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by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © 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: 19969 - Posted: 08.18.2014

By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 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: 19943 - Posted: 08.12.2014

Older people who have a severe vitamin D deficiency have an increased risk of developing dementia, a study has suggested. UK researchers, writing in Neurology, looked at about 1,650 people aged over 65. This is not the first study to suggest a link - but its authors say it is the largest and most robust. However, experts say it is still too early to say elderly people should take vitamin D as a preventative treatment. There are 800,000 people with dementia in the UK with numbers set to rise to more than one million by 2021. Vitamin D comes from foods - such as oily fish, supplements and exposing skin to sunlight. However older people's skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. The international team of researchers, led by Dr David Llewellyn at the University of Exeter Medical School, followed people for six years. All were free from dementia, cardiovascular disease and stroke at the start of the study. At the end of the study they found the 1,169 with good levels of vitamin D had a one in 10 chance of developing dementia. Seventy were severely deficient - and they had around a one in five risk of dementia. 'Delay or even prevent' Dr Llewellyn said: "We expected to find an association between low vitamin D levels and the risk of dementia and Alzheimer's disease, but the results were surprising - we actually found that the association was twice as strong as we anticipated." He said further research was needed to establish if eating vitamin D rich foods such as oily fish - or taking vitamin D supplements - could "delay or even prevent" the onset of Alzheimer's disease and dementia. But Dr Llewellyn added: "We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. BBC © 2014

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: 19923 - Posted: 08.07.2014

By Fredrick Kunkle The way older people walk may provide a reliable clue about how well their brain is aging and could eventually allow doctors to determine whether they are at risk of Alzheimer’s, researchers have found. The study, involving thousands of older people in several countries, suggests that those whose walking pace begins to slow and who also have cognitive complaints are more than twice as likely to develop dementia within 12 years. The findings are among the latest attempts to find and develop affordable, inexpensive diagnostic tools to determine whether a person is at risk for dementia. Last month, researchers attending the Alzheimer’s Association International Conference in Copenhagen presented several studies focused on locating biomarkers of dementia in its earliest stages. Among other things, scientists reported a connection between dementia and sense of smell that suggested a common scratch-and-sniff test could be used to help identify onset of dementia, while other researchers suggested that eye scans could also be useful someday be able to detect Alzheimer’s. Different studies found a new abnormal protein linked to Alzheimer’s and a possible link between sleep disorders and the onset of dementia. Now, researchers at the Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center say that a simple test to measure a patient’s cognitive abilities and walking speed could provide a new diagnostic tool to identify people at risk for dementia. It could be especially important tool in low- and middle-income countries with less access to sophisticated and costly technology, the scientists said.

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: 19910 - Posted: 08.02.2014

Tania Browne As a teenager, I lost my grandfather. But he wasn't dead. He still had his favourite music, he still loved to walk in the woods and name the flowers and plants, and he loved his soap operas. He was alive, but gone. A dignified man, a former aircraft engineer and oil company salesman, reduced to the status of a bewildered toddler lost in a shopping centre. When he died, our family felt an odd mix of relief, then guilt at the relief. The man we loved had left his body years before the body gave out. This was 30 years ago. But while a cure is still far away, two new techniques may at least be able to forewarn us of dementia, and allow us to plan treatment for ourselves or loved ones before any outward symptoms are apparent. According to Alzheimer's Research UK, my experience is currently shared by 24m relatives and close friends of the 800 000 diagnosed dementia sufferers in the UK. In December last year, a G8 summit was told by Alzheimer's Disease International that the worldwide figure was 44m and set to treble by 2050, as the life expectancy of people in middle and lower income countries soars – precisely the countries who have either depleted or non-existent healthcare systems. Dementia is a serious time bomb. “Dementia” covers about 100 conditions, all resulting from large scale brain cell death. People often think that when they're diagnosed they're in the early stages. Yet cell death can be occurring for 10-15 years or more before any outward symptoms occur, and by the time they're diagnosed many dementia patients have already lost one fifth of their memory cells. © 2014 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: 19856 - Posted: 07.21.2014

