mobility and reduce falls and fractures in seniors, even by up to 30%. As well Omega 3 provides significant health benefits to seniors. DO-HEALTH hopes to provide definitive evidence that the three interventions, alone or combined, are able to reduce the number of fractures, the functional and cognitive decline, the risk of hypertension and the risk of infections in the senior population".

Additionally, the study will measure several other important parameters, such as the severity of knee pain in patients with osteoarthritis, the ability to carry out daily life activities and the participants' general quality of life.

DO-HEALTH will start recruiting seniors in five European countries as of May 2012 and will observe more than 2,000 healthy-at-start community-dwelling seniors, aged 70 and older, for three years. Participants' follow-up will be in-person and in quarterly intervals, including yearly clinical visits. Participants will be recruited at the University of Zurich, Basel, Geneva, Toulouse, Innsbruck, Nuremberg, Coimbra and the Charité in Berlin.

Professor René Rizzoli, Board Member of the International Osteoporosis Foundation and Head of the Division of Bone Diseases, Department of Medical Specialties, Geneva University Hospitals and Faculty of Medicine, stated, "The findings of this important new study may provide the critical evidence that will result in the implementation of simple, cost-effective strategies and medical recommendations to help tackle the growing burden of chronic diseases in Europe's senior population. Health authorities must do all they can to ensure that senior citizens remain physically independent and active members of the community".

More information: http://europa.eu/r … iLanguage=en

Provided by International Osteoporosis Foundation

Same genes linked to early- and late-onset Alzheimer's disease

The PET image of the brain shows a build up of amyloid deposits (highest amounts in yellow and red) in a patient with Alzheimer's disease.

The same gene mutations linked to inherited, early-onset Alzheimer's disease have been found in people with the more common late-onset form of the illness.

05 feb 2012--The discovery by researchers at Washington University School of Medicine in St. Louis may lead doctors and researchers to change the way Alzheimer's disease is classified.

They report their findings Feb. 1 in the online journal PLoS One.

"We probably shouldn't think of early-onset disease as inherited and late-onset as sporadic because sporadic cases and familial clustering occur in both age groups," says senior investigator Alison M. Goate, DPhil. "I think it's reasonable to assume that at least some cases among both early- and late-onset disease have the same causes. Our findings suggest the disease mechanism can be the same, regardless of the age at which Alzheimer's strikes. People who get the disease at younger ages probably have more risk factors and fewer protective ones, while those who develop the disease later in life may have more protective factors, but it appears the mechanism may be the same for both."

The researchers used next-generation DNA sequencing to analyze genes linked to dementia. They sequenced the APP (amyloid precursor protein) gene, and the PSEN1 and PSEN2 (presenilin) genes. Mutations in those genes have been identified as causes of early-onset Alzheimer's disease. They also sequenced the MAPT (microtubule associated protein tau) gene and GRN (progranulin) gene, which have been associated with inherited forms of another illness involving memory loss called frontotemporal dementia.

For several years, scientists have known that genetic mutations are linked to inherited forms of early-onset Alzheimer's disease. But now researchers at Washington University School of Medicine in St. Louis have found that some of the same genes also play a role in more common late-onset forms of Alzheimer's. Credit: Washington University BioMed Radio

"We found an increase in rare variants in the Alzheimer's genes in families where four or more members were affected with late-onset disease," says Goate, the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry, professor of neurology, of genetics and co-director of the Hope Center Program on Protein Aggregation and Neurodegeneration. "Changes in these genes were more common in Alzheimer's cases with a family history of dementia, compared to normal individuals. This suggests that some of these gene variants are likely contributing to Alzheimer's disease risk."

The study also found mutations in the MAPT and GRN genes in some Alzheimer's patients, suggesting they had been incorrectly diagnosed as having Alzheimer's disease when they instead had frontotemporal dementia.

Goate and her colleagues studied the five genes in members of 440 families in which at least four individuals per family had been diagnosed with Alzheimer's disease. They found rare variants in key Alzheimer's-related genes in 13 percent of the samples they analyzed.

