Brain
Gene predicts how brain responds to fatigue, human study shows
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New imaging research in the June 24 issue of The Journal of Neuroscience helps explain why sleep deprivation affects some people more than others. After staying awake all night, those who are genetically vulnerable to sleep loss showed reduced brain activity, while those who are genetically resilient showed expanded brain activity, the study found. The findings help explain individual differences in the ability to compensate for lack of sleep.
“The extent to which individuals are affected by sleep deprivation varies, with some crashing out and others holding up well after a night without sleep,” said Michael Chee, MBBS, at the Duke–National University of Singapore Graduate Medical School, an expert on sleep deprivation who was not affiliated with the study. However, studying how the brain produces these behavioral differences is difficult: researchers usually do not know whether their study participants will be vulnerable to sleep deprivation until after a study is complete. Previous studies have shown conflicting results, perhaps because the study subjects differed widely in vulnerability to sleep deprivation.
In the current study, the researchers, led by Pierre Maquet, MD, at the University of Lìege in Belgium and Derk-Jan Dijk, PhD, at the University of Surrey in the United Kingdom, avoided this problem by selecting study participants based on their genes. Previous research showed that the PERIOD3 (PER3) gene predicts how people will respond to sleep deprivation. People carry either long or short variants of the gene. Those with the short PER3 variant are resilient to sleep loss — they perform well on cognitive tasks after sleep deprivation. However, those with the long PER3 variant are vulnerable — they show deficits in cognitive performance after sleep deprivation. Now the new study explains why.
Pathologists Pioneer Biomarker Test to Diagnose or Rule Out Alzheimer’s Disease
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A test capable of confirming or ruling out Alzheimer’s disease has been validated and standardized by researchers at the University of Pennsylvania School of Medicine. By measuring cerebrospinal fluid (CSF) concentrations of two of the disease’s biochemical hallmarks – amyloid beta42 peptide and tau protein – the test also predicted whether a person’s mild cognitive impairment would convert to Alzheimer’s disease over time. Researchers were able to detect this devastating disease at the earliest stages, before dementia symptoms appeared and widespread irreversible damage occurred. The findings hold promise in the search for effective pharmaceutical therapies capable of halting the disease.
Homing in on a previously suggested pathological CSF biomarker signature, a team of Penn Medicine researchers, led by Leslie M. Shaw, PhD, Co-Director of the Penn Alzheimer’s Disease Neuroimaging Initiative (ADNI) Biomarker Core, found evidence of neuron degeneration – marked by an increase in CSF concentration of tau proteins – and plaque deposition, indicated by a decrease in amyloid beta42 concentration. In addition, people with two copies of the genetic risk factor for Alzheimer’s disease, APOE ε4 , had the lowest concentrations of amyloid beta42, compared to those with one or no copies. The study appears in the online edition of the Annals of Neurology.
“With this test, we can reliably detect and track the progression of Alzheimer’s disease,” said Dr. Shaw. “Validated biomarker tests will improve the focus of Alzheimer’s clinical trials, enrolling patients at earlier stages of the disease to find treatments that can at least delay –and perhaps stop– neurodegeneration. In addition, prevention trials can test methods to delay or block mild cognitive impairment from converting to full-blown Alzheimer’s.”
Better Tests Needed to Pinpoint Memory Problems
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There’s a lot more to memory than the ability to remember a story, who the President is, or what you ate for lunch.
Do you recall who told you the story? How about whether you heard it before or after the President’s inauguration? Do you remember that you planned to meet a friend for lunch tomorrow?
According to new research by scientists at Washington State University (WSU), aspects of memory that record the source of information and the relative timing of events are at least as important to our everyday functioning as the ability to recall specific content.
“These other aspects of memory may actually have greater contributions to what people are reporting in their everyday lives as causing problems,” said Maureen Schmitter-Edgecombe, a WSU psychologist and leader of the study.
Formal “brain exercise” won’t help healthy seniors
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Healthy older people shouldn’t bother spending money on computer games and Web sites promising to ward off mental decline, the author of a review of scientific evidence for the benefits of these “brain exercise” programs says.
“These marketed products don’t confer any additional benefit over and above being socially and intellectually active in one’s normal daily life,” Dr. Peter J. Snyder of Lifespan Affiliated Hospitals in Providence, Rhode Island, told Reuters Health. “There are some things that we could be doing that have much more rigorous data to support their application.”
Types of “brain training” are known to help people with memory problems function better, but their benefits for those who don’t have measurable cognitive impairment isn’t clear, Snyder and his team note in the journal Alzheimer’s & Dementia. Meanwhile, Snyder said in an interview, the market for these products has swelled from $2 million in 2005 to an estimated $225 million this year.
