5.23.2012
New Research: Effects of Alcohol Both Positive and Negative for Cognition
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New cumulative research shows that alcohol consumption may affect cognitive function and the risk of dementia in the elderly, both adversely and favourably as alcohol may have both a neuro toxic and neuro protective effect, depending on the dose and drinking pattern.
This is according to a review by Kim JW et al on the association between alcohol consumption and cognition in the elderly.Longitudinal and brain imaging studies in the elderly show that excessive alcohol consumption may increase the risk of cognitive dysfunction and dementia, but regular low to moderate alcohol intake may protect against such conditions and provide cardiovascular benefits.
Studies published from 1971 to 2011 related to alcohol and cognition in the elderly were reviewed using a PubMed search.
At present, there are no proven agents to prevent cognitive decline or dementia, although a number of prospective epidemiologic studies have shown a lower risk of such conditions among light to moderate drinkers in comparison with non-drinkers.
Other studies have found that beneficial effects are seen only among certain sub-groups of subjects. A recent meta-analysis by Peters et al of subjects over the age of 65 in longitudinal studies concluded that light-to-moderate alcohol consumption, in comparison with abstinence, was associated with approximately 35-45 percent lower risk of cognitive decline or dementia.
This paper provides a summary of what is known about the mechanisms by which alcohol consumption, especially heavy drinking, can be neurotoxic, and how light-to-moderate drinking may help protect against cognitive decline and dementia.
The authors state that their intent is to determine if there is an 'optimal pattern of drinking' that may protect the elderly against such conditions.
At present, the mechanisms by which the moderate intake of wine and other alcoholic beverages reduces the risk of cardiovascular diseases are much better defined than they are for cognition. Forum members agree with the authors that further research is needed to evaluate a potential role that alcohol may play in reducing the risk of dementia.
Forum members also agree that, at present, the specific mechanisms of such putative protection are not well defined, and it would be premature to recommend light-to-moderate drinking for reducing the risk of dementia. On the other hand, current biomedical data supports the concept that regular, moderate intake of ethanol is not simply less dangerous for cognitive function, but is positively protective. This is the same conclusion reached by epidemiologic studies.'
The review paper was published in Psychiatry Investigation. (ANI)

5.18.2012
With fat: What's good or bad for the heart, may be the same for the brain
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It has been known for years that eating too many foods containing "bad" fats, such as saturated fats or trans fats, isn't healthy for your heart. However, according to new research from Brigham and Women's Hospital (BWH), one "bad" fat—saturated fat—was found to be associated with worse overall cognitive function and memory in women over time. By contrast, a "good" fat—mono-unsaturated fat was associated with better overall cognitive function and memory.
This study is published online by Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society, on May 18, 2012.
The research team analyzed data from the Women's Health Study—originally a cohort of nearly 40,000 women, 45 years and older. The researchers focused on data from a subset of 6,000 women, all over the age of 65. The women participated in three cognitive function tests, which were spaced out every two years for an average testing span of four years. These women filled out very detailed food frequency surveys at the start of the Women's Health Study, prior to the cognitive testing.
"When looking at changes in cognitive function, what we found is that the total amount of fat intake did not really matter, but the type of fat did," explained Olivia Okereke, MD, MS, BWH Department of Psychiatry.
Women who consumed the highest amounts of saturated fat, which can come from animal fats such as red meat and butter, compared to those who consumed the lowest amounts, had worse overall cognition and memory over the four years of testing. Women who ate the most of the monounsaturated fats, which can be found in olive oil, had better patterns of cognitive scores over time.
"Our findings have significant public health implications," said Okereke. "Substituting in the good fat in place of the bad fat is a fairly simple dietary modification that could help prevent decline in memory."
Okereke notes that strategies to prevent cognitive decline in older people are particularly important. Even subtle declines in cognitive functioning can lead to higher risk of developing more serious problems, like dementia and Alzheimer disease.
Read the Press Release at Eureka Alert
Labels: annals-of-neurology, brigham-and-women's-hospital, BWH, okereke

