ScienceDaily (Jan. 14, 2010) — Current Alzheimer's disease (AD) research indicates that accumulation of amyloid-beta (Aβ) protein plaques in the brain is central to the development of AD. Unfortunately, presence of these plaques is typically confirmed only at autopsy. In a special issue of the journal Behavioural Neurology, researchers review the evidence that Positron emission tomography (PET) can image these plaques during life. This exciting new technique provides researchers with an opportunity to test the amyloid hypothesis as it occurs in living patients.
In a review article with over 100 references, Dr. Gil Rabinovici and Dr. William Jagust from the University of California, San Francisco and Berkeley, summarize the results of experiments from their laboratories and others using the Aβ tracer Pittsburgh Compound-B (PIB). This compound binds to Aβ protein and allows the mapping of plaques in the brains of AD and non-AD volunteer subjects.
They report that PIB-PET can detect Aβ deposits in a significant proportion of cognitively normal older subjects and that these deposits are associated with brain atrophy even in the absence of cognitive symptoms. By the time patients develop mild cognitive impairment (MCI) amyloid load in the brain appears to have reached a plateau. As patients progress to dementia, neurodegeneration and cognitive decline proceed independently of further amyloid accumulation.
The authors interpret these results as consistent with a model in which amyloid deposition plays a critical early role on the path to AD, beginning years before onset of symptoms and triggering a series of events which ultimately leads to cognitive decline and dementia. While the use of PIB-PET is currently limited to research centers because of the compound's very short radioactive half-life (20 minutes), new amyloid imaging agents with longer half-lives are under development for more widespread use. Amyloid imaging is already playing an important role in the development of amyloid-based therapies for AD, and Dr. Rabinovici and Dr. Jagust speculate that in the future amyloid imaging will assist clinicians in identifying patients with mild or atypical symptoms who may be candidates for anti-amyloid treatments.
Writing in the article, the authors state, "PIB-PET has provided us with our first in vivo glance at the dynamic relationship between amyloid deposition, clinical symptoms, and structural and functional changes in the brain in the continuum between normal aging and AD…In the future, Aβ imaging will likely supplement clinical evaluation in selecting patients for anti-amyloid therapies both during drug development and in the clinic."
Friday, January 15, 2010
Exercise Associated With Preventing, Improving Mild Cognitive Impairment
ScienceDaily (Jan. 14, 2010) — Moderate physical activity performed in midlife or later appears to be associated with a reduced risk of mild cognitive impairment, whereas a six-month high-intensity aerobic exercise program may improve cognitive function in individuals who already have the condition, according to two reports in the January issue of Archives of Neurology, one of the JAMA/Archives journals.
Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group.
These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise -- such as brisk walking, aerobics, yoga, strength training or swimming -- during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group.
These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise -- such as brisk walking, aerobics, yoga, strength training or swimming -- during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
Neural Thermostat Keeps Brain Running Efficiently
ScienceDaily (Jan. 15, 2010) — Our energy-hungry brains operate reliably and efficiently while processing a flood of sensory information, thanks to a sort of neuronal thermostat that regulates activity in the visual cortex, Yale researchers have found.
actions of inhibitory neurons allow the brain to save energy by suppressing non-essential visual stimuli and processing only key information, according to research published in the January 13 issue of the journal Neuron.
"It's called the iceberg phenomenon, where only the tip is sharply defined yet we are aware that there is a much larger portion underwater that we can not see," said David McCormick, the Dorys McConnell Duberg Professor of Neurobiology at Yale School of Medicine, researcher of the Kavli Institute of Neuroscience and co-senior author of the study. "These inhibitory neurons set the water level and control how much of the iceberg we see. We don't need to see the entire iceberg to know that it is there."
The brain uses the highest percentage of the body's energy, so scientists have long wondered how it can operate both efficiently and reliably when processing a deluge of sensory information. Most studies of vision have concentrated on activity of excitatory neurons that fire when presented with simple stimuli, such as bright or dark bars. The Yale team wanted to measure what happens outside of the classical field of vision when the brain has to deal with more complex scenes in real life.
By studying brains of animals watching movies of natural scenes, the Yale team found that inhibitory cells in the visual cortex control how the excitatory cells interact with each other.
"We found that these inhibitory cells take a lead role in making the visual cortex operate in a sparse and reliable manner," McCormick said.
James Mazer was co-senior author of the paper with McCormick. Bilal Haider, a Yale graduate student, was lead author. Other Yale authors of the paper were Matthew R. Krause, Alvaro Duque, Yuguo Yu and Jonathan Touryan.
The work was funded by the National Eye Institute and the Kavli Foundation.
actions of inhibitory neurons allow the brain to save energy by suppressing non-essential visual stimuli and processing only key information, according to research published in the January 13 issue of the journal Neuron.
"It's called the iceberg phenomenon, where only the tip is sharply defined yet we are aware that there is a much larger portion underwater that we can not see," said David McCormick, the Dorys McConnell Duberg Professor of Neurobiology at Yale School of Medicine, researcher of the Kavli Institute of Neuroscience and co-senior author of the study. "These inhibitory neurons set the water level and control how much of the iceberg we see. We don't need to see the entire iceberg to know that it is there."
The brain uses the highest percentage of the body's energy, so scientists have long wondered how it can operate both efficiently and reliably when processing a deluge of sensory information. Most studies of vision have concentrated on activity of excitatory neurons that fire when presented with simple stimuli, such as bright or dark bars. The Yale team wanted to measure what happens outside of the classical field of vision when the brain has to deal with more complex scenes in real life.
By studying brains of animals watching movies of natural scenes, the Yale team found that inhibitory cells in the visual cortex control how the excitatory cells interact with each other.
"We found that these inhibitory cells take a lead role in making the visual cortex operate in a sparse and reliable manner," McCormick said.
James Mazer was co-senior author of the paper with McCormick. Bilal Haider, a Yale graduate student, was lead author. Other Yale authors of the paper were Matthew R. Krause, Alvaro Duque, Yuguo Yu and Jonathan Touryan.
The work was funded by the National Eye Institute and the Kavli Foundation.
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