Can Exercising Your Brain Prevent Memory Loss?
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Participating in certain mental activities, like reading magazines or crafting in middle age or later in life, may delay or prevent memory loss, according to a study released today that will be presented at the American Academy of Neurology’s 61st Annual Meeting in Seattle, April 25 to May 2, 2009.
The study involved 197 people between the ages of 70 and 89 with mild cognitive impairment, or diagnosed memory loss, and 1,124 people that age with no memory problems. Both groups answered questions about their daily activities within the past year and in middle age, when they were between 50 to 65 years old.
The study found that during later years, reading books, playing games, participating in computer activities and doing craft activities such as pottery or quilting led to a 30 to 50 percent decrease in the risk of developing memory loss compared to people who did not do those activities. People who watched television for less than seven hours a day in later years were 50 percent less likely to develop memory loss than people who watched for more than seven hours a day.
Forgotten and lost - when proteins “shut down” our brain
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Which modules of the tau protein, in neurons of Alzheimer disease patients, may act in a destructive manner were investigated by researchers from the Max Planck Institute for Biophysical Chemistry (Göttingen) and the Max Planck Unit for Structural Molecular Biology (Hamburg) with the help of Nuclear Magnetic Resonance Spectroscopy (PLoS Biology, February 17, 2009).
Coordination becomes difficult, items disappear, keeping new information in the mind is impossible. Worldwide almost 30 million people suffer from Alzheimer’s disease, a neurodegenerative, irreversible ailment which starts with memory gaps and ends in helplessness and the loss of personality. The most critical factor in developing Alzheimer’s disease is age. Most cases occur after the age of 65.
Two hallmarks are typical for Alzheimer affected brains. One of them, located between nerve cells, is amyloid plaques - extracellular protein aggregates mainly composed of a protein named beta-amyloid. The other clue is intracellular tau fibrils. In the interplay with genetic factors, the latter contribute to a disordered communication within the cell. This triggers cell death.
MRI shows brain atrophy pattern that predicts Alzheimer’s
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Using special MRI methods, researchers have identified a pattern of regional brain atrophy in patients with mild cognitive impairment (MCI) that indicates a greater likelihood of progression to Alzheimer’s disease. The findings are published in the online edition of Radiology.
“Previously, this pattern has been observed only after a diagnosis of probable Alzheimer’s disease,” said the study’s lead author, Linda K. McEvoy, Ph.D., assistant project scientist in the Department of Radiology at the University of California San Diego School of Medicine in La Jolla. “Our results show that some individuals with MCI have the atrophy pattern characteristic of mild Alzheimer’s disease, and these people are at higher risk of experiencing a faster rate of brain degeneration and a faster decline to dementia than individuals with MCI who do not show that atrophy pattern.”
According to the Alzheimer’s Association, more than five million Americans currently have Alzheimer’s disease. One of the goals of modern neuroimaging is to help in early and accurate diagnosis, which can be challenging. There is no cure for Alzheimer’s disease, but when it is diagnosed early, drug treatment may help improve or stabilize patient symptoms.
Mediterranean diet may protect the brain
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Eating a Mediterranean-style diet high in vegetables, fruits and nuts, legumes, fish and cereals, and low in dairy products, meat, and fat, with moderate alcohol consumption, is not only good for the heart, it’s also good for the brain, new research hints.
In a study, “following Mediterranean diet-type habits was associated with reduced risk for getting mild cognitive impairment—a transitional stage between normal cognition and dementia/Alzheimer’s disease,” Dr. Nikolaos Scarmeas told Reuters Health.
“Additionally, subjects who already had mild cognitive impairment and had a higher adherence to the Mediterranean diet had lower risk for converting to Alzheimer’s disease,” he noted.
Growth Factor Reverses Alzheimer’s-Like Signs in Animals
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Memory loss, cognitive impairment, brain cell degeneration and cell death were prevented or reversed in several animal models after treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF). The study by a University of California, San Diego-led team – published in the February 8, 2009 issue of Nature Medicine – shows that BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping the progression of Alzheimer’s disease in animal models.
“The effects of BDNF were potent,” said Mark Tuszynski, MD, PhD, professor of neurosciences at the UC San Diego School of Medicine and neurologist at the Veterans Affairs San Diego Health System. “When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease.”
BDNF is normally produced throughout life in the entorhinal cortex, a portion of the brain that supports memory. Its production decreases in the presence of Alzheimer’s disease. For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer’s disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage.
UCSB scientists make headway in understanding Alzheimer’s disease
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Scientists at UC Santa Barbara have discovered that a protein called BAG2 is important for understanding Alzheimer’s disease and may open up new targets for drug discovery. They are ready to move from studying these proteins in culture to finding out how they work with mice.