Associated Press The rate of Alzheimer's disease and other dementias is falling in the United States and some other rich countries - good news about an epidemic that is still growing simply because more people are living to an old age, new studies show. An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded. Dementia rates also are down in Germany, a study there found. "For an individual, the actual risk of dementia seems to have declined," probably because of more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer's Association International Conference in Copenhagen. The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising. More than 5.4 million Americans and 35 million people worldwide have Alzheimer's, the most common form of dementia. It has no cure, and current drugs only temporarily ease symptoms. A drop in rates is a silver lining in the so-called silver tsunami - the expected wave of age-related health problems from an older population. Alzheimer's will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said. © 2014 Hearst Communications, Inc.

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: 19838 - Posted: 07.16.2014

By PAULA SPAN What we really want, if we’re honest, is a pill or a shot that would allow us to stop worrying about ever sinking into dementia. Instead, what we’re hearing about preventing dementia is, in many ways, the same stuff we hear about preventing other kinds of illnesses. Healthy lifestyles. Behavioral modification. Stress reduction. At the Alzheimer’s Association International Conference in Copenhagen this week, researchers from Montefiore Medical Center and the Albert Einstein College of Medicine were among the scientists presenting findings that had little to do with amyloid in the brain and a lot to do with how people feel and act and cope with life. “A number of people have been interested in modifiable lifestyle factors for years,” said Richard Lipton, a neurologist at the college and director of the Einstein Aging Study, which has tracked cognition in elderly Bronx residents since the 1980s. But interest has increased lately, he said: “It’s at least in part a reflection of disappointing drug trials.” Medications have failed, over and over, to prevent or cure or substantially slow the ravages of dementing diseases. What else might help? Dr. Lipton and his colleagues, who monitor about 600 people aged 70 to 105, have been exploring the impact of stress. More specifically, they have been measuring “perceived stress,” a metric not so much about unpleasant things happening as how people respond to them. They use a scale based on the answers to 13 questions like, “In the past month, how often have you felt confident about your ability to handle your personal problems?” and “In the past month, how often have you felt difficulties were piling up so high you could not overcome them?” © 2014 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: 19837 - Posted: 07.16.2014

|By Maria Burke and ChemistryWorld The world needs to tackle head-on the market failures undermining dementia research and drug development, UK Prime Minister David Cameron told a summit of world health and finance leaders in London in June. He announced an investigation into how to get medicines to patients earlier, extend patents and facilitate research collaborations, to report this autumn. But just how much difference will these sorts of measures make when scientists are still grappling with exactly what causes different types of dementia? Added to these problems is that dementia has become a graveyard for a large number of promising drugs. A recent study looked at how 244 compounds in 413 clinical trials fared for Alzheimer's disease between 2002 and 2012. The researchers findings paint a gloomy picture. Of those 244 compounds, only one was approved. The researchers report that this gives Alzheimer's disease drug candidates one of the highest failures rates of any disease area – 99.6%, compared with 81% for cancer. ‘Dementia is a ticking bomb costing the global economy £350 billion and yet progress with research is achingly slow,’ warned the World Dementia Envoy, Dennis Gillings. Businesses need incentives to invest in research and bring in faster, cheaper clinical trials, or the world won’t meet the ambition to find a cure or disease-modifying therapy by 2025, he added. ‘We need to free up regulation so that we can test ground-breaking new drugs, and examine whether the period for market exclusivity could be extended.’ © 2014 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19828 - Posted: 07.15.2014

By Fredrick Kunkle Sleep disturbances such as apnea may increase the risk of Alzheimer’s disease, while moderate exercise in middle age and mentally stimulating games, such as crossword puzzles, may prevent the onset of the dementia-causing disease, according to new research to be presented Monday. The findings — which are to be introduced during the six-day Alzheimer’s Association International Conference in Copenhagen — bolster previous studies that suggest sleep plays a critical role in the aging brain’s health, perhaps by allowing the body to cleanse itself of Alzheimer's-related compounds during down time. The studies also add to a growing body of literature that suggests keeping the brain busy keeps it healthy. The battle against Alzheimer’s disease has become more urgent for the United States and other developing nations as their populations turn increasingly gray. The disease is the leading cause of dementia in older people and afflicts more than 5 million Americans. At its current pace, the number is expected to soar to 16 million people by 2050. In 2012, the United States adopted a national plan to combat the disease and the G-8 nations last year adopted a goal of providing better treatment and prevention by 2025. Erin Heintz, a spokeswoman for the Alzheimer’s Association, said U.S. government funding to combat the disease now stands at about $500 million a year. To reach its 2025 goal, the United States should be spending $2 billion a year, she said.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 19825 - Posted: 07.14.2014

