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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

Erin Allday A gene variant that scientists already knew to be associated with longer life also seems to make people smarter, and may help offset the effects of normal cognitive decline in old age, according to a team of San Francisco researchers. The findings, published Thursday in the journal Cell Reports, are encouraging news for the roughly 1 in 5 people who have the genetic trait, which is a variant of the klotho gene. Beyond that, scientists hope the findings will help them develop tools for retaining, or even boosting, intelligence in people who have suffered cognitive losses, either from disease or through the normal course of aging. 'Cognitive enhancer' "What we've discovered is a cognitive enhancer," said Dr. Dena Dubal, an assistant professor of neurology at UCSF and lead author of the study, which was done with researchers from the Gladstone Institutes. "This may represent a new way to treat problems of cognition in the brain." The name of the gene comes from Greek mythology - Klotho is one of the three sisters of fate, and she spins the thread of life. The gene is responsible for secretions of the hormone klotho, which is thought to have effects on a variety of biological systems and has been shown to disrupt some processes associated with aging. © 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: 19606 - Posted: 05.13.2014

Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer’s disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain. The study was partly funded by the National Institutes of Health. “This could be a major step toward helping millions around the world who are suffering from Alzheimer’s disease and other dementias,” said Dena Dubal, M.D., Ph.D., an assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at the University of California San Francisco (UCSF) and the lead author of the study published in Cell Reports. “If we could boost the brain’s ability to function, we may be able to counter dementias.” As people live longer the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing. Klotho is the name of a Greek mythological goddess of fate, “who spins the thread of life.” People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer’s disease.

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: 19594 - Posted: 05.10.2014

by Andy Coghlan HERE'S another reason to be fit and healthy. Staying free of "lifestyle diseases" and infections could put the brakes on Alzheimer's. The advice comes from teams that have pieced together how these bodily ailments create inflammation that ultimately spills over into the brain, sending its immune cells into a hyperactive, destructive state. "The idea is simple: monitoring and prompt treatment [of inflammation] could prevent the decline from Alzheimer's," said Hugh Perry of the University of Southampton, UK, as he presented the research at the Alzheimer's Research UK annual meeting in Oxford last month. As well as revealing step by step how disease and infection can aggravate and accelerate the early stages of Alzheimer's, Perry and his colleague Clive Holmes have begun a pioneering trial in 40 people to see if a drug that acts to dampen inflammation in the body can help delay the progress of the brain disease. Etanercept is already prescribed to people with rheumatoid arthritis, and works by sponging up a molecule that aggravates inflammation. According to Alzheimer's Disease International, 44 million people globally have dementia, of which Alzheimer's is the most common type. The beginnings of the disease are characterised by the appearance in the brain of plaques of amyloid proteins and tangles of tau proteins. They prompt the brain's native immune cells, the microglia, to multiply in a bid to dispose of the troublesome new debris. © 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: 19536 - Posted: 04.26.2014

Scientists haven’t pinpointed a definitive cause for Alzheimer’s disease—a fatal brain disorder that robs people of their memory and cognitive abilities. But now researchers have uncovered an intriguing clue about why more women than men develop the condition. A particular gene variant, found in a quarter of the population and long known to raise people’s risk for the disease, seems less menacing in men, new research shows. The findings could have implications for potential gender-specific treatments, some Alzheimer’s investigators suggest. Though a small percentage of Alzheimer’s cases arise from genetic mutations that cause obvious disease before the age of 65, the vast majority of people who develop the condition do so later in life from undefined triggers, some thought to be genetic. In 1993, scientists found that people who inherit a gene variant called apolipoprotein E4 (APOE4) are more prone to the common form of Alzheimer’s that strikes in late life. There’s also a “risk-neutral” variant (APOE3) and a much rarer version of the gene (APOE2) that decreases a person’s risk for Alzheimer’s. Shortly thereafter, other research groups replicated the finding and some data hinted that APOE4 raises Alzheimer’s risk more in women than in men. Indeed, when scientists combed through a massive data set containing 5930 Alzheimer’s patients and 8607 dementia-free elderly from 40 independent studies, they reported in 1997 that females with the APOE4 variant were four times more likely to have Alzheimer’s compared with people with the more common, neutral form of the gene. However, in men, APOE4 seemed virtually harmless. “It was a pretty big effect,” says Michael Greicius, a neurologist at Stanford University Medical Center in California, of the analysis. Yet the findings didn’t create much of a stir at the time. © 2014 American Association for the Advancement of Science

