Links for Keyword: Alzheimers

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By Kelli Whitlock Burton Evolutionarily speaking, we are born to make babies. Our bodies—and brains—don’t fall apart until we come to the end of our child-bearing years. So why are grandmothers, who don’t reproduce and who contribute little to food production, still around and still mentally sound? A new study offers an intriguing genetic explanation. Scientists have proposed several explanations for why our species lives as long and as healthily as it does. One idea is that grandmothers help out with child rearing. A 1998 study found, for example, that a Hadza group of hunter-gatherers in Tanzania had more babies if grandmothers helped feed their newly-weaned young grandchildren. The researchers speculated this kind of care freed up young mothers to reproduce, and ensured that the caregiver grandmother’s genes were passed on to more young. They called their theory the “grandmother hypothesis.” But grandmothers need to have all their wits about them to help out in this way, and the new study may explain how this happens. Physician-scientist Ajit Varki and evolutionary biologist Pascal Gagneux of the University of California, San Diego, arrived at the findings accidentally. The pair was studying a gene that helps control the body’s inflammatory and immune response to injury or infection. Previous studies have linked two forms of the gene—CD33—to Alzheimer’s disease. While one CD33 variant, or allele, predisposes a person to the disease, the other appears to protect against it by preventing the formation of protein clumps in the brain. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21669 - Posted: 12.01.2015

The town of Yarumal in Colombia is famous for all the wrong reasons: it has the world’s largest population of people with Alzheimer’s disease. In Yarumal and the surrounding state of Antioquia, 5000 people carry a gene mutation which causes early-onset Alzheimer’s – half of them will be diagnosed by the age of 45, and the other half will succumb by the time they are 65. Locals call the disease La Bobera, “the foolishness”, and the village bears uncanny parallels with the fictional Macondo in Gabriel Garcia Marquez’s novel One Hundred Years of Solitude, where people suffer memory disorders and hallucinations. But while Yarumal’s “curse” is well known, no one knew how the mutation first appeared. Now researchers have traced the ancestry of the mutation, concluding that it was probably introduced by a Spanish conquistador early in the 17th century. Ken Kosik at the University of California, Santa Barbara, and colleagues collected blood samples from 102 people in Antioquia and sequenced their genomes. The mutation causing this form of early-onset Alzheimer’s is called E280A and is found in a gene on chromosome 14 – 74 people had the mutation. Because Kosik’s team had information on the genome sequence around the mutation, they could use something called identity-by-descent analysis to determine how the people in the study were related. The analysis suggested the mutation arose from a common ancestor around 375 years ago. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21647 - Posted: 11.20.2015

By Gretchen Reynolds Sturdy legs could mean healthy brains, according to a new study of British twins. As I frequently have written in this column, exercise may cause robust improvements in brain health and slow age-related declines in memory and thinking. Study after study has shown correlations between physical activity, muscular health and mental acuity, even among people who are quite old. But these studies have limitations and one of them is that some people may be luckier than others. They may have been born to have a more robust brain than someone else. Their genes and early home environment might have influenced their brain health as much as or more than their exercise habits. Their genes and early home environment also might have influenced those exercise habits, as well as how their bodies and brains responded to exercise. In other words, genes and environment can seriously confound experimental results. That problem makes twins so valuable for scientific purposes. (Full disclosure, I am a twin, although not an identical one.) Twins typically share the same early home environment and many of the same genes, and if they are identical, all their genes are the same. So if one twin’s body, brain and thinking abilities begin to differ substantially over the years from their twin’s, the cause is less likely to be solely genetic or the early environment, and more likely to be attributable to lifestyle, including exercise habits. It was that possibility that recently prompted Claire Steves, a senior lecturer in twin research at King’s College London, to consider twins and their thighs. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 21641 - Posted: 11.18.2015