One in three cases of Alzheimer's disease worldwide is preventable, according to research from the University of Cambridge. The main risk factors for the disease are a lack of exercise, smoking, depression and poor education, it says. Previous research from 2011 put the estimate at one in two cases, but this new study takes into account overlapping risk factors. Alzheimer's Research UK said age was still the biggest risk factor. Writing in The Lancet Neurology, the Cambridge team analysed population-based data to work out the main seven risk factors for Alzheimer's disease. These are: Diabetes Mid-life hypertension Mid-life obesity Physical inactivity Depression Smoking Low educational attainment They worked out that a third of Alzheimer's cases could be linked to lifestyle factors that could be modified, such as lack of exercise and smoking. The researchers then looked at how reducing these factors could affect the number of future Alzheimer's cases. They found that by reducing each risk factor by 10%, nearly nine million cases of the disease could be prevented by 2050. In the UK, a 10% reduction in risk factors would reduce cases by 8.8%, or 200,000, by 2050, they calculated. BBC © 2014

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: 19824 - Posted: 07.14.2014

By Fredrick Kunkle A simple test of a person’s ability to identify odors and noninvasive eye exams might someday help doctors learn whether their patients are at risk of Alzheimer’s disease, according to research to be presented Sunday. With Alzheimer’s disease growing fast among the world’s aging population, researchers are increasingly focused on the search for new ways to detect and treat the brain-killing disease in its earliest stages. In two separate studies on the connection between dementia and sense of smell, teams of researchers found that a decreased ability to detect odors in older people, as determined by a common scratch-and-sniff test, could point to brain cell loss and the onset of dementia. In two other studies, researchers showed that noninvasive eye exams also might offer a way to identify Alzheimer’s in its early stages. The findings — which are to be presented at the Alzheimer’s Association International Conference in Copenhagen on Sunday — raise hopes that doctors could develop simple, inexpensive diagnostic tools that would hunt down reliable biomarkers of a disease that affects more than 5 million people in the United States. Alzheimer’s is a progressive and incurable disease that begins in areas of the brain associated with memory. It is the leading cause of dementia in older people, usually striking after the age of 65. It robs people of their cognitive abilities, speech and, ultimately, their identities. Eventually, it shuts down the most basic body functions, resulting in death.

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: 19823 - Posted: 07.14.2014

by Helen Thomson A blood test for Alzheimer's might be just two years away. Abdul Hye at King's College London and his colleagues have identified 10 proteins in blood that can predict who will develop Alzheimer's disease a year after having mild memory problems. Its accuracy is almost 90 per cent. That could prove a huge boost for researchers seeking treatments. So far, trials of Alzheimer's drugs are thought to have failed because they have been given too late in the course of the disease to halt progression. The new blood test will initially be used to identify those people with mild cognitive impairment who are likely to get Alzheimer's disease and so might be good candidates for clinical trials to find drugs that halt disease progression. "Having a blood test is a really big step forward," says team member Ian Pike of Proteome Sciences in Cobham, UK. "The most important thing we can do is get the correct patients into clinical trials so we can tell, for example, whether it is a drug that is slowing the progression of the disease or the fact that we just happen to have a group of patients who have a slow progressing form of the disease." "This [blood test] is a technical tour de force," says Eric Karran, director of research at the Alzheimer's Research UK charity. However, he remains cautious about its use beyond clinical research. For every 10 people who take the test, one will get an incorrect result. "Alzheimer's is the most feared diagnosis, so we have to be careful, particularly in the absence of any treatment," he says. © 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: 19802 - Posted: 07.08.2014