5.12.2012
Berries Protect Brain in Older Women?
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Lucky for us that we live in an area where there's fresh blueberries and strawberries in abundance.
Older women who consume these berries may delay decline in cognitive abilities by as much as 2.5 years, according to a study published today in the Annals of Neurology.
The berries contain flavonoids, compounds found in plants that can have antioxidant and anti-inflammatory properties. Stress and inflammation are thought to contribute to cognitive impairment or a reduction in ability to communicate and process information.
Between 1995 and 2001, cognitive function was measured in 16,010 women over the age of 70 at two-year intervals.
Increased consumption of blueberries and strawberries appear to slow cognitive decline in older women — the first evidence of this association.
However, part of the trend in maintaining cognitive function may also have been influenced by other lifestyle choices, such as exercising more, according to researchers.
Older women who consume these berries may delay decline in cognitive abilities by as much as 2.5 years, according to a study published today in the Annals of Neurology.
The berries contain flavonoids, compounds found in plants that can have antioxidant and anti-inflammatory properties. Stress and inflammation are thought to contribute to cognitive impairment or a reduction in ability to communicate and process information.
Between 1995 and 2001, cognitive function was measured in 16,010 women over the age of 70 at two-year intervals.
Increased consumption of blueberries and strawberries appear to slow cognitive decline in older women — the first evidence of this association.
However, part of the trend in maintaining cognitive function may also have been influenced by other lifestyle choices, such as exercising more, according to researchers.
Labels: 16010-women, annals-of-neurology, anti-oxidants, berries, flavanoids, sharon-salyer

5.11.2012
Reducing brain activity may help restore memory after cognitive decline
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Scientists have discovered a potential new therapeutic approach for improving memory and interrupting disease progression in patients with a form of cognitive impairment that often leads to full-blown Alzheimer's disease.
A study led by a Johns Hopkins neuroscientist focused on "excessbrain activity" commonly associated with conditions that cause mild cognitive decline and memory loss, and are linked to an increased risk of Alzheimer's.
Previously, it had been thought that this neural hyperactivity in thehippocampus was the brain's attempt to compensate for a weakness in forming new memories. Instead, the team found that this excess activity is contributing to conditions such as amnestic mild cognitive impairment (aMCI), in which patients' memories are worse than would be expected in healthy people the same age.
"In the case of aMCI, it has been suggested that the increased hippocampal activation may serve a beneficial function by recruiting additional neural 'resources' to compensate for those that are lost," explained lead author Michela Gallagher, the Krieger-Eisenhower Professor of Psychological and Brain Sciences in the Johns Hopkins University's Krieger School of Arts and Sciences.
"However, animal studies have raised the alternative view that this excess activation may be contributing to memory impairment," he stated.
To test how a reduction in that hippocampal activity would affect human patients with aMCI, Gallagher's team administered a low dose of a drug clinically used to treat epilepsy.
The goal was to reduce the test subjects' activity to levels that were similar to those of healthy, age-matched subjects in a control group. They used functional magnetic resonance imaging both to determine the levels of excess activity, and the reduction of it by way of the drug.
Gallagher and her team found that those subjects who had been treated with an effective dose of the drug did better on a memory task, pointing to the therapeutic potential of reducing this excess activation of the hippocampus in patients with aMCI.
These findings in human patients with aMCI are the first to clinically demonstrate that over activity in the hippocampus has no benefit for cognition, and are consistent with Gallagher's research in an animal model of memory loss: aged rodents.
The findings may have broad clinical implications because increased hippocampal activation occurs not only in patients with aMCI, but also in other conditions of risk, such as familial Alzheimer's disease (AD).
Research in mouse models of familial AD conducted at the Gladstone Institutes of San Francisco has identified mechanisms of the brain that contribute to abnormal excitatory brain activity, as reported in a paper published in the April 27 issue of the journal Cell. In addition, the results of other studies in mice using the same drug used in aMCI patients were presented at last year's International Congress on Alzheimer's disease in Paris, showing both improved memory performance and neuronal function in the hippocampus.
"From both a scientific and clinical perspective, I am thrilled about the consistency of findings obtained in aMCI patients and related animal models," said Lennart Mucke, director of the Gladstone Institute of Neurological Disease and professor of neurology and neuroscience at the University of California San Francisco.
According to Gallagher, the elevated hippocampal activity observed in conditions that precede AD may be one of the underlying mechanisms contributing to neurodegeneration and memory loss.
Studies have found that if patients with MCI are followed for a number of years, those with the greatest excess activation have the greatest further decline in memory, and are more likely to receive a diagnosis of Alzheimer's over the next four to six years.
"Apart from a direct role in memory impairment, there is concern that elevated activity in vulnerable neural networks could be causing additional damage and possibly promoting the widespread disease-related degeneration that underlies cognitive decline and the conversion to Alzheimer's disease," said Gallagher.
"Therefore, reducing the elevated activity in the hippocampus may help to restore memory and protect the brain. It will require a carefully monitored, lengthier clinical trial to determine if that is the case," he added.he study has been published in the May 10 issue of the journal Neuron. (ANI)
Labels: ANI, Cell, gallagher, gladstone-institute, leonard-mucke

