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By Jessica Hamzelou Having an agile mind in your 90s might sound like wishful thinking, but some people manage to retain youthful memories until their dying days. Now post mortems have revealed that these “superagers” manage to do this even when their brains have the hallmarks of Alzheimer’s diseases. Superagers have the memory and cognition of the average person almost half their age, and manage to avoid Alzheimer’s symptoms. Aras Rezvanian at Northwestern University in Chicago, Illinois, and his colleagues have been looking at brain samples donated by such people to try to understand what their secret might be. The group looked at eight brains, all from people who had lived into their 90s, and had memory and cognition scores of the average 50-year-old until their final days. Specifically, the team studied two brain regions – the hippocampus, which is involved in memory, and the prefrontal cortex, which is key for cognition. They found that the brain samples of the superagers had plaques and tangles in them to varying degrees. These are sticky clumps and twisted fibres of protein that seem to be linked to the death of neurons, and are usually found in the brains of people with Alzheimer’s disease after they die. Of the eight superager samples, two had such a high density and distribution of these proteins that they resembled the most severe cases of Alzheimer’s. © 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: 22868 - Posted: 11.15.2016

Kathleen Taylor The global rise in dementia should surprise no one. The figures — such as the 9.9 million new diagnoses each year — have been known for decades. As slow as we are to accept such vast changes on a personal, societal and political level, so research is slow to uncover why our brains become fragile with age. Neuroscientist and writer Kathleen Taylor's The Fragile Brain is about that research. But it is much more than a simple reflection on the best published hypotheses. Taylor has crafted a personal, astonishingly coherent review of our current state of knowledge about the causes of Alzheimer's disease and dementia, as well as possible solutions, from lifestyle adjustments to drug developments. Filled with elegant metaphors, her study covers the detail of molecular biology and larger-scale analysis, including epidemiological observations and clinical studies. It extends to dementia due to multiple sclerosis, stroke and encephalitis. For instance, some 5–30% of people who have a first stroke develop dementia. But the book's focus is Alzheimer's disease, and rightly so: it is what up to 80% of people with dementia are diagnosed with. Taylor begins with a shocking juxtaposition, setting the costs of age-related disorders and of dementia alongside the scarcity in funding. In Britain, Australia and the United States, for example, funding for dementia research is a fraction of that for cancer — in the United States, just 18%. She contextualizes with reflections on the history of dementia research, deftly unravelling the roles of pioneering scientists Alois Alzheimer, Franz Nissl and Emil Kraepelin in describing the condition. © 2016 Macmillan Publishers Limited,

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: 22851 - Posted: 11.10.2016

Elie Dolgin There are not a lot of things that could bring together people as far apart on the US political spectrum as Republican Newt Gingrich and Democrat Bob Kerrey. But in 2007, after leading a three-year commission that looked into the costs of care for elderly people, the political rivals came to full agreement on a common enemy: dementia. At the time, there were fewer than 30 million people worldwide diagnosed with the condition, but it was clear that the numbers were set to explode. By 2050, current predictions suggest, it could reach more than 130 million, at which point the cost to US health care alone from diseases such as Alzheimer’s will probably hit US$1 trillion per year in today’s dollars. “We looked at each other and said, ‘You know, if we don’t get a grip on Alzheimer’s, we can’t get anything done because it’s going to drown the system,’” recalls Gingrich, the former speaker of the US House of Representatives. He still feels that sense of urgency, and for good reason. Funding has not kept pace with the scale of the problem; targets for treatments are thin on the ground and poorly understood; and more than 200 clinical trials for Alzheimer’s therapies have been terminated because the treatments were ineffective. Of the few treatments available, none addresses the underlying disease process. “We’re faced with a tsunami and we’re trying to deal with it with a bucket,” says Gingrich. But this message has begun to reverberate around the world, which gives hope to the clinicians and scientists. Experts say that the coming wave can be calmed with the help of just three things: more money for research, better diagnostics and drugs, and a victory — however small — that would boost morale. © 2016 Macmillan Publishers 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: 22848 - Posted: 11.09.2016