By Helen Briggs Health editor, BBC News website More than 99% of drug trials for Alzheimer's disease during the past decade have failed, according to a study. There is an urgent need to increase the number of potential therapies being investigated, say US scientists. Only one new medicine has been approved since 2004, they report in the journal Alzheimer's Research & Therapy. The drug failure rate is troubling and higher than for other diseases such as cancer, says Alzheimer's Research UK. Dr Jeffrey Cummings, of the Cleveland Clinic Lou Ruvo Center for Brain Health, in Las Vegas, and colleagues, examined a public website that records clinical trials. Between 2002 and 2012, they found 99.6% of trials of drugs aimed at preventing, curing or improving the symptoms of Alzheimer's had failed or been discontinued. This compares with a failure rate of 81% for cancer drugs. The failure rate was "especially troubling" given the rising numbers of people with dementia, said Dr Simon Ridley, of Alzheimer's Research UK. "The authors of the study highlight a worrying decline in the number of clinical trials for Alzheimer's treatments in more recent years," he said. "There is a danger that the high failure rates of trials in the past will discourage pharmaceutical companies from investing in dementia research. BBC © 2014

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: 19793 - Posted: 07.04.2014

By GRETCHEN REYNOLDS Exercise may help to keep the brain robust in people who have an increased risk of developing Alzheimer’s disease, according to an inspiring new study. The findings suggests that even moderate amounts of physical activity may help to slow the progression of one of the most dreaded diseases of aging. For the new study, which was published in May in Frontiers in Aging Neuroscience, researchers at the Cleveland Clinic in Ohio recruited almost 100 older men and women, aged 65 to 89, many of whom had a family history of Alzheimer’s disease. Alzheimer’s disease, characterized by a gradual and then quickening loss of memory and cognitive functioning, can strike anyone. But scientists have discovered in recent years that people who harbor a specific variant of a gene, known as the APOE epsilon4 allele or the e4 gene for short, have a substantially increased risk of developing the disease. Genetic testing among the volunteers in the new study determined that about half of the group carried the e4 gene, although, at the start of the study, none showed signs of memory loss beyond what would be normal for their age. Then the scientists set out to more closely examine their volunteers’ brains. For some time, researchers have suspected that Alzheimer’s disease begins altering the structure and function of the brain years or even decades before the first symptoms appear. In particular, it’s been thought that the disease silently accelerates the atrophy of the hippocampus, a portion of the brain critical for memory processing. Brain scans of people who have Alzheimer’s show that their hippocampi are considerably more shrunken than those of people of the same age without the disease. There’s been less study, though, of possible shrinkage in the brains of cognitively normal people at risk for Alzheimer’s. One reason is that, until recently, few interventions, including drugs, had shown much promise in slowing or preventing the disease’s progression, so researchers – and patients – have been reluctant to identify markers of its potential onset. © 2014 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: 19783 - Posted: 07.02.2014

|By Lisa Marshall Is Alzheimer's disease an acquired form of Down syndrome? When neurobiologist Huntington Potter first posed the question in 1991, Alzheimer's researchers were skeptical. They were just beginning to explore the causes of the memory-robbing neurological disease. Scientists already knew that by age 40, nearly 100 percent of patients with Down syndrome, who have an extra copy of chromosome 21, had brains full of beta-amyloid peptide—the neuron-strangling plaque that is a hallmark of Alzheimer's. They also knew that the gene that codes for that protein lives on chromosome 21, suggesting that people acquire more plaque because they get an extra dose of the peptide. Potter, though, suggested that if people with Down syndrome develop Alzheimer's because of an extra chromosome 21, healthy people may develop Alzheimer's for the same reason. A quarter of a century later mounting evidence supports the idea. “What we hypothesized in the 1990s and have begun to prove is that people with Alzheimer's begin to make molecular mistakes and generate cells with three copies of chromosome 21,” says Potter, who was recently appointed director of Alzheimer's disease research at the University of Colorado School of Medicine, with the express purpose of studying Alzheimer's through the lens of Down syndrome. He is no longer the only one exploring the link. In recent years dozens of studies have shown Alzheimer's patients possess an inordinate amount of Down syndrome–like cells. One 2009 study by Russian researchers found that up to 15 percent of the neurons in the brains of Alzheimer's patients contained an extra copy of chromosome 21. Others have shown Alzheimer's patients have 1.5 to two times as many skin and blood cells with the extra copy as healthy controls. Potter's own research in mice suggests a vicious cycle: when normal cells are exposed to the beta-amyloid peptide, they tend to make mistakes when dividing, producing more trisomy 21 cells, which, in turn, produce more plaque. In August, Potter and his team published a paper in the journal Neurobiology of Aging describing why those mistakes may occur: the inhibition of a specific enzyme. © 2014 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: 19771 - Posted: 06.25.2014

