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By KATIE THOMAS The drug maker Eli Lilly & Company said on Wednesday that it planned an additional study of an experimental Alzheimer’s drug that failed to improve the condition of people with the disease, saying that it remained hopeful about the drug’s prospects. The newest study is expected to get under way in the third quarter of 2013 and will focus on patients with mild Alzheimer’s disease. Lilly released results of two clinical trials in August that showed the drug, called solanezumab, did not significantly improve either the cognition or the daily functioning of people with mild and moderate forms of the disease. But despite that failure, the results also gave some reason for hope: when patients with mild Alzheimer’s were separated out, the drug was shown to significantly slow their decline in cognition. In a statement on Wednesday, the company said it decided not to pursue approval of the drug based on existing study results after it met with officials from the Food and Drug Administration. A Lilly executive said, however, that the company was still optimistic. “We remain encouraged and excited by the solanezumab data,” David Ricks, a senior vice president at Lilly and president of Lilly Bio-Medicines, said in the statement. “We are committed to working with the F.D.A. and other regulatory authorities to bring solanezumab to the millions of patients and caregivers suffering from this devastating disease who urgently need this potential treatment.” The Lilly drug is the second Alzheimer’s treatment to fail in clinical trials this year. Pfizer and Johnson & Johnson stopped development of a similar treatment, bapineuzumab, after it, too, was not shown to work. Both drugs target beta amyloid, a protein in the brain that is found in people with Alzheimer’s disease. © 2012 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: 17598 - Posted: 12.13.2012

Analysis by Emily Sohn Older people who remembered going hungry as children were slower to lose their mental sharpness as they reached old age. The new finding was only true for African-Americans, suggesting that the study hit on a particularly resilient group of people who thrived despite extreme childhood adversity. Even so, the study offers insight into how the experiences we have at very young ages can affect our health much later in life. "We know that the social experiences of African-Americans and Caucasians in this country have been very different, at least for people over age 65," said Lisa Barnes, a cognitive neuropsychologist at Rush University Medical Center in Chicago. "We wanted to measure that and see if it had any effect at all." In an effort to add to a growing interest in the long-term health influence of childhood adversity, Barnes and colleagues started by interviewing about 6,100 people who lived in Chicago and were enrolled in a study of Alzheimer's. All participants were at least 65 years old when the study began. The average starting age was 75. In the first interview, seniors answered questions about their childhoods, including details about health, the financial situations of their families and how often someone read books to them. They also took a cognitive exam that included tests of memory. © 2012 Discovery Communications, LLC.

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: 17596 - Posted: 12.11.2012

By Laura Sanders A new therapy busts up deposits of sticky plaques associated with Alzheimer’s disease in the brains of mice. Further tests with the experimental drug could help settle the question of how important the plaques are to the disease, and might even lead to a treatment for its most advanced stages. The study, described in the Dec. 6 Neuron, tested an antibody called mE8 in the brains of older mice that had been genetically altered to accumulate amyloid-beta, a protein that forms plaques in the brains of people with Alzheimer’s. “We removed 50 percent of the plaque,” says study coauthor Ronald DeMattos of Eli Lilly and Co. in Indianapolis. “This is a big deal.” The scientists haven’t yet looked for any behavioral improvements in the mice. Nor is it clear that the drug would work the same way in people. But DeMattos and his Lilly colleagues are hopeful that the therapy will lead to new treatments for patients in later stages of Alzheimer’s, who carry large amounts of plaque in their brains. Other researchers say that busting plaques may be the wrong approach to slowing or stopping the dementia that plagues Alzheimer’s patients. Another antibody recently failed to change the course of Alzheimer’s disease in two large clinical trials. Although the drug developers haven’t yet released the full details of those trials, that antibody — called bapineuzumab — appears to reduce levels of A-beta and shrink plaques. But with no improvement in symptoms, the trial results, reported in August, are a setback on the path to new Alzheimer’s drugs. © Society for Science & the Public 2000 - 2012