In a paper published this week in the Journal of Neuroscience, the scientists describe important activities of BAG2 in cleaning up brain cells. The protein tau is normally found in brain cells, but scientists don’t know why it clumps into tangles in people with Alzheimer’s disease.
Senior author Kenneth S. Kosik, co-director of UCSB’s Neuroscience Research Institute, and Harriman Chair in Neuroscience, has been involved in the study of neurons that develop neurofibrillary tangles, one of the hallmarks of the disease, since he was a postdoctoral fellow. “Early on in my career, we were one of several labs to discover that tau was in the neurofibrillary tangles,” said Kosik.
1 gene regulates pain, learning and memory
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In 2002, a group of scientists at the University of Toronto was able to identify a gene which they dubbed DREAM (downstream regulatory element antagonistic modulator). The gene’s function was highly interesting: it obviously served as a key regulator in the perception of pain. Mice who lacked the gene showed clear signs of markedly reduced sensitivity to all kinds of pain, whether chronic or acute. Otherwise, the mice appeared perfectly normal.
The work leading to these findings was carried out in the lab of Josef Penninger, then principal investigator at the Amgen Institute in Toronto. The publication describing the gene’s function was received with great interest (Cell, Vol. 108, 31-43, 11.1.2002) and DREAM was subsequently termed the “Master-Gene of pain perception”.
Josef Penninger, meanwhile scientific director of IMBA, the Institute of Molecular Biotechnology of the Austrian Academy of Sciences in Vienna, continued to wonder what other surprises DREAM might have in store. In a collaborative effort with neurobiologists from the University Pablo de Olivade (Seville) he devised experiments to follow up on the previous findings. A team of scientists under Ángel Manuel Carrión subjected DREAM-less mice to numerous neurological tests and analyzed their memory skills. The results were striking: without DREAM, mice were able to learn faster and remember better. Fascinatingly, the brains of aged mice (18 months) showed learning capacities similar to those of very young mice.
Alzheimer’s: Who’s Taking Care of the Caregiver?
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About 300,000 Canadians over 65 suffer from Alzheimer’s disease, and 17% of Canadians have someone with the disease in their family, according to the Alzheimer Society of Canada. People who suffer from Alzheimer’s usually receive long-term help and support from caregivers. But who is taking care of these caregivers? Researchers are finding ways to help caregivers stay mentally and physically healthy, overcome their challenges, and better understand the disease.
Several experts from the Canadian Institutes of Health Research (CIHR) are available to comment on different aspects related to the health issues experienced by caregivers of Alzheimer’s patients on January 13.
Experts:
Preventing distress in Alzheimer’s caregivers
Gout may protect against Parkinson’s disease
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Having gout apparently lowers the risk of developing Parkinson’s disease in older individuals, new research hints.
Gout is caused by high levels of uric acid in the blood. Some studies have shown that uric acid exerts beneficial antioxidant effects on neurons. With these antioxidant properties, uric acid has been hypothesized to protect against oxidative stress, a process in which cell-damaging free radical particles are produced, which is a prominent contributor to nerve degeneration seen in Parkinson’s disease (PD).
Dr. Hyon Choi, of the University of British Columbia, Vancouver, BC, Canada, and colleagues assessed the relationship between gout and the risk of PD in a large group of people aged 65 and older. They compared rates of PD between 11,258 people with gout and 56,199 matched control subjects.
People With Intellectual Disabilities Face Health Care Hurdles
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People with intellectual disabilities face a variety of barriers when it comes to organizing their health care, and there’s little research to direct health care providers in helping them, according to a new review of studies.
“At a personal level, there are communication problems. They’re not able to communicate their health issues as well as the general population. At a community level, sometimes there are access problems; a lot of people have physical problems also, so they can’t get to the places that provide services,” said Robert Balogh, the lead review author.
Barriers also exist at the health service provider level. “Some of them are not trained to work with that population, are reluctant to see them and they don’t have very good attitudes,” Balogh said.
Occasional Memory Loss Tied to Lower Brain Volume
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People who occasionally forget an appointment or a friend’s name may have a loss of brain volume, even though they don’t have memory deficits on regular tests of memory or dementia, according to a study published in the October 7, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology.
The study involved 500 people age 50 to 85 with no dementia who lived in the Netherlands. Participants were asked about occasional memory problems such as having trouble thinking of the right word or forgetting things that happened in the last day or two, or thinking problems such as having trouble concentrating or thinking more slowly than they used to.
Participant’s brains were scanned to measure the size of the hippocampus, an area of the brain important for memory and one of the first areas damaged by Alzheimer’s disease.