Laura Sanders In an unexpected twist, two antibodies designed to fight Alzheimer’s disease instead made nerve cells in mice misbehave more. The results, published online November 9 in Nature Neuroscience, highlight how little is known about how these drugs actually work, says study coauthor Marc Aurel Busche of Technical University Munich. “We need to understand what these antibodies do in the brains of patients better,” he says. The treatment approach relies on antibodies that target amyloid-beta, a protein that builds up in the brains of people with Alzheimer’s. One of the antibodies used in the new study, bapineuzumab, failed to show benefits in much-anticipated trials described in the New England Journal of Medicine in 2014. Despite that setback, some researchers say antibodies are still the best option to halt Alzheimer’s. The bapineuzumab trial was flawed, says neurologist Dennis Selkoe of Harvard Medical School and Brigham and Women’s Hospital. And the new results, which come from mice, have little relevance for ongoing tests of other antibodies in people, he says. “A-beta immunotherapy is the most promising approach right now, and nothing in their paper undercuts that,” he says. Several other antibodies have recently shown modest benefits in people with Alzheimer’s, he adds. Representatives from Eli Lilly and Biogen, pharmaceutical companies that are developing antibody treatments, declined to comment on the new study. © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21622 - Posted: 11.10.2015

By Michelle Roberts Health editor, BBC News online An increasingly warped sense of humour could be an early warning sign of impending dementia, say UK experts. The University College London study involved patients with frontotemporal dementia, with the results appearing in the Journal of Alzheimer's Disease. Questionnaires from the friends and family of the 48 patients revealed many had noticed a change in humour years before the dementia had been diagnosed. This included laughing inappropriately at tragic events. Experts say more studies are now needed to understand how and when changes in humour could act as a red flag for dementia. There are many different types of dementia and frontotemporal dementia is one of the rarer ones. The area of the brain it affects is involved with personality and behaviour, and people who develop this form of dementia can lose their inhibition, become more impulsive and struggle with social situations. Dr Camilla Clark and colleagues recruited 48 patients from their dementia clinic at University College London. And they asked the friends or relatives of the patients to rate their loved one's liking for different kinds of comedy - slapstick comedy such as Mr Bean, satirical comedy such as Yes, Minister or absurdist comedy such as Monty Python - as well as any examples of inappropriate humour. Nearly all of the respondents said, with hindsight, that they had noticed a shift in the nine years before the dementia had been diagnosed. Many of the patients had developed a dark sense of humour - for example, laughing at tragic events in the news or in their personal lives. The dementia patients also tended to prefer slapstick to satirical humour, when compared with 21 healthy people of a similar age. © 2015 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21617 - Posted: 11.10.2015

By DAVE ITZKOFF and BENEDICT CAREY For the first time in more than a year, the widow of the actor Robin Williams is speaking publicly about the circumstances that preceded Mr. Williams’s death, and sharing details about a disease he had when he died. Stories from Our Advertisers In interviews with People magazine and with ABC News, the widow, Susan Schneider Williams, laid the blame for her husband’s suicide in 2014 not on depression but on diffuse Lewy body dementia. “It was not depression that killed Robin,” Mrs. Williams said in the People magazine interview. “Depression was one of let’s call it 50 symptoms and it was a small one.” She added: “This was a very unique case and I pray to God that it will shed some light on Lewy bodies for the millions of people and their loved ones who are suffering with it. Because we didn’t know. He didn’t know.” Parts of an interview with Mrs. Williams were shown Tuesday on ABC’s “Good Morning America,” with further segments scheduled for that evening on the network’s “World News Tonight” and “Nightline” programs, and Friday on its morning talk show “The View.” Robin Williams was one of the most explosively, exhaustingly, prodigiously verbal comedians who ever lived, says film critic A. O. Scott. And the only thing faster than Williams’s mouth was his mind. By Adam Freelander on Publish Date August 12, 2014. Photo by ABC, via Associated Press. Watch in Times Video » Mr. Williams, the stand-up comic and star of “Mork & Mindy,” “Good Morning, Vietnam,” “Good Will Hunting” (for which he won an Oscar) and “Dead Poets Society,” killed himself on Aug. 11, 2014, in the home he shared with Mrs. Williams in Tiburon, Calif. He was 63. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21601 - Posted: 11.04.2015