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: 17585 - Posted: 12.08.2012

By Maggie Fox, NBC News Seniors who fit in the most daily physical activity – from raking leaves to dancing – can have more gray matter in important brain regions, researchers reported on Monday. The scientists have images that show people who were the most active had 5 percent more gray matter than people who were the least active. Having more little gray brain cells translates into a lower risk of Alzheimer’s disease, other studies have shown. “People really want to know what they can do to reduce their risk of Alzheimer’s disease,” said Dr. Cyrus Raji of the University of California in Los Angeles, who presented his team’s findings to a meeting of the Radiological Society of North America. Raji’s team looked at the records of 876 adults, who were recruited into a larger study on heart health starting in 1989. They all got magnetic resonance imaging (MRI) brain scans in 1998 and 1999, when they were on average 78 years old, and filled out detailed questionnaires on exercise and other types of activity. Most of them were a little overweight – with a body mass index or BMI of 27. People with BMIs above 25 are considered overweight and at 30 they are considered clinically obese. The researchers found a huge difference in the amount of activity people reported. They were asked about everything from cycling to yard work, dancing and bicycle riding. © 2012 NBCNews.com

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: 17543 - Posted: 11.27.2012

By Carrie Arnold Researchers have untangled some of the neurological events that may ultimately lead to Alzheimer's disease. Two new studies show that a protein implicated in this form of dementia can infect other neurons to spread disease across the brain. These problematic proteins clump together, which can lead to cognitive problems. A protein's shape—the way its chains of amino acids fold—determines its function. If a protein misfolds, its structure and function change. In Alzheimer's, researchers have long suspected that misfolded versions of a protein called amyloid-beta might travel from cell to cell and cause more amyloid-beta proteins to take on a deformed shape. To test this idea, biophysicist Jan Stöhr of the University of California, San Francisco, and his colleagues injected synthetic amyloid-beta proteins into the brains of mice and found that plaques began to form in less than six months. Even when the synthetic proteins were injected into only one side of the brain, over time plaques materialized throughout the organ, the researchers found. “If these aggregates are not cleared by the brain, they will start to recruit more amyloid-beta peptides into the diseased conformation, and the spread throughout the brain begins,” Stöhr says. The results appeared in the June Proceedings of the National Academy of Sciences USA. In a separate study using a cell culture, a team of researchers led by Martin Hallbeck of Linköping University in Sweden tracked amyloid-beta transmission from neuron to neuron for the first time. The results, published in the June 27 Journal of Neuroscience, also show that neurons containing misfolded amyloid-beta can cause neighboring, connected neurons to break down, eventually infecting the entire culture. © 2012 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: 17532 - Posted: 11.24.2012

By GINA KOLATA He learned there was a new brain scan to diagnose the disease and nervously agreed to get her one, secretly hoping it would lay his fears to rest. In June, his wife became what her doctor says is the first private patient in Arizona to have the test. “The scan was floridly positive,” said her doctor, Adam S. Fleisher, director of brain imaging at the Banner Alzheimer’s Institute in Phoenix. The Jimenezes have struggled ever since to deal with this devastating news. They are confronting a problem of the new era of Alzheimer’s research: The ability to detect the disease has leapt far ahead of treatments. There are none that can stop or even significantly slow the inexorable progression to dementia and death. Families like the Jimenezes, with no good options, can only ask: Should they live their lives differently, get their affairs in order, join a clinical trial of an experimental drug? “I was hoping the scan would be negative,” Mr. Jimenez said. “When I found out it was positive, my heart sank.” The new brain scan technology, which went on the market in June, is spreading fast. There are already more than 300 hospitals and imaging centers, located in most major metropolitan areas, that are ready to perform the scans, according to Eli Lilly, which sells the tracer used to mark plaque for the scan. © 2012 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: 17501 - Posted: 11.17.2012