|By Tori Rodriguez One of the most devastating aspects of Alzheimer's is its effect on patients' ability to recall life events. Several studies have found that music helps to strengthen these individuals' autobiographical memories, and a paper in the November 2013 Journal of Neurolinguistics builds on these findings by exploring the linguistic quality of those recollections. Researchers instructed 18 patients with Alzheimer's and 18 healthy control subjects to tell stories from their lives in a silent room or while listening to the music of their choice. Among the Alzheimer's patients, the music-cued stories contained a greater number of meaningful words, were more grammatically complex and conveyed more information per number of words. Music may enhance narrative memories because “music and language processing share a common neural basis,” explains study co-author Mohamad El Haj of Lille University in France. © 2014 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: 19762 - Posted: 06.24.2014

Associated Press In one of the most ambitious attempts yet to thwart Alzheimer's disease, a major study got under way Monday to see if an experimental drug can protect healthy seniors whose brains harbor silent signs that they're at risk. Scientists plan to eventually scan the brains of thousands of older volunteers in the U.S., Canada and Australia to find those with a sticky build-up believed to play a key role in development of Alzheimer's - the first time so many people without memory problems get the chance to learn the potentially troubling news. Having lots of that gunky protein called beta-amyloid doesn't guarantee someone will get sick. But the big question: Could intervening so early make a difference for those who do? "We have to get them at the stage when we can save their brains," said Dr. Reisa Sperling of Boston's Brigham and Women's Hospital and Harvard Medical School, who is leading the huge effort to find out. Researchers are just beginning to recruit volunteers, and on Monday, a Rhode Island man was hooked up for an IV infusion at Butler Hospital in Providence, the first treated. Peter Bristol, 70, of Wakefield, R.I., figured he was at risk because his mother died of Alzheimer's and his brother has it. "I felt I needed to be proactive in seeking whatever therapies might be available for myself in the coming years," said Bristol, who said he was prepared when a PET scan of his brain showed he harbored enough amyloid to qualify for the research. "Just because I have it doesn't mean I'm going to get Alzheimer's," he stressed. But Bristol and his wife are "going into the situation with our eyes wide open." He won't know until the end of what is called the A4 Study - it stands for Anti-Amyloid Treatment in Asymptomatic Alzheimer's - whether he received monthly infusions of the experimental medicine, Eli Lilly & Co.'s solanezumab, or a dummy drug. © 2014 Hearst Communications, Inc.

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: 19717 - Posted: 06.10.2014

