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By Emily Underwood More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons. “It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville. Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work. What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. © 2016 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: 22062 - Posted: 04.01.2016

By Patrick Monahan Yesterday, mountaineer Richard Parks set out for Kathmandu to begin some highly unusual data-gathering. As part of Project Everest Cynllun, he will climb Mount Everest without supplemental oxygen and perform—on himself—a series of blood draws, muscle biopsies, and cognitive tests. If he makes it to the summit, these will be the highest-elevation blood and tissue samples ever collected. Damian Bailey, a physiologist at the University of South Wales, Pontypridd, in the United Kingdom and the project’s lead scientist, hopes the risky experiment will yield new information about how the human body responds to low-oxygen conditions, and how similar mechanisms might drive cognitive decline with aging. As Parks began the acclimatization process with warm-up climbs on two smaller peaks, Bailey told ScienceInsider about his ambitions for the project. This interview has been edited for clarity and brevity. Q: Parks is an extreme athlete who has climbed Everest before. What can his performance tell us about regular people? A: What we’re trying to understand is, what is it about Richard’s brain that is potentially different from other people’s brains, and can that provide us with some clues to accelerated cognitive decline, which occurs with aging [and] dementia. We know that sedentary aging is associated with a progressive decline in blood flow to the brain. … And the main challenge for sedentary aging is we have to wait so long to see the changes occurring. So this is almost a snapshot, a day in the life of a patient with cognitive decline. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 22043 - Posted: 03.29.2016

By Emily Underwood When pharmaceutical company Eli Lilly in Indianapolis last week announced a major change to its closely watched clinical trial for the Alzheimer’s drug solanezumab, some in the scientific community and drug development industry cried foul. To critics, the company’s decision to eliminate changes in a person’s daily ability to function as a primary measure of solanezumab’s efficacy and focus solely on a cognitive test seemed like a last-ditch attempt to keep a doomed drug from failing its third trial. Lilly’s stock plunged by nearly 5%, apparently reflecting that sentiment. Largely lost in the online “chatter,” however, was that Lilly’s move reflects a growing scientific consensus about how the early stages of Alzheimer’s disease progress, says Dennis Selkoe, a neurologist at Brigham and Women’s Hospital in Boston, who is not involved in the Lilly trial. “From the point of view of a neurologist who’s seen hundreds of patients, [Lilly’s decision] makes clinical sense,” he says. Solanezumab is an antibody designed to bind to and promote the clearance of the β-amyloid protein, which forms plaques around the neurons of people with Alzheimer’s. Not everyone agrees that these plaques are at the root of the disease—a concept called the amyloid hypothesis, of which Selkoe is a major proponent—but fighting them is the foundation of nearly all current efforts in Alzheimer’s drug development. By helping destroy the plaques in people with early stages of Alzheimer’s, Lilly hopes solanezumab can slow the disease’s progression. © 2016 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: 22011 - Posted: 03.22.2016

Alison Abbott In the 25 years that John Collinge has studied neurology, he has seen hundreds of human brains. But the ones he was looking at under the microscope in January 2015 were like nothing he had seen before. He and his team of pathologists were examining the autopsied brains of four people who had once received injections of growth hormone derived from human cadavers. It turned out that some of the preparations were contaminated with a misfolded protein — a prion — that causes a rare and deadly condition called Creutzfeldt–Jakob disease (CJD), and all four had died in their 40s or 50s as a result. But for Collinge, the reason that these brains looked extraordinary was not the damage wrought by prion disease; it was that they were scarred in another way. “It was very clear that something was there beyond what you'd expect,” he says. The brains were spotted with the whitish plaques typical of people with Alzheimer's disease. They looked, in other words, like young people with an old person's disease. For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone — the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures. © 2016 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22003 - Posted: 03.17.2016