A drug for Alzheimer’s seems to delay the point at which a person with the condition needs to be moved into a nursing home. Donepezil is usually given to people with moderate forms of the disease, but continuing to take the drug once the disease becomes more severe seems to prolong the period of time a person can remain in their own home. Previously, the drug was not thought to benefit people once they had developed more severe forms of Alzheimer’s. But a study that followed 295 people with moderate to severe Alzheimer’s disease found that those who continued to take donepezil were nearly half as likely to end up in a care home within the next year. “It could mean thousands of patients per year not going into care homes,” says Robert Howard of University College London, who led the study. His team found that those who continued to take donepezil had a 20 per cent chance of being moved into a care home within the first year of the trial, compared to 37 per cent in those who stopped taking the drug. However the effect didn’t last. The trial lasted for three years, and after the first year, those who taking donepezil were just as likely to be moved into a home than those who weren’t, suggesting that the drug does not have a longer-term effect on the care needs of those with Alzheimer’s. “For every six patients treated with donepezil for 12 months, you would prevent one moving into a nursing home,” says Howard. “It’s a modest effect, but it’s important if it’s your mother or your wife.” © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21577 - Posted: 10.28.2015

By GINA KOLATA Three diseases, leading killers of Americans, often involve long periods of decline before death. Two of them — heart disease and cancer — usually require expensive drugs, surgeries and hospitalizations. The third, dementia, has no effective treatments to slow its course. So when a group of researchers asked which of these diseases involved the greatest health care costs in the last five years of life, the answer they found might seem surprising. The most expensive, by far, was dementia. The study looked at patients on Medicare. The average total cost of care for a person with dementia over those five years was $287,038. For a patient who died of heart disease it was $175,136. For a cancer patient it was $173,383. Medicare paid almost the same amount for patients with each of those diseases — close to $100,000 — but dementia patients had many more expenses that were not covered. On average, the out-of-pocket cost for a patient with dementia was $61,522 — more than 80 percent higher than the cost for someone with heart disease or cancer. The reason is that dementia patients need caregivers to watch them, help with basic activities like eating, dressing and bathing, and provide constant supervision to make sure they do not wander off or harm themselves. None of those costs were covered by Medicare. For many families, the cost of caring for a dementia patient often “consumed almost their entire household wealth,” said Dr. Amy S. Kelley, a geriatrician at Icahn School of Medicine at Mt. Sinai in New York and the lead author of the paper published on Monday in the Annals of Internal Medicine. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21571 - Posted: 10.27.2015

Alzheimer's disease can be detected decades before onset, using a virtual reality test, a study suggests. People aged 18 to 30 were asked to navigate through a virtual maze to test the function of certain brain cells. Those with a high genetic risk of Alzheimer's could be identified by their performance, according to German neuroscientists. The findings could help future research, diagnosis and treatment, they report in the journal Science. The scientists, led by Lukas Kunz of the German Centre for Neurodegenerative Diseases in Bonn, say the high risk group navigated the maze differently and had reduced functioning of a type of brain cell involved in spatial navigation. The findings could give an insight into why people with dementia can find navigating the world around them challenging, they say. "Our results could provide a new basic framework for preclinical research on Alzheimer's disease and may provide a neurocognitive explanation of spatial disorientation in Alzheimer's disease," they report in Science. Although genes play a role in dementia, their effects are complex with many unknowns. Dr Laura Phipps of Alzheimer's Research, said the latest study focused on healthy younger people at higher genetic risk of Alzheimer's, suggesting they may already show alterations in spatial navigation several decades before the disease could start. © 2015 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21555 - Posted: 10.23.2015

By Nicholas Bakalar Agitation and aggression are common in Alzheimer’s patients, and there is no known safe and effective treatment. Now researchers report that a combination drug already in use for treating certain neurological problems may be a better remedy. Dextromethorphan is a cough suppressant commonly found in over-the-counter cough medicines, and quinidine is a drug used to control heart rhythm disorders. In combination, they are used to treat certain neurological disorders involving involuntary movement of the facial muscles. The scientists randomized 152 Alzheimer’s patients to a 10-week course of dextromethorphan-quinidine and 127 to placebo. Researchers then rated them using a well-validated scale that measures aggression and agitation. The study is in the Sept. 22 issue of JAMA. Aggression scores declined to 3.8 from 7.1 in the dextromethorphan-quinidine group and to 5.3 from 7.0 in those who took a placebo. Then the researchers re-randomized those who did not respond to placebo to receive either drugs or placebo, and found similar encouraging results for the drug combination. “Fifty-five percent of the people who were on drugs had a 50 percent reduction in their agitation,” said the lead author, Dr. Jeffrey L. Cummings, director of the Cleveland Clinic Lou Ruvo Center for Brain Health. “That’s a lot when a patient is striking and hitting and cussing. There are no currently approved treatments for agitation, and we’re very enthusiastic about this finding.” © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21459 - Posted: 09.30.2015

