Links for Keyword: Alzheimers

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 61 - 80 of 1090

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

Jon Hamilton The face of Alzheimer's isn't always old. Sometimes it belongs to someone like Giedre Cohen, who is 37, yet struggles to remember her own name. Until about a year ago, Giedre was a "young, healthy, beautiful" woman just starting her life, says her husband, Tal Cohen, a real estate developer in Los Angeles. Now, he says, "her mind is slowly wasting away." People like Giedre have a rare gene mutation that causes symptoms of Alzheimer's to appear before they turn 60. Until recently, people who inherited this gene had no hope of avoiding dementia and an early death. Now there is a glimmer of hope, thanks to a project called DIAN TU that is allowing them to take part in a study of experimental Alzheimer's drugs. The project also could have a huge payoff for society, says Dr. Randall Bateman, a professor of neurology at Washington University in St. Louis. "It's highly likely," he says, that the first drug able to prevent or delay Alzheimer's will emerge from studies of people genetically destined to get the disease. Giedre Cohen enrolled in the DIAN TU study in 2013, when she still had no symptoms of Alzheimer's, her husband says. Their story began more than a decade earlier. In 2002, Tal Cohen was on a trip to Miami to attend a wedding. He met Giedre, who was born in Lithuania, and the two fell in love. © 2015 NPR

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: 21211 - Posted: 07.23.2015

By James Gallagher Health editor, BBC News website The first hints a drug can slow the progression of Alzheimer's disease have emerged at a conference. Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third. The results are being met with cautious optimism, with a separate trial due to report next year. The death of brain cells in Alzheimer's is currently inexorable. Solanezumab may be able to keep them alive. Current medication, such as Aricept, can only manage the symptoms of dementia by helping the dying brain cells function. But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer's. It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death. Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012. But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease. So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years. And the results from this extension of the original trial have now been presented, at the Alzheimer's Association International Conference. Dr Eric Siemers, from the Lilly Research Laboratories, in Indiana, told the BBC: "It's another piece of evidence that solanezumab does have an effect on the underlying disease pathology. "We think there is a chance that solanezumab will be the first disease-modifying medication to be available." The company also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug. © 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: 21203 - Posted: 07.22.2015

By BENEDICT CAREY Women who develop slight but detectable deficits in memory and mental acuity late in life tend to decline faster than men with mild impairment, researchers reported on Tuesday. Some two-thirds of the five million Americans with Alzheimer’s disease are women, in part because women live longer. Researchers have searched in vain for decades to determine other reasons for the disparity. The authors of the new study, who presented their work at the Alzheimer’s Association International Conference in Washington, said their findings indicated nothing about possible causes of gender differences and had no immediate implications for treatment. “All we can say at this point is that there appears to be a faster trajectory for women than men” toward dementia, said Dr. P. Murali Doraiswamy, a professor of psychiatry at the Duke Institute for Brain Sciences and the study’s senior author. Katherine Amy Lin, a student of Dr. Doraiswamy’s and a co-author, presented the study. Previous research had found a steeper decline in women with mild deficits over a period of about a year. The new study extends that finding to up to eight years. “It’s a very interesting finding, but it’s also still early, so we’re limited in what conclusions we can draw,” said Dr. Edward D. Huey, a geriatric psychiatrist at Columbia University, who was not involved in the study. “I think of this as an excellent hypothesis generator. It’s something we need to investigate more deeply.” In the study, the Duke researchers analyzed scores on standard cognitive tests taken by 398 men and women, most in their 70s, being followed as part of a large, continuing Alzheimer’s trial. The participants have been taking the cognitive tests — as well as other tests, like PET scans — on average for four years, and as long as eight years. Controlling for factors that influence memory and mental acuity, like age, education and genetic predisposition, the research team found that women’s scores slipped by an average of about two points a year, compared with one point for men. The team also looked at a standard measure of life quality, rating how well people functioned socially: at home, at work and with family. That, too, slipped faster for women than for men, at about the same rate. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21202 - Posted: 07.22.2015