Tom Pugh A gene with links to late-onset dementia is also suspected of boosting people's brains in their youth, according to a study. People who inherit one copy of the gene variant, known as APOE e4, have up to four times the normal risk of developing Alzheimer's disease in later life. Neuroscientists tested the cognitive skills of those with the gene variant, which is found in around a quarter of the population, against those without it. They also looked at the brain structure and brain activities of both groups during the tasks. The study, led by the University of Sussex, found that young people with the same variant performed better in attention tests, including episodic memory of words and spotting number sequences. Experts suggested that while the e4 variant might help boost the brain in early life, it could also increase the possibility of "burnout" in old age. Lead researcher Professor Jennifer Rusted said: "Earlier studies suggested that those with the e4 variant outperform those without it in tasks such as memory, speed of processing, mental arithmetic and verbal fluency. "But it is also well-established that this gene is a risk factor for Alzheimer's 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: 17492 - Posted: 11.14.2012

By NICHOLAS BAKALAR High blood pressure may cause harmful brain changes in people as young as 40, a study suggests. In the report, published online Nov. 2 in Lancet Neurology, researchers measured blood pressure in 579 men and women whose average age was 39, then examined their brains with magnetic resonance imaging. After adjusting for smoking, hypertension treatment and total cranial volume, they found that higher systolic blood pressure — the most common form of hypertension — was associated with decreases in gray matter volume and significant injury to white matter. Moreover, there was a dose-response relationship: The higher the blood pressure, the greater the visible changes. These changes also occur in people over 55 with high blood pressure and are associated with decreased cognitive performance. Essentially, these young people with high blood pressure had brains that were older than their chronological age. The authors acknowledge that their sample was mostly healthy, white volunteers, and that the study represents a snapshot, not a long-term picture. The senior author, Dr. Charles DeCarli, a neurologist at the University of California, Davis, urged caution. “Most people at this age have no symptoms at all, even if they have high blood pressure,” he said. “Get your blood pressure measured when you’re young, and treated if necessary.” Copyright 2012 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: 17483 - Posted: 11.13.2012

By JIM DENT Three days before his death last week at 88, Darrell Royal told his wife, Edith: “We need to go back to Hollis” — in Oklahoma. “Uncle Otis died.” “Oh, Darrell,” she said, “Uncle Otis didn’t die.” Royal, a former University of Texas football coach, chuckled and said, “Well, Uncle Otis will be glad to hear that.” The Royal humor never faded, even as he sank deeper into Alzheimer’s disease. The last three years, I came to understand this as well as anyone. We had known each other for more than 40 years. In the 1970s, Royal was a virile, driven, demanding man with a chip on his shoulder bigger than Bevo, the Longhorns mascot. He rarely raised his voice to players. “But we were scared to death of him,” the former quarterback Bill Bradley said. Royal won 3 national championships and 167 games before retiring at 52. He was a giant in college football, having stood shoulder to shoulder with the Alabama coach Bear Bryant. Royal’s Longhorns defeated one of Bryant’s greatest teams, with Joe Namath at quarterback, in the 1965 Orange Bowl. Royal went 3-0-1 in games against Bryant. Royal and I were reunited in the spring of 2010. I barely recognized him. The swagger was gone. His mind had faded. Often he stared aimlessly across the room. I scheduled an interview with him for my book “Courage Beyond the Game: The Freddie Steinmark Story.” Still, I worried that his withering mind could no longer conjure up images of Steinmark, the undersize safety who started 21 straight winning games for the Longhorns in the late 1960s. Steinmark later developed bone cancer that robbed him of his left leg. © 2012 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: 17477 - Posted: 11.12.2012