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: 19490 - Posted: 04.15.2014

Want to live a long, dementia-free life? Stress your cells out. That’s the conclusion of a new study, which finds that heightened cellular stress causes brain cells to produce a protein that staves off Alzheimer’s disease and other forms of dementia. The work could lead to new ways to diagnose or treat such diseases. “This paper is very impressive,” says neuroscientist Li-Huei Tsai of the Massachusetts Institute of Technology in Cambridge, who was not involved in the new work. “It puts a finger on a particular pathway that can provide some explanation as to why some people are more susceptible to Alzheimer’s.” Alzheimer’s disease, characterized by a progressive loss of memory and cognition, affects an estimated 44.4 million people worldwide, mostly over the age of 65. The illness has been linked to the accumulation of certain proteins in the brain, but what causes symptoms has been unclear. That’s because the brains of some elderly people without dementia have the same clumps of so-called amyloid β and τ proteins typically associated with Alzheimer’s. The new study deals with a protein called repressor element 1-silencing transcription factor (REST), which turns genes and off. Scientists knew that REST played a key role in fetal brain development by controlling the activity of certain genes, but they thought it was absent in adult brains. However, when Bruce Yankner, a neurologist at Harvard Medical School in Boston, looked at all the genes and proteins that change in brains as people age, he found that REST levels begin increasing again when a person hits their 30s. Stumped as to why, he and his colleagues isolated human and mouse brain cells and probed what factors altered REST levels and what consequences those levels had. © 2014 American Association for the Advancement of Science

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: 19389 - Posted: 03.20.2014

By Maggie Fox and Erika Edwards Women are carrying the bigger burden of Alzheimer’s disease in the U.S., according to a new report — making up not only most of the cases, but paying more of the cost of caring for the growing population of people with the mind-destroying illness. The new report from the Alzheimer’s Association paints Alzheimer’s as a disease that disproportionately affects women, both as patients and as caregivers. It points out that women in their 60s are about twice as likely to develop Alzheimer’s over the rest of their lives as they are to develop breast cancer. “So women are at the epicenter of Alzheimer's disease today, not only by being most likely to be diagnosed with Alzheimer's, but also by being the caregiver most of the time,” said Maria Carrillo, vice president of the advocacy group. Alzheimer’s affects more than 5 million Americans, a number projected to soar to 13 million over the next 35 years. A study published earlier this year suggested it’s a big killer, taking down more than 500,000 Americans every year. Three out of five of those living with Alzheimer’s are women, the report finds. “The surprising statistic we pulled out of this report actually is that women over 65 have a one in six chance of developing Alzheimer's disease, in comparison to one out of 11 in men,” Carrillo said. And that compares to a one in eight lifetime risk for developing breast cancer.

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: 19381 - Posted: 03.19.2014

by Colin Barras Amyloid plaques, a hallmark of diseases like Alzheimer's, are bad news for humans – but they could have been drivers of the earliest life on Earth. A new study shows that these amyloid clusters can behave as catalysts, backing a theory that they helped trigger the reactions that sustain life, long before modern enzymes appeared. Without enzymes, life's metabolic reactions simply wouldn't occur. But making enzymes from scratch isn't easy. They are normally large, complicated proteins folded into a specific three-dimensional shape. It's difficult to see how these large proteins could have popped out of the primordial soup fully formed. Even if they did, nature faced another problem. There are 20 naturally occurring amino acids, which are the building blocks for all proteins, and each enzyme is made up of a unique sequence of at least 100 amino acids. This means there is a mind-bogglingly vast number – 20100 – of possible enzymes, each with a different amino acid sequence and a slightly different 3D structure. But very few of these 3D structures will work effectively as enzymes because they have to be an exact fit for the substrate they react with – in the same way that a lock can only be opened by one particular key. Even with millions of years to work at the problem, says Ivan Korendovych at Syracuse University in New York, nature would have struggled to build and test all possible enzyme molecules to identify the relatively few that catalyse today's metabolic reactions. © 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: 19372 - Posted: 03.17.2014