Kashmira Gander Performing well at school and going on to have a complex job could lower the risk of dementia, scientists have found. On the contrary, loneliness, watching too much TV and a sedentary lifestyle can make a person’s cognitive abilities decline more quickly, according to new research being presented to experts at the international Alzheimer's Association International Conference in Washington DC. Researchers are also due to show attendees the results from trials Solanezumab – believed to be the first drug to halt the progression of the disease if a patient is diagnosed early enough. One study involving 7,500 people aged 65 and above in Sweden over a 20-year period showed that dementia rates were 21 per cent higher in those whose grades were in the bottom fifth of the population. Meanwhile, participants with complex jobs involving data and numbers saw their chance of developing the disease cut by 23 per cent. Read more: Why fish oil pills may not be so healthy after all Proof that dementia risk can be reduced by improving lifestyle Charity warns of a 'worrying' lack of support for dementia patients Dementia research: Drug firms despair of finding cure and withdraw funding after a catalogue of failures For separate study in Sweden, scientists followed the lives of 440 people aged 75 or over for nine years, and discovered that those in the bottom fifth for school grades were found to have a 50 per cent increase in the risk of developing dementia. © independent.co.uk

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: 21195 - Posted: 07.21.2015

Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.

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: 21190 - Posted: 07.20.2015

By Fredrick Kunkle A new study suggests that Alzheimer’s disease may affect the brain differently in black people compared with whites. The research, conducted by Lisa L. Barnes at the Rush University Medical Center, suggests that African Americans are less likely than Caucasians to have Alzheimer’s disease alone and more likely to have other pathologies associated with dementia. These include the presence of Lewy bodies, which are abnormal proteins found in the brain, and lesions arising from the hardening of tiny arteries in the brain, which is caused mainly by high blood pressure and other vascular conditions. The findings suggest that researchers should seek different strategies to prevent and treat Alzheimer’s disease in blacks. While many therapeutic strategies focus on removing or modifying beta amyloid – a key ingredient whose accumulation leads to the chain of event triggering the neurodegenerative disease – the study suggests that possible treatments should pursue additional targets, particularly for African Americans. But the study also points up the critical need to enroll more black people in clinical trials. Although Barnes said the research was the largest sample of its kind, she also acknowledged that the sample is still small. And that’s at least partially because blacks, for a variety of cultural and historical reasons, are less likely to participate in scientific research.

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: 21176 - Posted: 07.16.2015

Hannah Devlin Science correspondent Two licensed drugs have been shown to halt brain degeneration in mice, raising the prospect of a rapid acceleration in the search for a medicine to beat Alzheimer’s disease. The results, presented on Tuesday at the Alzheimer’s Society annual research conference in Manchester, have been hailed as “hugely promising” because they involve medicines that are already known to be safe and well-tolerated in people – potentially cutting years from the timeline for drugs to reach patients. Speaking ahead of her presentation, Giovanna Mallucci, professor of clinical neuroscience at the University of Cambridge, said: “It’s really exciting. They’re licensed drugs. This means you’d do a straightforward basic clinical trial on a small group of patients because these are not new compounds, they’re known drugs.” The scientists have chosen not to name the two drugs, which are currently used for conditions unrelated to dementia, to avoid the possibility of patients seeking to use them ahead of any clinical trial to prove their efficacy. The findings build on a landmark study two years ago, showing that brain cell death could be halted in mice by switching off a faulty signal in the brain that stops new proteins being produced. However, the breakthrough relied on a compound that had severe physical side-effects including weight loss and diabetes, making it unsuitable for use in humans. The two drugs were identified after Mallucci’s team screened hundreds of licensed compounds in search for something safe that had the same protective effects on the brain. Clare Walton, research manager at the Alzheimer’s Society, said: “The new results are hugely promising because the drugs are already given to people and we know they’re safe.” © 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: 21114 - Posted: 07.01.2015

By Ariana Eunjung Cha One of the most heartbreaking things about Alzheimer's is that it has been impossible for doctors to predict who will get it before symptoms begin. And without early detection, researchers say, a treatment or cure may be impossible. Governments, drug companies and private foundations have poured huge amounts of money into trying to come up with novel ways to detect risk through cutting-edge technologies ranging from brain imaging, protein analysis of cerebrospinal fluid and DNA profiling. Now a new study, published in the journal Neurology, shows that perhaps something more old-fashioned could be the answer: a memory test. The researchers tracked 2,125 participants in four Chicago neighborhoods for 18 years, giving them tests of memory and thinking every three years. They found that those who scored lowest on the tests during the first year were 10 times more likely to be diagnosed with Alzheimer's down the road -- indicating that cognitive impairment may be affecting the brain "substantially earlier than previously established," the researchers wrote.

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: 21109 - Posted: 06.30.2015