"Of those rare gene variants, we think about 5 percent likely contribute to Alzheimer's disease," says first author Carlos Cruchaga, PhD, assistant professor of psychiatry. "That may not seem like a lot, but so many people have the late-onset form of Alzheimer's that even a very small percentage of patients with changes in these genes could represent very large numbers of affected individuals."

Goate, who in 1991 was the first scientist to identify a mutation in the APP gene linked to inherited, early-onset Alzheimer's disease, now wants to look closely at families with multiple cases of Alzheimer's but no mutations in previously identified Alzheimer's genes. She says it's likely they carry mutations in genes that scientists don't yet know about. And she believes that new sequencing techniques could speed the discovery of these genes. In fact, the researchers say a study like this would have been impossible only a few years ago.

"With next-generation sequencing technology, it's now possible to sequence all of these genes at the same time," Cruchaga says. "One reason we didn't do this study until now is that 15 to 20 years ago when these genes were first identified, it would have taken years to sequence each gene individually."

Cruchaga and Goate say the new technology and their new findings suggest that it may be worthwhile to sequence these genes in people with a strong family history of Alzheimer's disease.

"We would like to see physicians who treat patients with late-onset disease ask detailed questions about family history," Goate says. "I'm sure many probably do that already, but in those families with very strong histories, it's not unreasonable to think about screening for genetic mutations."

She says such screenings also may weed out people thought to have Alzheimer's disease who actually have changes in genes related to frontotemperal dementia.

Both Goate and Cruchaga agree that one result of their discovery that the same genes can be connected with both early- and late-onset forms of Alzheimer's disease may be changes in the way the disease is classified.

"It's always been somewhat arbitrary, figuring out where early-onset ends and late-onset begins," Goate says. "So I no longer look at early- and late-onset disease as being different illnesses. I think of them as stages along a continuum."

More information: Cruchaga C, et al, Rare variants in APP, PSEN1 and PSEN2 increase risk for AD in late-onset Alzheimer's disease families. PLoS One, Feb. 1, 2012. http://dx.plos.org … pone.0031039

Provided by Washington University School of Medicine

Why two new studies represent important breakthrough in Alzheimer's disease research

Two different research groups have independently made the same important discoveries on how Alzheimer's disease spreads in the brain. The groups' findings have the potential to give us a much more sophisticated understanding of what goes wrong in Alzheimer's disease and, more importantly, what can be done to prevent or repair damage in the brain.

04 feb 2012--The Times reported on the research teams of Bradley T. Hyman, MD, Ph.D., at Massachusetts General Hospital in Boston, and Karen E. Duff, Ph.D., of Columbia University Medical Center in New York.

Each research group found that the Alzheimer's disease protein called tau can apparently spread from one part of the brain to other connected areas by effectively "jumping" from one nerve cell (neuron) to another. This is good news for scientists exploring pathways for treating Alzheimer's disease, which is now a growing epidemic with the aging of the Baby Boomer generation and the sixth leading cause of death in the U.S. If scientists can determine how tau jumps from neuron to neuron, Alzheimer's disease can potentially be stopped from spreading.

Results of Dr. Hyman's AHAF-funded research will be published later this month in the journal Neuro. Dr. Duff's research was published this week in PLoS ONE.

The two research groups also made similar advances in how to study the development of the disease in mice, by making new "mouse models" that better represent the human form of Alzheimer's at later stages of the disease. This will allow scientists to develop a much more detailed understanding of what goes awry with the spread of Alzheimer's disease over time, and what can be done to stop it.

It is important to note that these scientists' findings build on an idea studied by a number of others over the years—the idea that cells can infect neighboring cells. This concept—now significantly advanced by the work of Hyman and Duff—was previously pursued by several scientists including AHAF grantees Joanna Jankowsky, Ph.D., of Baylor College of Medicine in Houston, and Marc Diamond, M.D., of Washington University School of Medicine in St. Louis.

The announcement this week reminds us why early-stage basic research is so crucial to fighting costly and devastating diseases. Only with solid investment in this type of research will solutions ultimately be developed that improve the lives of people affected by this disease.