By Simon Makin Cerebral autopsy specimen of a patient diagosed having Alzheimer Disease. In the HE stain numerous plaque formations within the neuropil background are visible. Credit: WIKIPEDIA, CC BY-SA 3.0 On Monday Pres. Barack Obama proclaimed November “National Alzheimer's Disease Awareness Month.” The administration’s ambitious goal is to prevent and treat Alzheimer's by 2025. Although there are currently no approved therapies that slow or stop progression of the disease, several approaches are showing promise. In a study published today in Science Translational Medicine, a team from Merck Research Laboratories reports results of early human and animal trials of a drug called verubecestat, which targets the production of protein plaques associated with the disease. “It's a summary of the discovery and early-stage profiling of what we hope is going to be a new therapeutic for Alzheimer's,” says team leader Matthew Kennedy. “It represents well over a decade of investment in this project by many, many scientists.” Definitive conclusions will have to await the results of larger, ongoing phase III clinical trials to assess their efficacy, effectiveness and safety, but the results are promising, experts say. Verubecestat is a so-called BACE1 inhibitor. BACE1 (for Beta-site Amyloid precursor protein Cleaving Enzyme 1, aka beta-secretase 1) is an enzyme involved in producing amyloid beta (Ab), a protein that clumps together, eventually forming the plaques surrounding neurons that are the disease's key hallmark. The amyloid hypothesis of Alzheimer's proposes that the accumulation of amyloid beta aggregates in the brain drives a cascade of biological events leading to neurodegeneration. By blocking BACE1, the hope is this approach could prevent the buildup of these clumps in the first place. But until now, development of these drugs has been hindered by problems finding molecules with the right characteristics, and concerns over theoretical and actual side effects. © 2016 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: 22827 - Posted: 11.03.2016

By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 22754 - Posted: 10.13.2016

By Smitha Mundasad Health reporter People who experience frequent drops in blood pressure or dizziness when suddenly standing up are at increased risk of dementia, scientists say. Writing in Plos Medicine they suggest that less blood reaches the brain during these moments, leading to brain cell damage over time. Dementia experts say this is a "robust study" and "plausible explanation" that needs further investigation. Charities point out that factors such as smoking carry higher risks. But they say the work adds to growing evidence that changes in blood pressure have an impact on the brain. Previous studies have linked high blood pressure to types of dementia. But in this paper scientists focused on transient periods of low blood pressure - also known as postural hypotension - which become more common in older age. These episodes can sometimes leave people feeling dizzy or give them "head rushes" when standing up suddenly. Researchers from the Erasmus Medical Center, in the Netherlands, tracked 6,000 people for an average of 15 years. They found those who suffered repeated periods of low blood pressure on standing were more likely to develop dementia in the years that followed. Researcher Dr Arfan Ikram said: "Even though the effect can be seen as subtle - with an increased risk of about 4% for people with postural hypotension compared to those without it - so many people suffer from postural hypotension as they get older that it could have a significant impact on the burden of dementia across the world." He told the BBC: "If people experience frequent episodes of dizziness on standing, particularly as they get older, they should see their GPs for advice." © 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: 22753 - Posted: 10.13.2016

By Rebecca Robbins, In the months before his death, Robin Williams was besieged by paranoia and so confused he couldn’t remember his lines while filming a movie, as his brain was ambushed by what doctors later identified as an unusually severe case of Lewy body dementia. “Robin was losing his mind and he was aware of it. Can you imagine the pain he felt as he experienced himself disintegrating?” the actor’s widow, Susan Schneider Williams, wrote in a wrenching editorial published this week in the journal Neurology. The title of her piece: “The terrorist inside my husband’s brain.” Susan Williams addressed the editorial to neurologists, writing that she hoped husband’s story would “help you understand your patients along with their spouses and caregivers a little more.” Susan Williams has previously blamed Lewy body dementia for her husband’s death by suicide in 2014. About 1.3 million Americans have the disease, which is caused by protein deposits in the brain. Williams was diagnosed with Parkinson’s disease a few months before he died; the telltale signs of Lewy body dementia in his brain were not discovered until an autopsy. The editorial chronicles Williams’s desperation as he sought to understand a bewildering array of symptoms that started with insomnia, constipation, and an impaired sense of smell and soon spiraled into extreme anxiety, tremors, and difficulty reasoning. © 2016 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: 22721 - Posted: 10.02.2016

Jon Hamilton What rats can remember may help people who forget. Researchers are reporting evidence that rats possess "episodic memories," the kind of memories that allow us to go back in time and recall specific events. These memories are among the first to disappear in people who develop Alzheimer's disease. The finding, which appears Thursday in Current Biology, suggests that rats could offer a better way to test potential drugs for Alzheimer's. Right now, most of these drugs are tested in mice. "We need to have a way to study the exact type of memory that we think is impaired in Alzheimer's disease," says Bruce Lamb, a professor of medical and molecular genetics at Indiana University in Indianapolis. He was not involved in the study. The lack of an adequate animal model of Alzheimer's disease may be one reason drugs that seemed to work in mice have failed when given to people, Lamb says. Loss of episodic memories, especially recent ones, is a key sign of Alzheimer's, says Jonathon Crystal, an author of the study and director of the neuroscience program at Indiana University in Bloomington. "So if you visit your grandmother who has Alzheimer's, [she] isn't going to remember that you were visiting a couple of weeks ago and what you described about things that are going on in your life," he says. Crystal and a team of researchers thought rats might have some form of episodic memory. So they began doing studies that relied on the animals' remarkable ability to recognize a wide range of odors, like basil and banana and strawberry. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22711 - Posted: 09.30.2016