Alison Abbott A simple blood test has the potential to predict whether a healthy person will develop symptoms of dementia within two or three years. If larger studies uphold the results, the test could fill a major gap in strategies to combat brain degeneration, which is thought to show symptoms only at a stage when it too late to treat effectively. The test was identified in a preliminary study involving 525 people aged over 70. The work identified a set of ten lipid metabolites in blood plasma that distinguished with 90% accuracy between people who would remain cognitively healthy from those who would go on to show signs of cognitive impairment. “These findings are potentially very exciting,” says Simon Lovestone, a neuroscientist at the University of Oxford, UK, and a cordinator of a major European public-private partnership seekimg biomarkers for Alzheimer's. But he points out that only 28 participants developed symptoms similar to those of Alzheimer's disease during the latest work. “So the findings need to be confirmed in independent and larger studies.” There is not yet a good treatment for Alzheimer’s disease, which affects 35 million people worldwide. Several promising therapies have been tested in clinical trials over the last few years, but all have failed. However, those trials involved people who had already developed symptoms. Many neuroscientists fear that any benefits of a treatment would be missed in such a study, because it could be impossible to halt the disease once it has manifested. “We desperately need biomarkers which would allow patients to be identified — and recruited into trials — before their symptoms begin,” says Lovestone. © 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: 19340 - Posted: 03.10.2014

By Tara Bahrampour, Alzheimer’s disease likely plays a much larger role in the deaths of older Americans than is reported, according to a new study that says the disease may be the third-leading cause of death in the United States. The Centers for Disease Control and Prevention lists Alzheimer’s as the sixth-leading cause of death, far below heart disease and cancer. But the new report, published Wednesday in the medical journal of the American Academy of Neurology, suggests that the current system of relying on death certificates for causes misses the complexity of dying for many older people and underestimates the impact of Alzheimer’s. While the CDC attributed about 84,000 deaths in 2010 to Alzheimer’s, the report estimated that number to be 503,400 among people 75 and older. That puts it in a close third place, behind heart disease and cancer, and well above chronic lung disease, stroke and accidents, which rank third, fourth and fifth. Alzheimer’s is somewhat of a sleeping giant compared with other leading killers that have received more funding over the years. While deaths from these diseases have been going down thanks to better treatment and prevention, the number of people suffering from Alzheimer’s is quickly rising and the disease is always fatal. More than 5 million people in the United States are estimated to have Alzheimer’s. With the aging of the baby-boom generation, this number is expected to nearly triple by 2050 if there are no significant medical breakthroughs, according to the Alzheimer’s Association. © 1996-2014 The Washington Post

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: 19326 - Posted: 03.06.2014

Ian Sample, science correspondent, in Chicago Regular brisk walks can slow down the shrinking of the brain and the faltering mental skills that old age often brings, scientists say. Studies on men and women aged 60 to 80 found that taking a short walk three times a week increased the size of brain regions linked to planning and memory over the course of a year. The prefrontal cortex and hippocampus increased in size by only 2% or 3%, but that was enough to offset the steady shrinkage doctors expected to see over the same period. "It may sound like a modest amount but that's actually like reversing the age clock by about one to two years," said Professor Kirk Erickson, a neuroscientist at the University of Pittsburgh. "While the brain is shrinking, we actually saw not a levelling out but an increase in the size of these regions. It was better than before we started the study." People who took part in the study scored higher on spatial memory tests, and some reported feeling more mentally alert, according to Erickson. "They feel better, they feel as if the fog has lifted. Anecdotally, it seems to benefit these cognitive functions," he said. Erickson recruited more than 100 adults who confessed to doing little if any exercise in their daily lives. Half were randomly assigned to walk for 30 to 45 minutes three days a week. The rest spent a similar amount of time doing stretching exercises. Medical scans showed minor increases in the two brain regions in both groups. But the effect was greater in the walkers, Erickson said at the annual meeting of the American Association for the Advancement of Science. © 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: 19271 - Posted: 02.20.2014