By Dominic Howell BBC News Gum disease has been linked to a greater rate of cognitive decline in people with Alzheimer's disease, early stage research has suggested. The small study, published in PLOS ONE, looked at 59 people who were all deemed to have mild to moderate dementia. It is thought the body's response to gum inflammation may be hastening the brain's decline. The Alzheimer's Society said if the link was proven to be true, then good oral health may help slow dementia. The body's response to inflammatory conditions was cited as a possible reason for the quicker decline. Inflammation causes immune cells to swell and has long been associated with Alzheimer's. Researchers believe their findings add weight to evidence that inflammation in the brain is what drives the disease. 'Six-fold increase' The study, jointly led by the University of Southampton and King's College London, cognitively assessed the participants, and took blood samples to measure inflammatory markers in their blood. Their oral health was also assessed by a dental hygienist who was unaware of the cognitive outcomes. Of the sample group, 22 were found to have considerable gum disease while for the remaining 37 patients the disease was much less apparent. The average age of the group with gum disease was 75, and in the other group it was 79. A majority of participants - 52 - were followed up at six months, and all assessments were repeated. The presence of gum disease - or periodontitis as it is known - was associated with a six-fold increase in the rate of cognitive decline, the study suggested. © 2016 BBC

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21976 - Posted: 03.12.2016

By GINA KOLATA Marty and Matt Reiswig, two brothers in Denver, knew that Alzheimer’s disease ran in their family, but neither of them understood why. Then a cousin, Gary Reiswig, whom they barely knew, wrote a book about their family, “The Thousand Mile Stare.” When the brothers read it, they realized what they were facing. In the extended Reiswig family, Alzheimer’s disease is not just a random occurrence. It results from a mutated gene that is passed down from parent to child. If you inherit the mutated gene, Alzheimer’s will emerge at around age 50 — with absolute certainty. Your child has a 50-50 chance of suffering the same fate. The revelation came as a shock. And so did the next one: The brothers learned that there is a blood test that can reveal whether one carries the mutated gene. They could decide to know if they had it. Or not. It’s a dilemma more people are facing as scientists discover more genetic mutations linked to diseases. Often the newly discovered gene increases risk, but does not guarantee it. Sometimes knowing can be useful: If you have a gene mutation that makes colon cancer much more likely , for example, then frequent colonoscopies may help doctors stave off trouble. But then there are genes that make a dreaded disease a certainty: There is no way to prevent it, and no way to treat it. Marty Reiswig, 37, saw his father, now in the final stages of Alzheimer’s, slowly lose his ability to think, to remember, to care for himself, or even to recognize his wife and sons. Mr. Reiswig knows that if he has the gene, he has perhaps a bit more than a decade before the first symptoms appear. If he has it, his two young children may have it, too. He wavers about getting tested. © 2016 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: 21967 - Posted: 03.08.2016

By Nicholas Bakalar The popular heartburn drugs known as proton pump inhibitors have been linked to a range of ills: bone fractures, kidney problems, infections and more. Now a large new study has found that they are associated with an increased risk for dementia as well. Proton pump inhibitors, or P.P.I.s, are widely available both by prescription and over the counter under various brand names, including Prevacid, Prilosec and Nexium. German researchers, using a database of drug prescriptions, studied P.P.I. use in 73,679 men and women older than 75 who were free of dementia at the start of the study. Over an average follow-up period of more than five years, about 29,000 developed Alzheimer’s disease or other dementias. The study is in JAMA Neurology. After controlling for age, sex, depression, diabetes, stroke, heart disease and the use of other medicines, they found that regular use of P.P.I.s increased the risk for dementia in men by 52 percent and in women by 42 percent, compared with nonusers. “Our study does not prove that P.P.I.s cause dementia,” said the senior author, Britta Haenisch of the German Center for Neurodegenerative Diseases. “It can only provide a statistical association. This is just a small part of the puzzle. “Clinicians, pharmacists and patients have to weigh the benefits against the potential side effects,” she continued, “and future studies will help to better inform these decisions.” © 2016 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: 21910 - Posted: 02.19.2016