By James Gallagher Health and science reporter, BBC News Researchers have found some of the earliest signs of Alzheimer's disease, more than two decades before the first symptoms usually appear. Treating the disease early is thought to be vital to prevent damage to memory and thinking. A study, published in the Lancet Neurology, found differences in the brains of an extended Colombian family predisposed to develop an early form of Alzheimer's. Experts said the US study may give doctors more time to treat people. Alzheimer's disease starts long before anyone would notice; previous studies have shown an effect on the brain 10-15 years before symptoms. It is only after enough brain cells have died that the signs of dementia begin to appear - some regions of the brain will have lost up to 20% of their brain cells before the disease becomes noticeable. However, doctors fear so much of the brain will have degenerated by this time that it will be too late to treat patients. The failure of recent trials to prevent further cognitive decline in patients with mild to moderate Alzheimer's disease has been partly put down to timing. BBC © 2012

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: 17457 - Posted: 11.06.2012

By ANAHAD O'CONNOR Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Physical exercise not only protected against such age-related brain changes, but also had more of an effect than mentally and socially stimulating activities. In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities. Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the brain’s white matter, which is considered the “wiring” of the brain’s communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and I.Q. As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study and a senior research fellow at Edinburgh. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.” Copyright 2012 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 17427 - Posted: 10.27.2012

By Michelle Roberts Health editor, BBC News online Exercising in your 70s may stop your brain from shrinking and showing the signs of ageing linked to dementia, say experts from Edinburgh University. Brain scans of 638 people past the age of retirement showed those who were most physically active had less brain shrinkage over a three-year period. Exercise did not have to be strenuous - going for a walk several times a week sufficed, the journal Neurology says. But giving the mind a workout by doing a tricky crossword had little impact. The study found no real brain-size benefit from mentally challenging activities, such as reading a book, or other pastimes such as socialising with friends and family. When the researchers examined the brain's white matter - the wiring that transmits messages round the brain - they found that the people over the age of 70 who were more physically active had fewer damaged areas than those who did little exercise. And they had more grey matter - the parts of the brain where the messages originate. Experts already know that our brains tend to shrink as we age and that this shrinkage is linked to poorer memory and thinking. BBC © 2012

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: 17410 - Posted: 10.23.2012

Mo Costandi A disturbed night's sleep might signal a future diagnosis of Alzheimer’s disease, according to findings presented this week at the annual meeting of the Society for Neuroscience in New Orleans, Louisiana. Patients with Alzheimer’s often complain of changes in their sleep patterns during the early stages of the disease. In healthy people, for example, daytime naps usually last around 20 minutes, but they can be to 3 hours long in patients with Alzheimer’s disease. Roxanne Sterniczuk, a neurophysiologist at Dalhousie University in Halifax, Canada, and her colleagues wanted to determine how early these changes occur and if they could predict a person’s future risk of developing the disease. Sterniczuk and her colleagues analysed data from around 14,600 healthy people, collected as part of the Survey of Health, Ageing and Retirement in Europe (SHARE), a long-term observational study of people aged 50 and over from 12 European countries. They looked at various measures of sleep quality, and used them to produce a ‘sleep disturbance index’. The researchers found that participants who reported sleeping restlessly, feeling tired during the day and taking sleep medication were more likely to be diagnosed with Alzheimer’s within the next 2 years, and that the greater the extent of these problems, the more severe were the symptoms of the subsequent disease. “Increased daytime sleepiness was the biggest predictor,” says Sterniczuk. “It would appear that subtle changes in the sleep–wake cycle are taking place before any disease pathology.” © 2012 Nature Publishing Group

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: 17395 - Posted: 10.20.2012

Elizabeth Lopatto , Bloomberg News Three studies set to explore the use of experimental drugs that may become the first to change the course of Alzheimer's disease aren't looking to cure the illness. Their goal is to prevent it altogether. The independent trials will begin in 2013 and run for three to five years, testing as many as five drugs in almost 1,500 volunteers who haven't shown any of Alzheimer's mind-altering symptoms, yet carry a strong genetic risk for the disease or display early physical evidence in the brain. A decision on the final study drug is expected in December. The newest strategy abandons a drive that failed to stop Alzheimer's once memories recede. Instead, as with heart disease, scientists are exploring if the mind-robbing ailment can be prevented or at least delayed using drugs that act roughly like Pfizer's Lipitor and other statins. The idea, driven by new information that tracks the disease's progression back through time, is to act years before symptoms occur to rid the brain of proteins that can later destroy nerve cells. "We now can see changes 10 to 15 years before symptoms develop," said Neil Buckholtz, director of the division of neuroscience at the National Institute on Aging in Bethesda, Maryland. "If you can stop them, you have a chance of slowing down or possibly even stopping progression." A breakthrough can't come soon enough. The number of Alzheimer's cases globally is expected to double within 20 years as the world's population ages, to as many as 65.7 million people in 2030 and 115 million by 2050, the Geneva- based World Health Organization said in April. © 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: 17394 - Posted: 10.20.2012