By CONOR DOUGHERTY SAN FRANCISCO — Every now and again, when I’m feeling a little down, I go to Baseball-Reference.com and look up the San Francisco Giants’ box score from July 29, 2012. It’s an odd choice for a Giants fan. The Los Angeles Dodgers won, 4-0, completing a weekend sweep in which they outscored the Giants by 19-3 and tied them for the lead in the National League West. The Giants went on to win the World Series that year, but that’s not why I remember the July 29 game. I remember that afternoon because my mom, in the throes of Alzheimer’s, left the house she shared with my dad in the Noe Valley neighborhood, walked four or so miles and somehow ended up at AT&T Park. Then she went inside and watched her team. It took a while for me to believe this. When Mom told me she had gone to the park — my dad barely watches baseball, so the Giants have always been a thing between me and Mom — I assumed it was an old memory misplaced on a new day. But it turned out that Sunday game did overlap with the hours she had been out, and a month or so later my dad got a credit card bill with the charge for the ticket. I can’t tell you when Mom cheered or if she managed to find her seat. All I know is Clayton Kershaw struck out seven, the Giants had five hits, and even though I’ve committed these statistics to memory, I still like looking them up. On the chance that this hasn’t been clubbed into your head by now, the Giants have won the World Series in every even-numbered year this decade. And for reasons that I choose to see as cosmic, this run of baseball dominance has tracked my mom’s descent into Alzheimer’s. The disease doesn’t take people from you in a day or a week or a season. You get years of steady disappearance, with an indeterminate end. So for me and Mom and baseball, this decade has been a long goodbye. © 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: 22690 - Posted: 09.24.2016

Laura Sanders An experimental drug swept sticky plaques from the brains of a small number of people with Alzheimer’s disease over the course of a year. And preliminary results hint that this cleanup may have staved off mental decline. News about the new drug, an antibody called aducanumab, led to excitement as it trickled out of recent scientific meetings. A paper published online August 31 in Nature offers a more comprehensive look at the drug’s effects. “Overall, this is the best news that we’ve had in my 25 years doing Alzheimer’s clinical research,” study coauthor Stephen Salloway of Brown University said August 30 at a news briefing. “It brings new hope for patients and families most affected by the disease.” The results are the most convincing evidence yet that an antibody can reduce amyloid in the brain, says Alzheimer’s researcherRachelle Doody of Baylor College of Medicine in Houston, who was not involved in the study. Still, experts caution that the results come from 165 people, a relatively small number. The seemingly beneficial effects could disappear in larger clinical trials, which are under way. “These new data are tantalizing, but they are not yet definitive,” says neuroscientist John Hardy of University College London. Like some other drug candidates for Alzheimer’s, aducanumab is an antibody that targets amyloid-beta, a sticky protein that accumulates in the brains of people with the disease. Delivered by intravenous injection, aducanumab appeared to get inside the brains of people with mild Alzheimer’s (average age about 73) and destroy A-beta plaques, the results suggest. After a year of exposure to the drug, A-beta levels had dropped. This reduction depended on the dose — the more drug, the bigger the decline in A-beta. In fact, people on the highest dose of the drug had almost no A-beta plaques in their brains after a year. |© 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: 22621 - Posted: 09.01.2016

By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © 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: 22588 - Posted: 08.23.2016

By Roni Caryn Rabin Dementia is a general term for a set of symptoms that includes severe memory loss, a significant decline in reasoning and severely impaired communication skills; it most commonly strikes elderly people and used to be referred to as “senility.” Alzheimer’s disease is a specific illness that is the most common cause of dementia. Though many diseases can cause dementia, Alzheimer’s accounts for 60 percent to 80 percent of dementia cases, “which is why you’ll often hear the terms used interchangeably,” said Heather Snyder, the senior director of medical and scientific operations for the Alzheimer’s Association. She said the question comes up frequently because patients may receive an initial diagnosis of dementia followed by an evaluation that yields the more specific diagnosis of Alzheimer’s disease, and they may be confused. The second most common form of dementia is vascular dementia, which is caused by a stroke or poor blood flow to the brain. Other diseases that can lead to dementia include Huntington’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Some patients may have more than one form of dementia. Dementia is caused by damage to brain cells. In the case of Alzheimer’s disease, that damage is characterized by telltale protein fragments or plaques that accumulate in the space between nerve cells and twisted tangles of another protein that build up inside cells. In Alzheimer’s disease, dementia gets progressively worse to the point where patients cannot carry out daily activities and cannot speak, respond to their environment, swallow or walk. Although some treatments may temporarily ease symptoms, the downward progression of disease continues and it is not curable. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Brain Asymmetry, Spatial Cognition, and Language
Link ID: 22559 - Posted: 08.16.2016

Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22543 - Posted: 08.11.2016

By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 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: 22520 - Posted: 08.06.2016

By Andy Coghlan Mysterious shrunken cells have been spotted in the human brain for the first time, and appear to be associated with Alzheimer’s disease. “We don’t know yet if they’re a cause or consequence,” says Marie-Ève Tremblay of Laval University in Québec, Canada, who presented her discovery at the Translational Neuroimmunology conference in Big Sky, Montana, last week. The cells appear to be withered forms of microglia – the cells that keep the brain tidy and free of infection, normally by pruning unwanted brain connections or destroying abnormal and infected brain cells. But the cells discovered by Tremblay appear much darker when viewed using an electron microscope, and they seem to be more destructive. “It took a long time for us to identify them,” says Tremblay, who adds that these shrunken microglia do not show up with the same staining chemicals that normally make microglia visible under the microscope. Compared with normal microglia, the dark cells appear to wrap much more tightly around neurons and the connections between them, called synapses. “It seems they’re hyperactive at synapses,” says Tremblay. Where these microglia are present, synapses often seem shrunken and in the process of being degraded. Tremblay first discovered these dark microglia in mice, finding that they increase in number as mice age, and appear to be linked to a number of things, including stress, the neurodegenerative condition Huntington’s disease and a mouse model of Alzheimer’s disease. “There were 10 times as many dark microglia in Alzheimer’s mice as in control mice,” says Tremblay. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22503 - Posted: 08.02.2016

By Tanya Lewis The tangled buildup of tau protein in brain cells is a hallmark of the cognitive decline linked with Alzheimer’s disease. Antibodies have been shown to block tau’s spread, but some scientists worry it could also fuel inflammation. Now, researchers from Genentech in San Francisco and colleagues have found that an antibody’s ability to recruit immune cells—known as its effector function—is not necessary for stopping tau’s spread, the team reported today (July 28) in Cell Reports. “Our results suggest that, given that effector function is not required for efficacy [in treating tau accumulation], going without it could offer a safer approach for immunotherapy,” study coauthor Gai Ayalon of Genentech told The Scientist. Alzheimer’s disease causes a characteristic constellation of pathologies: accumulation of amyloid-β plaques outside neurons, neurofibrillary tangles of tau inside brain cells, and chronic inflammation. Clinical research has mostly focused on targeting amyloid-β with antibody therapies, and several treatments based on this approach are currently in clinical trials. But recent efforts have zeroed in on tau as a new potential target. Antibodies are known to spur the brain’s defense system, microglia, to absorb and degrade tau, but their recruitment of immune cells may also worsen inflammation. Ayalon and colleagues wondered whether effector function was necessary for stopping tau’s spread. © 1986-2016 The Scientist

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: 22492 - Posted: 07.30.2016

By ANDREW POLLACK A new type of drug for Alzheimer’s disease failed to slow the rate of decline in mental ability and daily functioning in its first large clinical trial. There was a hint, though, that it might be effective for certain patients. The drug, called LMTX, is the first one with its mode of action — trying to undo so-called tau tangles in the brain — to reach the final stage of clinical trials. So the results of the study were eagerly awaited. The initial reaction to the outcome was disappointment, with perhaps a glimmer of hopefulness. Over all, the patients who received LMTX, which was developed by TauRx Therapeutics, did not have a slower rate of decline in mental ability or daily functioning than those in the control group. However, the drug did seem to work for the subset of patients — about 15 percent of those in the study — who took LMTX as their only therapy. The other 85 percent of patients took an existing Alzheimer’s drug in addition to either LMTX or a placebo. “There were highly significant, clinically meaningful, large effects in patients taking the drug as monotherapy, and no effect in patients taking it as an add-on,” Claude Wischik, a founder and the chief executive of TauRx, said in an interview. He spoke from Toronto, where the results were being presented at the Alzheimer’s Association International Conference. Dr. Wischik said a second clinical trial sponsored by the company, whose results will be announced later, found the same phenomenon. He said the company planned to apply for approval of LMTX to be used by itself. But some experts not involved in the study were skeptical about drawing conclusions from a small subset of patients, especially since there was no obvious explanation why LMTX would be expected to work only in patients not getting other drugs. on © 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: 22488 - Posted: 07.28.2016