Alan Yuhas in Washington DC Scientists working on genetically modified worms have made what they hope are the first steps towards developing a preventative treatment for Alzheimer’s disease. The study, published in the journal Science Advances and presented at the American Association for the Advancement of Science conference, describes how researchers modified nematode worms to develop Alzheimer’s-like symptoms, and then applied the existing anti-cancer drug, bexarotene, at various stages of the disease. “We showed that these worms that were doomed to develop Alzheimer’s disease could be rescued,” said study author Michele Vendruscolo, of the University of Cambridge. “It is a powerful first step,” he said. “It is very exciting, but at the same time we are very aware it the first step and many things can go wrong.” Researchers believe that Alzheimer’s destroys brain function through a catastrophic cascade of events: natural proteins start folding and glomming onto each other in dysfunctional ways, a process that in turn creates the toxic molecules thought to kill brain cells. When the proteins started malfunctioning in the worms, the drug could do nothing to save them. But if administered before symptoms developed, it prevented the first stage of the process. © 2016 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: 21890 - Posted: 02.13.2016

By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21887 - Posted: 02.11.2016

By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 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: 21879 - Posted: 02.10.2016

Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016

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: 21871 - Posted: 02.09.2016

Alison Abbott For the second time in four months, researchers have reported autopsy results that suggest Alzheimer’s disease might occasionally be transmitted to people during certain medical treatments — although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly1 on 26 January, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater — the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD. But in addition to the damage caused by the prions, five of the brains displayed some of the pathological signs that are associated with Alzheimer’s disease, researchers from Switzerland and Austria report. Plaques formed from amyloid-β protein were discovered in the grey matter and blood vessels. The individuals, aged between 28 and 63, were unusually young to have developed such plaques. A set of 21 controls, who had not had surgical grafts of dura mater but died of sporadic CJD at similar ages, did not have this amyloid signature. According to the authors, it is possible that the transplanted dura mater was contaminated with small ‘seeds’ of amyloid-β protein — which some scientists think could be a trigger for Alzheimer’s — along with the prion protein that gave the recipients CJD. © 2016 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21822 - Posted: 01.26.2016

By Esther Landhuis Amid gloomy reports of an impending epidemic of Alzheimer’s and other dementias, emerging research offers a promising twist. Recent studies in North America, the U.K. and Europe suggest that dementia risk among seniors in some high-income countries has dropped steadily over the past 25 years. If the trend is driven by midlife factors such as building “brain reserve” and maintaining heart health, as some experts suspect, this could lend credence to staying mentally engaged and taking cholesterol-lowering drugs as preventive measures. At first glance, the overall message seems somewhat confusing. Higher life expectancy and falling birth rates are driving up the global elderly population. “And if there are more 85-year-olds, it’s almost certain there will be more cases of age-related diseases,” says Ken Langa, professor of internal medicine at the University of Michigan. According to the World Alzheimer Report 2015 (pdf), 46.8 million people around the globe suffered from dementia last year, and that number is expected to double every 20 years. Looking more closely, though, new epidemiological studies reveal a surprisingly hopeful trend. Analyses conducted over the last decade in the U.S., Canada, England, the Netherlands, Sweden and Denmark suggest that “a 75- to 85-year-old has a lower risk of having Alzheimer’s today than 15 or 20 years ago,” says Langa, who discussed the research on falling dementia rates in a 2015 Alzheimer’s Research & Therapy commentary (pdf). © 2016 Scientific America

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: 21821 - Posted: 01.26.2016

By David Shultz A rat navigating a maze has to rank somewhere near the top of science tropes. Now, scientists report that they’ve developed an analogous test for humans—one that involves driving through a virtual landscape in a simulated car. The advance, they say, may provide a more sensitive measure for detecting early signs of Alzheimer’s disease. “I think it’s a very well-done study,” says Keith Vossel, a translational neuroscientist at the University of California, San Francisco (UCSF), who was not involved with the work. In the rodent version of the so-called Morris Maze Test, researchers fill a large cylindrical container with water and place a platform just above the waterline. A scientist then places a rat into the tank, and the rodent must swim to the platform to avoid drowning. The experimenter then raises the water level just above the height of the platform and adds a compound to the water to make it opaque. The trial is repeated, but now the rat must find the platform without seeing it, using only its memory of where the safe zone exists relative to the tank’s walls and the surrounding environment. In subsequent trials, researchers place the rat at different starting points along the tank’s edge, but the platform stays put. In essence, the task requires the rat to move to a specific but invisible location within a circular arena from different starting points. © 2016 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: 21803 - Posted: 01.20.2016