By GINA KOLATA Scientists have selected three different types of Alzheimer’s drugs to be tested in the first large-scale international attempt to prevent the disease in people who are otherwise doomed to get it. It is one of three studies with the same goal that will start early next year. This one involves 160 people from the United States, Britain and Australia with a variety of gene mutations that cause Alzheimer’s with absolute certainty. Most of the test subjects will have no symptoms yet of the degenerative disease that ravages the brain, destroying memory and thought. But they would be expected to start showing signs of problems with memory and thinking within five years unless the drugs work. The hope is that by intervening early, the disease might be headed off. Another study starting next year involves an extended family in Colombia that shares the same mutation. Anyone who inherits that mutated gene get Alzheimer’s disease. A third study will involve people in the United States age 70 and older who seem perfectly healthy and who do not have any known Alzheimer’s mutations but in whom, brain scans show, the disease is starting to manifest itself. In recent years, as studies involving people who already have Alzheimer’s have failed, researchers increasingly have called for studies in those who do not yet have the disease, arguing that the time to intervene is before the brain is irreversibly damaged. So the new study with people who are destined to get Alzheimer’s unless a drug can stop it is a way to test that idea. © 2012 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: 17355 - Posted: 10.11.2012

By Anna-Marie Lever Health reporter, BBC News An aspirin a day may slow brain decline in elderly women at high risk of cardiovascular disease, research finds. Around 500 at risk women, between the ages of 70 to 92, were tracked for five years - their mental capacity was tested at the start and end of the study. Those taking aspirin for the entire period saw their test scores fall much less than those who had not. The Swedish study is reported in the journal BMJ Open. Dr Silke Kern, one of paper's authors, said: "Unlike other countries - Sweden is unique, it is not routine to treat women at high risk of heart disease and stroke with aspirin. This meant we had a good group for comparison." The women were tested using a mini mental state exam (MMSE) - this tests intellectual capacity and includes orientation questions like, "what is today's date?", "where are we today?" and visual-spatial tests like drawing two interlinking pentagons. But the report found that while aspirin may slow changes in cognitive ability in women at high risk of a heart attack or stroke, it made no difference to the rate at which the women developed dementia - which was also examined for by a neuropsychiatrist. BBC © 2012

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: 17332 - Posted: 10.04.2012

By Deborah Kotz, Globe Staff Is Alzheimer’s disease really a form of diabetes? Let’s call it type 3, because that’s what a Brown Medical School researcher dubbed it back in 2005 when she autopsied the brains of Alzheimer’s patients and found that they had signs of insulin resistance -- an early indicator of diabetes. Since then, however, we haven’t seen a sea-change in preventive treatments based on this idea. Those who carry the gene for hereditary Alzheimer’s aren’t given diabetes drugs to help stave off dementia. Nor are Alzheimer’s patients given insulin injections. What has been getting attention, however, is whether we should make extra efforts to eat a low glycemic diet -- which is low in processed foods, sugar, and starchy carbohydrates that cause quick spikes in blood sugar -- to help protect our brains from developing those gunky amyloid plaques associated with Alzheimer’s. The September issue of the New Scientist advocates for changing our eating patterns with a frightening image of a cracked chocolate brain on its cover. (Chocolate consumption, though, hasn’t been linked to cognitive decline, much to my relief.) New York Times food columnist Mark Bittman pointed out in a recent post that the latest studies provide some persuasive evidence linking diet to the development of Alzheimer’s. I’ve covered those studies too, including this one that measured a smaller Alzheimer’s risk in people who eat a diet rich in fish, veggies, and fruit compared with those who eat a diet centered on processed foods containing trans fats. © 2012 NY Times Co.