Jon Hamilton Two studies released at an international Alzheimer's meeting Tuesday suggest doctors may eventually be able to screen people for this form of dementia by testing the ability to identify familiar odors, like smoke, coffee and raspberry. In both studies, people who were in their 60s and older took a standard odor detection test. And in both cases, those who did poorly on the test were more likely to already have — or go on to develop — problems with memory and thinking. "The whole idea is to create tests that a general clinician can use in an office setting," says Dr. William Kreisl, a neurologist at Columbia University, where both studies were done. The research was presented at the Alzheimer's Association International Conference in Toronto. Currently, any tests that are able to spot people in the earliest stages of Alzheimer's are costly and difficult. They include PET scans, which can detect sticky plaques in the brain, and spinal taps that measure the levels of certain proteins in spinal fluid. The idea of an odor detection test arose, in part, from something doctors have observed for many years in patients with Alzheimer's, Kreisl says. "Patients will tell us that food does not taste as good," he says. The reason is often that these patients have lost the ability to smell what they eat. That's not surprising, Kreisl says, given that odor signals from the nose have to be processed in areas of the brain that are among the first to be affected by Alzheimer's disease. But it's been tricky to develop a reliable screening test using odor detection. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22485 - Posted: 07.27.2016

By PAM BELLUCK “Has the person become agitated, aggressive, irritable, or temperamental?” the questionnaire asks. “Does she/he have unrealistic beliefs about her/his power, wealth or skills?” Or maybe another kind of personality change has happened: “Does she/he no longer care about anything?” If the answer is yes to one of these questions — or others on a new checklist — and the personality or behavior change has lasted for months, it could indicate a very early stage of dementia, according to a group of neuropsychiatrists and Alzheimer’s experts. They are proposing the creation of a new diagnosis: mild behavioral impairment. The idea is to recognize and measure something that some experts say is often overlooked: Sharp changes in mood and behavior may precede the memory and thinking problems of dementia. The group made the proposal on Sunday at the Alzheimer’s Association International Conference in Toronto, and presented a 38-question checklist that may one day be used to identify people at greater risk for Alzheimer’s. “I think we do need something like this,” said Nina Silverberg, the director of the Alzheimer’s Disease Centers program at the National Institute on Aging, who was not involved in creating the checklist or the proposed new diagnosis. “Most people think of Alzheimer’s as primarily a memory disorder, but we do know from years of research that it also can start as a behavioral issue.” Under the proposal, mild behavioral impairment (M.B.I.) would be a clinical designation preceding mild cognitive impairment (M.C.I.), a diagnosis created more than a decade ago to describe people experiencing some cognitive problems but who can still perform most daily functions. © 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: 22480 - Posted: 07.26.2016

By Sharon Begley, STAT For the first time ever, researchers have managed to reduce people’s risk for dementia — not through a medicine, special diet, or exercise, but by having healthy older adults play a computer-based brain-training game. The training nearly halved the incidence of Alzheimer’s disease and other devastating forms of cognitive and memory loss in older adults a decade after they completed it, scientists reported on Sunday. If the surprising finding holds up, the intervention would be the first of any kind — including drugs, diet, and exercise — to do that. “I think these results are highly, highly promising,” said George Rebok of the Johns Hopkins Bloomberg School of Public Health, an expert on cognitive aging who was not involved in the study. “It’s exciting that this intervention pays dividends so far down the line.” The results, presented at the Alzheimer’s Association International Conference in Toronto, come from the government-funded ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) study. Starting in 1998, ACTIVE’s 2,832 healthy older adults (average age at the start: 74) received one of three forms of cognitive training, or none, and were evaluated periodically in the years after. In actual numbers, 14 percent of ACTIVE participants who received no training had dementia 10 years later, said psychologist Jerri Edwards of the University of South Florida, who led the study. Among those who completed up to 10 60-to-75-minute sessions of computer-based training in speed-of-processing — basically, how quickly and accurately they can pay attention to, process, and remember brief images on a computer screen — 12.1 percent developed dementia. Of those who completed all 10 initial training sessions plus four booster sessions a few years later, 8.2 percent developed dementia. © 2016 Scientific American

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: 22479 - Posted: 07.26.2016