Blocking the production of new immune cells in the brain could reduce memory problems seen in Alzheimer's disease, a study suggests. University of Southampton researchers said their findings added weight to evidence that inflammation in the brain is what drives the disease. A drug used to block the production of these microglia cells in the brains of mice had a positive effect. Experts said the results were exciting and could lead to new treatments. Up until now, most drugs used to treat dementia have targeted amyloid plaques in the brain which are a characteristic of people with the Alzheimer's disease. But this latest study, published in the journal Brain, suggests that in fact targeting inflammation in the brain, caused by a build-up of immune cells called microglia, could halt progression of the disease. Researchers found increased numbers of microglia in the post-mortem brains of people with Alzheimer's disease. Previous studies have also suggested that these cells could play an important role. Dr Diego Gomez-Nicola, lead study author from the university, said: "These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease. "The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans." © 2016 BBC

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: 21762 - Posted: 01.08.2016

By Karen Weintraub Mild cognitive impairment, or M.C.I., is not a disease in itself. Rather, it is a clinical description based on performance on a test of memory and thinking skills. Depending on its cause, mild cognitive impairment is potentially reversible. Poor performance on a cognitive test could be caused by certain medications, sleep apnea, depression or other problems, said Dr. Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School and Beth Israel Deaconess Medical Center. In those cases, when the underlying disease is treated, cognitive abilities can bounce back. But in about half of people with M.C.I. – doctors are not sure of the exact number — memory problems are the first sign of impending Alzheimer’s disease. If M.C.I. progresses to Alzheimer’s, there is no recovery. Alzheimer’s is marked by an inexorable decline that is always fatal, although the path from the first signs of cognitive impairment to death may take three to 15 years, said Dr. David Knopman, a professor of neurology at the Mayo Clinic in Rochester, Minn. As many as 20 percent to 30 percent of those with M.C.I. who score below but near the cutoff for normal can cross back above in a subsequent cognitive test – perhaps because they are having a better day, he said. But someone whose score is borderline is at higher risk of developing Alzheimer’s than someone who scores higher, said Dr. Knopman, also vice chair of the medical and scientific advisory council of the Alzheimer’s Association. Doctors may be hesitant to label someone with early Alzheimer’s, which can be difficult to diagnose in the early stages, so they often call it mild cognitive impairment instead, said Dr. John C. Morris, a professor of neurology and the director of the Knight Alzheimer's Disease Research Center at Washington University School of Medicine in St. Louis. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21728 - Posted: 12.29.2015

A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease, creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of Alzheimer’s may prevent dementia and reduce damage to the brain. “This exciting research advances our understanding of the role of the proteasomes in neurodegeneration and provides a potential way to alleviate symptoms of neurodegenerative disorders,” said Roderick Corriveau, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. The proteasome is a hollow, cylindrical structure which chews up defective proteins into smaller, pieces that can be recycled into new proteins needed by a cell. To understand how neurodegenerative disorders affect proteasomes, Natura Myeku, Ph.D., a postdoctoral fellow working with Karen E. Duff, Ph.D., professor of pathology and cell biology at Columbia University, New York City, focused on tau, a structural protein that accumulates into clumps called tangles in the brain cells of patients with Alzheimer’s disease and several other neurodegenerative disorders known as tauopathies. Using a genetically engineered mouse model of tauopathy, as well as looking at cells in a dish, the scientists discovered that as levels of abnormal tau increased, the proteasome activity slowed down.