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: 17328 - Posted: 10.03.2012

by Jessica Hamzelou ALZHEIMER'S disease is more prevalent in older people, but we have never known why. Now it seems that about 80 per cent of our brain cells are vulnerable to a process that can turn them toxic. For the first time, cells in the brains of people with Alzheimer's have been shown to "senesce" - a mechanism that stops them dividing and starts them on a path of destruction. With hundreds of experimental treatments for the disease falling by the wayside, we need a new target and it seems as if we have now found one. The discovery of huge numbers of senescent cells in people with Alzheimer's suggests that they play a key role in the condition. Cells that continually replicate in the body, such as those in the skin, lung and kidney, eventually accumulate DNA damage - typically with age. Not all of these damaged cells die though, instead some senesce. When this happens, biological changes within the cell prevent it from dividing or carrying out its normal functions. Research suggests that senescing cells also start producing proteins that trigger inflammation. "It's pretty clear that cell senescence evolved to protect us against cancer," says Judith Campisi of the Buck Institute for Research on Aging in Novato, California. The idea is that once cells accumulate DNA damage, they senesce to avoid incorrect division that can lead to cancer. The benefit of this mechanism over self-destruction is that it sends out a call to the immune system to destroy nearby cells that might also be affected. © 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: 17306 - Posted: 09.27.2012

Problems sleeping may be an early sign of Alzheimer's if a study in mice also applies to people, say researchers. Clumps of protein, called plaques, in the brain are thought to be a key component of the illness. A study, published in the journal Science Translational Medicine, showed that when plaques first developed, the mice started having disrupted sleep. Alzheimer's Research UK argued that if the link was proven it could become a useful tool for doctors. The hunt for early hints that someone is developing Alzheimer's is thought to be crucial for treating the disease. People do not show problems with their memory or clarity of thought until very late on in the disease. At this point, parts of the brain will have been destroyed, meaning treatment will be very difficult or maybe even impossible. It is why researchers want to start early, years before the first symptoms. One large area of research is in plaques of beta amyloid which form on the brain. Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people. However, the protein forms permanent plaques in Alzheimer's disease. BBC © 2012

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: 17228 - Posted: 09.07.2012

by Greg Miller Earlier this summer, Alzheimer's researchers got disappointing—but not entirely unexpected—news from a phase III clinical trial of bapineuzumab, an antibody that targets β amyloid, the protein fragment that forms pathological clumps in the brains of patients. Bapineuzumab failed to improve cognition in two large trials of patients with mild to moderate Alzheimer’s disease. Today, Eli Lilly and Company announced slightly more encouraging results from another closely watched trial, for an anti-amyloid antibody called solanezumab. First the bad news: Solanezumab failed to slow cognitive decline in two trials with more than 2000 people with mild to moderate Alzheimer’s disease. However, the company says in a statement, a secondary analysis of data from the mild Alzheimer's patients enrolled in both trials indicated that the drug did slow cognitive decline in this subgroup. A similar analysis of the moderate Alzheimer’s patients in both trials showed no effect. Lilly says its plans for solanezumab are still undecided, pending discussions with regulators, but it will continue an open-label extension study in which patients from the two recently completed trials can continue to take the drug. "We see hopeful and encouraging information here," says Maria Carrillo, senior director of medical and scientific relations for the Alzheimer's Association. So far, Lilly has released only preliminary findings, but Carrillo says they appear to be the best evidence yet that anti-amyloid therapy can slow cognitive decline in some patients. © 2010 American Association for the Advancement of Science

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: 17198 - Posted: 08.25.2012