5.09.2012
Omega 3 Associated with Lower Levels of Alzheimer's Causing Proteins
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A New Study shows that Omega 3, a fatty-acid substance commonly found in fish, is linked to lower levels of the proteins Abeta 40-42, two proteins that are linked with the formation of Alzheimer's and cognitive decline. Therefore, the consumption of Omega 3 in the diet, either through fish such as salmon or through tablets, may offer a degree of protection against the start of the disease.
Read the Press Release on this topic.
Read the Press Release on this topic.

5.07.2012
Did a Copying Mistake Make Humans Smarter?
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Summary:
- -Critical features of the modern human brain may have come to be through an internal copyediting error.
- -When DNA is duplicated during cell division, accidental copies can lead to mutations, some good, some bad.
- -Good mutations may have allowed our brains to become more sophisticated, new research finds.
- A copyediting error appears to be responsible for critical features of the human brain that distinguish us from our closest primate kin, new research finds.
- When tested out in mice, researchers found this "error" caused the rodents' brain cells to move into place faster and enabled more connections between brain cells.When any cell divides, it first copies its entire genome. During this process, it can make errors. The cell usually fixes errors in the DNA. But when they aren't fixed, they become permanent changes called mutations, which are sometimes hurtful and sometimes helpful, though usually innocuous.One type of error is duplication, when the DNA-copying machinery accidentally copies a section of the genome twice. The second copy can be changed in future copies — gaining mutations or losing parts.The researchers scanned the human genome for these duplications, and found that many of them seem to play a role in the developing brain."There are approximately 30 genes that were selectively duplicated in humans," study researcher Franck Polleux, of The Scripps Research Institute in La Jolla, Calif., said in a statement. "These are some of our most recent genomic innovations."An extra copy of a gene gives evolution something to work with: Like modeling clay, this gene isn't essential like the original copy, so changes can be made to it without damaging the resulting organism.
Labels: franck-polleux, scripps-research-institute, SRGAP2

5.05.2012
Biosynthetic polyphenol improves cognitive function in mice with AD
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Mount Sinai School of Medicine researchers have succeeded in developing a biosynthetic polyphenol that improves cognitive function in mice with Alzheimer's disease (AD). The findings, published in a recent issue of the Journal of Neuroscience, provide insight in determining the feasibility of biosynthetic polyphenols as a possible therapy for AD in humans, a progressive neurodegenerative disease for which there is currently no cure.
Polyphenols, which occur naturally in grapes, fruits, and vegetables, have been shown to prevent the cognitive decline associated with AD in a mouse model, but the molecules are very complex and are extensively metabolized in the body. This is the first study to determine which specific subfraction of these molecules penetrates the animal brain, and demonstrate that a drug compound similar to polyphenols can exert similar bioactivities.
A research group led by Giulio Maria Pasinetti, MD, PhD, Saunders Family Professor and Chair in Neurology at Mount Sinai School of Medicine, has been exploring the application of specific grape-derived polyphenols for the treatment of AD. Previously, this group found that certain grape-seeds extracts, comprised of a complex mixture of naturally occurring polyphenols, were capable of lessening cognitive deterioration and reducing brain neuropathology in an animal model of AD, but they did not know how to manipulate the natural extract into a pharmaceutical compound that could be used by the brain.
"My team, along with many members of the scientific community, did not know how we could harness the efficacy of naturally occurring polyphenols in food for treatment of Alzheimer's disease," Dr. Pasinetti said. "We were skeptical that these naturally occurring polyphenols would reach the brain because they are extensively metabolized following ingestion."
Labels: alzheimers-disease, bioactivities, giulio-maria-pasinetti, mt-sinai-school-of-medicine, saunders-family-professor