On that front, important bipartisan legislation was unveiled this week by Senators Barbara Mikulski (D-MD) and Susan Collins (R-ME) and Representatives Chris Smith (R-NJ) and Ed Markey (D-MA). The Spending Reductions through Innovations in Therapies (SPRINT) Agenda Act of 2012 would ultimately reduce America's healthcare costs, by spurring public and private research funding and streamlining the regulatory review of treatments needed for Alzheimer's and other costly diseases. Read more information from Sen. Mikulski, and Sen. Collins. Provided by American Health Assistance Foundation

Study of Alzheimer's-related protein in healthy adults may shed light on earliest signs of disease

These are positron emission tomography scans of the brains of healthy adults showing low (left) and high (right) levels of beta-amyloid protein. Credit: Image courtesy of the Center for Vital Longevity, The University of Texas at Dallas

Researchers from the Center for Vital Longevity at the University of Texas at Dallas and UT Southwestern Medical Center have completed a large-scale neuroimaging study of healthy adults from age 30 to 90 that measured beta-amyloid protein—a substance whose toxic buildup in the brain is a diagnostic marker for Alzheimer's disease.

03 feb 2012--The findings, published in the February 1, 2012 online issue of Neurology, the medical journal of the American Academy of Neurology, mark a crucial step toward being able to predict who may be at risk for developing Alzheimer's disease long before symptoms appear.

Relatively few studies have looked at levels of beta-amyloid in healthy living adults, as until recently, beta-amyloid levels could only be measured at autopsy. Few, if any, studies have looked at beta-amyloid levels in middle-aged and younger adults. Many investigators now believe that the beginning stages of Alzheimer's disease can precede symptoms of dementia by a decade or more, so data on middle-aged adults is critically important to understanding the transition from a healthy brain to a diseased brain.

In the new study, researchers measured levels of beta-amyloid protein in the brains of 137 cognitively healthy adults between the ages of 30 and 89 using an amyloid imaging agent. The researchers found that beta-amyloid levels increased with age across the entire age span and that about 20% of adults aged 60 and older had particularly high levels of beta-amyloid.

"We found that this high-amyloid group showed deficits in cognitive performance even though the individuals were well educated and scored normally on our standard tests of cognition," said Dr. Karen Rodrigue, a postdoctoral fellow at the Center for Vital Longevity and lead author of the study. On tests of processing speed, working memory, and reasoning ability—three major aspects of cognition—higher levels of beta-amyloid correlated with lower test scores.

That beta-amyloid burden has detectable effects on cognitive function even in adults with apparently good cognitive health underscores the need to better understand the recently proposed preclinical phase of Alzheimer's disease, which suggests that beta-amyloid deposits in healthy adults do not exert a strong effect on cognition for some time.

"Our findings suggest that subtle effects on cognition occur early," said principal investigator Dr. Denise Park, co-director of the Center for Vital Longevity and Distinguished University Chair in the School of Behavioral and Brain Sciences at UT Dallas. "These are important findings because imaging patients when they first show signs of very mild cognitive impairment could be essential to determining their risk of future disease."

Long-term follow-up studies led by Dr. Park as part of the Dallas Lifespan Brain Study, one of the nation's largest projects examining neural and cognitive aging across the entire adult lifespan, are already underway to help researchers determine whether high beta-amyloid burden in healthy people necessarily predetermines occurrence of Alzheimer's disease later in life.

"Knowing this information will help us determine at what stage potential interventions, once available, may be most critical and most effective," said Park. Many researchers believe that interventions to slow or halt the progression of Alzheimer's will be most effective during middle age, before irreparable damage to the brain is done. "Just as many adults take aspirin to lower their risk of heart disease or stroke, one day we may be able to help protect our brains and cognitive health by starting a treatment in our 40s or 50s," Park said.

Another of the study's interesting findings was that some people well into their 60s, 70s, and even 80s, had beta-amyloid levels as low or lower than people at middle age or younger.

"Another avenue of our future work will be to investigate what factors enable these individuals to maintain cognitive health well into old age, whether they be genetic factors, lifestyle factors, or environmental issues," said Park.

"Understanding how the brain and mind stay healthy and vital over the long term will help guide our efforts to delay or even prevent the devastation caused by diseases like Alzheimer's."

Provided by University of Texas at Dallas