Steve Connor A painkiller widely used to treat rheumatoid arthritis has been shown to reverse the symptoms of dementia in the brains of laboratory mice, raising hope that there may soon be an effective treatment for Alzheimer’s disease, scientists have said. The drug, salsalate, is a licensed pain killer but in mice with a form of dementia similar to Alzheimer’s it reversed the changes to a key protein in the brain that builds up in patients with the debilitating neurological disease, they found. The researchers said it is the first time any drug has been shown to have an effect on the “tau” protein that accumulates in the brain of people with Alzheimer’s and a range of similar dementias known as “tauopathies”. It could lead to an effective therapy even for patients in the later stages of disease, the researchers said. “We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity," said Li Gan, PhD of the Gladstone Institutes, a non-profit research organisation affiliated with the University of California, San Francisco. “Remarkably, the profound protective effects of salsalate were achieved even though it was administered after disease onset, indicating that it may be an effective treatment option,” said Dr Gan a senior co-author of the study published in the journal Nature Medicine. As many as 800,000 people in Britain are already affected by Alzheimer’s disease and a new study has suggested that as many as one in three babies born this year will get dementia in their lifetime, largely as a result of people living longer. Age is the biggest risk factor for the disease. © independent.co.uk

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21428 - Posted: 09.22.2015

Nancy Shute There have been suggestions that low levels of vitamin D might be a factor in cognitive decline and Alzheimer's disease, but there's no proof that the lack of D is actually causing the problems. A study published Monday doesn't prove that link, but it does find that people with low levels of vitamin D lost key thinking skills more quickly than people with enough. The study is notable because of the diversity of the participants: 62 percent were women, 30 percent were African-American, 25 percent Hispanic and 41 percent white. Most earlier studies looking at cognitive decline and vitamin D were in white people. The participants lived in California's Sacramento Valley and were mostly in their 70s when they entered the study. The researchers followed up with them for about five years, having them take annual neurological exams and neuropsychological testing at the University of California, Davis, Alzheimer's Disease Center. Most of the 382 people in the study were low on vitamin D, tested by measuring 25-hydroxyvitamin D in the blood. One-quarter of the participants were deficient in vitamin D, and 35 percent had levels deemed insufficient. That's not a surprise — most older people are below the "adequate" level of 20 to less than 50 ng/ml, often because they're not outside much. And most of the people in the study weren't getting the recommended three servings of dairy foods daily that could help. © 2015 NPR

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21414 - Posted: 09.16.2015

A study suggests that a chemical in dark chocolate and red wine can slow the progression of Alzheimer’s disease. But how conclusive is the data, and does this mean we should all drink more wine? New Scientist looks at the evidence. What is resveratrol? Found in grapes, red wine and dark chocolate, many claims have been made about resveratrol. It has been touted as a potential panacea for a range of age-related disorders, including cancer, diabetes and neurological problems, but so far most of the data supporting these claims has come from lab studies and work in animals. There have been only a few, small studies in humans. How might resveratrol protect us from age-related illness? Extremely calorie-restricted diets greatly reduce age-related diseases in lab animals. This is thought to happen through the activation of a group of enzymes called sirtuins, which seem to affect gene expression and protect against the effects of stress, including a poor diet. The hope is that resveratrol activates sirtuins to get the same benefits – like preventing the onset of age-related diseases, including Alzheimer’s – without having to stick to such a low-energy diet. But some experiments have suggested slowed ageing from caloric restriction may not be down to sirtuins after all. What does the latest study show? To see if resveratrol could delay the progression of Alzheimer’s disease in people , Scott Turner at Georgetown University Medical Centre in Washington DC and his team gave 119 people with mild to moderate symptoms of the disease either a gram of synthesised resveratrol twice a day in pills for a year, or a placebo. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21404 - Posted: 09.14.2015