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: 21716 - Posted: 12.22.2015

By Gretchen Reynolds Physical fitness may be critical for maintaining a relatively youthful and nimble brain as we age, according to a new study of brain activation patterns in older people. For most of us, our bodies begin to lose flexibility and efficiency as we enter our 40s. Running and other movements slow down and become more awkward, and something similar seems to occur within our heads. As middle age encroaches, our thinking becomes less efficient. We don’t toggle between mental tasks as nimbly as we once did or process new information with the same aplomb and clarity. Recently, neuroscientists have begun to quantify how those cognitive changes play out in our brains, to disquieting effect. In studies comparing brain activation in young people with that of people past 40, they have found notable differences, especially during mental tasks that require attention, problem solving, decision-making and other types of high-level thinking. Such thinking primarily involves activation of the brain’s prefrontal cortex. In young people, activation in the cortex during these cognitive tasks tends to be highly localized. Depending on the type of thinking, young people’s brains light up almost exclusively in either the right or left portion of the prefrontal cortex. But in older people, studies show, brain activity during the same mental tasks requires far more brainpower. They typically display activity in both hemispheres of their prefrontal cortex. In effect, they require more of their brains’ resources to complete the same tasks that young people do with less cognitive effort. Neuroscientists coined an acronym for this phenomenon: Harold, for hemispheric asymmetry reduction in older adults. Most agree that it represents a general reorganization and weakening of the brain’s function with age. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 21688 - Posted: 12.10.2015

By Lindzi Wessel Nighttime restlessness is common among people with Alzheimer’s, and many stay awake agitated and pacing long after their family members have gone to sleep. Now, scientists may have figured out why: The disease appears to degrade a special type of eye cell that tells the brain when it’s day or night. If the discovery holds up, it might offer clinicians a new way to monitor the progression of Alzheimer’s and could lead to treatments that restore a good night’s sleep. The cells in question are known as melanopsin retinal ganglion cells. They send signals to the brain center responsible for circadian rhythms, our body’s daily clock. The cells make up 1% to 2% of the eye’s light-responsive sensors, but they play no role in vision, says lead author Chiara La Morgia, a neuroscientist at the University of Bologna in Italy. Rather, they sense light levels around us, telling us when to get sleepy and when to be alert. La Morgia and her colleagues, aware of the profound sleep problems often seen in Alzheimer’s, wondered whether the cells may stop doing their job as the disease progresses. “If you lose them, you should see dysfunction of the circadian rhythms and see disrupted sleep,” says Alfredo Sadun, neuro-opthamologist at the University of California, Los Angeles, and co-author of the study. “That is the exact symptomology we see in Alzheimer’s disease.” To learn more, the researchers used dyes to mark melanopsin cells in the eyes of 30 recently deceased organ donors. They found approximately 24% fewer melanopsin cells in the eyes of people with Alzheimer’s than in the eyes of donors without the disease. © 2015 American Association for the Advancement of Science.

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: 21686 - Posted: 12.09.2015

Ian Sample Science editor Scientists have discovered a chemical that destroys toxic plaques which build up in the brain in the early stages of Alzheimer’s disease. Preliminary tests found that when added to drinking water, the compound cleared amyloid beta plaques from the brains of mice with Alzheimer’s-like symptoms, and restored their cognitive function to normal. The work is at a very early stage, but raises hopes for drugs that can prevent the accumulation of amyloid plaques and potentially halt the progression of the disease. Amyloid plaques are one of the first hallmarks of Alzheimer’s disease and are thought to contribute to neurodegeneration by killing off brain cells. Researchers in Korea discovered the chemical, EPPS, while screening a variety of molecules for their effects on amyloid plaques. In the latest study, they added the substance to the drinking water of mice that had symptoms of Alzheimer’s disease. They found that administering EPPS for a week improved how well mice performed on maze tests, and cleared amyloid plaques from the animals’ brains. “Our findings clearly support the view that aggregated amyloid-beta is the pathological culprit of Alzheimer’s disease,” said YoungSoo Kim, who led the team at the Korea Institute of Science and Technology in Seoul. The study used mice that had amyloid plaques injected into their brains. The animals suffered cognitive impairments as a result, but they did not develop the kind of widespread brain damage seen in Alzheimer’s patients which would not be reversed by removing amyloid plaques. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21685 - Posted: 12.09.2015