Laura Spinney One day in 1991, neurologist Warren Strittmatter asked his boss to look at some bewildering data. Strittmatter was studying amyloid-β, the main component of the molecular clumps found in the brains of people with Alzheimer's disease. He was hunting for amyloid-binding proteins in the fluid that buffers the brain and spinal cord, and had fished out one called apolipoprotein E (ApoE), which had no obvious connection with the disease. Strittmatter's boss, geneticist Allen Roses of Duke University in Durham, North Carolina, immediately realized that his colleague had stumbled across something exciting. Two years earlier, the group had identified a genetic association between Alzheimer's and a region of chromosome 19. Roses knew that the gene encoding ApoE was also on chromosome 19. “It was like a lightning bolt,” he says. “It changed my life.” In humans, there are three common variants, or alleles, of the APOE gene, numbered 2, 3 and 4. The obvious step, Roses realized, was to find out whether individual APOE alleles influence the risk of developing Alzheimer's disease. The variants can be distinguished from one another using a technique called the polymerase chain reaction (PCR). But Roses had little experience with PCR, so he asked the postdocs in his team to test samples from people with the disease and healthy controls. The postdocs refused: they were busy hunting for genes underlying Alzheimer's, and APOE seemed an unlikely candidate. The feeling in the lab, recalls Roses, was that “the chief was off on one of his crazy ideas”. Roses then talked to his wife, Ann Saunders, a mouse geneticist who was skilled at PCR. She had just given birth to their daughter and was on maternity leave, so they struck a deal. “She did the experiments while I held the baby,” he says. Within three weeks, they had collected the data that would fuel a series of landmark papers showing that the APOE4 allele is associated with a greatly increased risk of Alzheimer's disease1. © 2014 Nature Publishing Group,

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: 19696 - Posted: 06.05.2014

By GINIA BELLAFANTE The opening shots of “The Normal Heart,” HBO’s adaptation of Larry Kramer’s 1985 play about the early days of the AIDS crisis in New York, reveal a crew of sinewy and amorous young men disembarking from a ferry on Fire Island on a beautiful July day in 1981. The tableau is meant to suggest the final hour of unburdened desire, the moment before so much youth and beauty would be sacrificed to the cruelest attacks of physiology and cultural indifference. On the way home from the weekend, Ned Weeks, Mr. Kramer’s proxy, a man distanced from the surrounding hedonism, is shown reading a piece in The New York Times headlined, “Rare Cancer Seen in 41 Homosexuals.” The film (which will make its debut on May 25) arrives at a transformative time in the history of AIDS prevention. On May 14, federal health officials, in a move that would have been unimaginable 30 years ago, recommended the use of a prophylactic drug regimen to prevent infection with H.I.V. The drug currently used is known as Truvada, and two years ago, David Duran, a writer and gay-rights campaigner, coined the term “Truvada whore,” controversially, as a judgment against gay men who were abandoning safer sex in favor of taking the antiretroviral. Though he has since characterized this view as “prudish,” there are doctors in the city who continue to harangue patients for what the longtime AIDS activist Peter Staley calls “any break with the condom code.” And yet whatever ideological divisions existed in the period Mr. Kramer’s narrative recalls and whatever have emerged since, the fight against AIDS has been one of the most successful and focused public health movements. In another distinguishing moment, the city health department announced this year that for the first time AIDS had fallen out of the 10 leading causes of death in New York. Replacing it was Alzheimer’s, whose damage is sure to multiply as the number of older New Yorkers increases — by 2030 there will be close to 500,000 more people over age 60 than there were at the beginning of the century. According to a study from Rush University Medical Center in March, the number of deaths attributable to the disease had been vastly undercalculated. The research showed that Alzheimer’s was the underlying cause in 500,000 deaths in the United States in 2010, a figure close to six times the estimate from the Centers for Disease Control. This means that in a single year, Alzheimer’s claimed nearly as many lives as AIDS — responsible for 636,000 deaths in this country — had taken in more than three decades. © 2014 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: 19628 - Posted: 05.18.2014

By Pippa Stephens Health reporter, BBC News An anti-depressant drug could be used to slow the onset of Alzheimer's disease, say scientists in the US. Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer's patients. Scientists said they hoped the study could help prevent the disease. Experts said the study was "interesting" and that using an approved drug could be beneficial. Alzheimer's disease is the most common cause of dementia, affecting around 496,000 people in the UK. It affects the brain through protein plaques and tangles which lead to the death of brain cells, and a shortage of chemicals important for transmitting messages. Symptoms include loss of memory, mood changes, and problems with communication and reasoning. Researchers at the University of Pennsylvania and Washington University School of Medicine carried out the study between 2012 and 2014. They bred mice with Alzheimer's disease and looked at the levels of the peptide - or protein component - amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer's. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number. BBC © 2014

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: Biological Basis of Behavioral Disorders
Link ID: 19616 - Posted: 05.15.2014