Alison Abbott Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception. The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease. “This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.” If confirmed, the findings raise the spectre that tens of thousands of other people treated with the human growth-hormone (hGH) extracts might be at risk of Alzheimer’s. And although there is no suggestion that Alzheimer’s could be contracted through normal contact with patients, some scientists worry that the findings may have broader implications: that Alzheimer’s could be passed on by other routes through which CJD can be transmitted, such as blood transfusions or contaminated surgical instruments. © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21395 - Posted: 09.10.2015

An experimental gene therapy reduces the rate at which nerve cells in the brains of Alzheimer’s patients degenerate and die, according to new results from a small clinical trial, published in the current issue of the journal JAMA Neurology. Targeted injection of the Nerve Growth Factor gene into the patients’ brains rescued dying cells around the injection site, enhancing their growth and inducing them to sprout new fibres. In some cases, these beneficial effects persisted for 10 years after the therapy was first delivered. Alzheimer’s is the world’s leading form of dementia, affecting an estimated 47 million people worldwide. This figure is predicted to almost double every 20 years, with much of this increase is likely to be in the developing world. And despite the huge amounts of time, effort, and money devoted to developing an effective cure, the vast majority of new drugs have failed in clinical trials. The new results are preliminary findings from the very first human trials designed to test the potential benefits of nerve growth factor (NGF) gene therapy for Alzheimer’s patients. NGF was discovered in the 1940s by Rita Levi-Montalcini, who convincingly demonstrated that the small protein promotes the survival of certain sub-types of sensory neurons during development of the nervous system. Since then, others have shown that it also promotes the survival of acetylcholine-producing cells in the basal forebrain, which die off in Alzheimer’s. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21360 - Posted: 08.29.2015

By Dina Fine Maron Whenever the fictional character Popeye the Sailor Man managed to down a can of spinach, the results were almost instantaneous: he gained superhuman strength. Devouring any solid object similarly did the trick for one of the X-Men. As we age and begin to struggle with memory problems, many of us would love to reach for an edible mental fix. Sadly, such supernatural effects remain fantastical. Yet making the right food choices may well yield more modest gains. A growing body of evidence suggests that adopting the Mediterranean diet, or one much like it, can help slow memory loss as people age. The diet's hallmarks include lots of fruits and vegetables and whole grains (as opposed to ultrarefined ones) and a moderate intake of fish, poultry and red wine. Dining mainly on single ingredients, such as pumpkin seeds or blueberries, however, will not do the trick. What is more, this diet approach appears to reap brain benefits even when adopted later in life—sometimes aiding cognition in as little as two years. “You will not be Superman or Superwoman,” says Miguel A. Martínez González, chair of the department of preventive medicine at the University of Navarra in Barcelona. “You can keep your cognitive abilities or even improve them slightly, but diet is not magic.” Those small gains, however, can be meaningful in day-to-day life. Scientists long believed that altering diet could not improve memory. But evidence to the contrary started to emerge about 10 years ago. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21350 - Posted: 08.28.2015

By Emily Underwood It is famous for robbing Lou Gehrig of his life and Stephen Hawking of his mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now, scientists are converging on an explanation, at least for a fraction of the ALS cases caused by a specific mutation. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become clogged, preventing vital molecules from passing through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9orf72—a DNA stutter in which a short nucleotide sequence, GGGGCC, is repeated hundreds to thousands of times in a gene on chromosome 9. Nor do the multiple labs reporting results this week agree on exactly what plugs those nuclear pores and how the cells die. Still, the work is “a major breakthrough” in ALS research, says Amelie Gubitz, program director of the neurodegeneration division at the National Institute of Neurological Disorders in Bethesda, Maryland. The groups worked independently, starting with different hypotheses and experimental designs, yet reached similar conclusions, making the finding more convincing. And it suggests that boosting 
traffic through nuclear pores could be a new strategy for treating some cases of ALS and frontotemporal dementia (FTD), another neurodegenerative condition C9orf72 can cause. Based on past work by their own and other groups, neuroscientists Jeff 
Rothstein and Tom Lloyd at Johns Hopkins University in Baltimore, Maryland, suspected that the long strands of excess RNA produced by C9orf72 cause neurodegeneration by binding to, and thus sequestering, key cellular proteins. The team tested the idea in fruit flies with the mutation, which display damage in the nerve cells of their eyes and in motor neurons. © 2015 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 21349 - Posted: 08.27.2015

While some research suggests that a diet high in omega-3 fatty acids can protect brain health, a large clinical trial by researchers at the National Institutes of Health found that omega-3 supplements did not slow cognitive decline in older persons. With 4,000 patients followed over a five-year period, the study is one of the largest and longest of its kind. It was published today in the Journal of the American Medical Association. “Contrary to popular belief, we didn’t see any benefit of omega-3 supplements for stopping cognitive decline,” said Emily Chew, M.D., . Dr. Chew leads the Age-Related Eye Disease Study (AREDS), which was designed to investigate a combination of nutritional supplements for slowing age-related macular degeneration (AMD), a major cause of vision loss among older Americans. That study established that daily high doses of certain antioxidants and minerals — called the AREDS formulation — can help slow the progression to advanced AMD. A later study, called AREDS2, tested the addition of omega-3 fatty acids to the AREDS formula. But the omega-3’s made no difference. Omega-3 fatty acids are made by marine algae and are concentrated in fish oils; they are believed to be responsible for the health benefits associated with regularly eating fish, such as salmon, tuna, and halibut.*Where studies have surveyed people on their dietary habits and health, they’ve found that regular consumption of fish is associated with lower rates of AMD, cardiovascular disease, and possibly dementia. “We’ve seen data that eating foods with omega-3 may have a benefit for eye, brain, and heart health,” Dr. Chew explained.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21340 - Posted: 08.26.2015

By Katie Free Shouting during a nightmare. Struggling to balance a checkbook. A weakened sense of smell. Hallucinations. Chronic constipation. This bizarre mix of symptoms often stumps doctors, but they are some of the telltale signs of Lewy body dementia—the second most common type (after Alzheimer's disease), affecting an estimated 1.4 million Americans. Lewy bodies are protein clumps that kill neurons. Depending on where they cluster in the brain, they can cause either Parkinson's disease or Lewy body dementia, although the two conditions tend to overlap as they progress. Lewy body dementia is more difficult to diagnose and treat, in part because the earliest warning signs have remained unknown. Now a new study finds that certain sensory and motor symptoms can help predict who will acquire the disease, paving the way for targeted studies. Researchers at the Center for Advanced Research in Sleep Medicine (which is associated with the University of Montreal) and at McGill University followed 89 patients with a history of acting out their dreams—not sleepwalking but moving or vocalizing in bed during rapid eye movement (REM) sleep. The failure to suppress such nighttime activity can be an early sign that something is going wrong in the brain; past studies have shown that up to 80 percent of patients who act out their dreams will eventually develop some form of neurodegeneration. Over 10 years the McGill researchers carefully tracked the patients' other potential symptoms of neural disease, such as mild cognitive impairment, depression and movement problems. They found a cluster of symptoms—abnormal color vision, loss of smell and motor dysfunction—that doubled the chance that a person with the REM sleep disorder would develop Parkinson's or Lewy body dementia within three years, according to the study published in February in Neurology. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21237 - Posted: 07.30.2015

Sara Reardon After years of disappointment, clinical-trial results released on 22 July suggest that antibody treatments may produce small improvements in people with Alzheimer’s disease. The drugs — Eli Lilly’s solanezumab and Biogen’s aducanumab — target the amyloid-β protein that accumulates in the brains of people with Alzheimer’s. Many researchers question whether the findings will hold up, given that antibody drugs against amyloid have failed in every previous test against the disease. Details of the results were presented at the Alzheimer's Association International Conference in Washington DC. Lilly, of Indianapolis, Indiana, says that in a trial with 440 participants, solanezumab seemed to slow the cognitive decline of people with mild Alzheimer’s by about 30%. The loss of mental acuity in these patients over 18 months was equivalent to the deterioration that participants with a similar level of Alzheimer's disease in a placebo group experienced in just 12 months. Lilly snatched this small victory from the jaws of defeat. In 2012, the company reported no difference between patients who had taken solanezumab for 18 months and those who had received a placebo. But when the company reanalyzed that trial it found a slight improvement in participants whose symptoms were mild when the trial began. Lilly continued the test for six months and began giving solanezumab to the 440-member control group, whose disease was by then more advanced. © 2015 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21212 - Posted: 07.23.2015