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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

By Minaz Kerawala, For years, gamers, athletes and even regular people trying to improving their memory have resorted, with electrified enthusiasm, to "brain zapping" to gain an edge. The procedure, called transcranial direct current stimulation (tDCS), uses a battery and electrodes to deliver electrical pulses to the brain, usually through a cap or headset fitted close to the scalp. Proponents say these currents are beneficial for a range of neurological conditions like Alzheimer's and Parkinson's diseases, stroke and schizophrenia, but experts are warning that too little is known about the safety of tDCS. "You might end up with a placement of electrodes that doesn't do what you think it does and could potentially have long-lasting effects," said Matthew Krause, a neuroscientist at the Montreal Neurological Institute. All functions of the brain—thought, emotion and coordination—are carried out by neurons using pulses of electricity. "The objective of all neuroscience is to influence these electrical processes," Krause said. The brain's activity can be influenced by drugs that alter its electrochemistry or by external external electric fields. While mind-altering headsets may seem futuristic, tDCS is not a new procedure. Much of the pioneering work in the field was done in Montreal by Dr. Wilder Penfield in the 1920s and 30s. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 22464 - Posted: 07.21.2016

By Maggie Koerth-Baker When former Tennessee women’s basketball coach Pat Summitt died Tuesday morning, news outlets, including ESPN, reported the cause of her death as “early-onset dementia, Alzheimer’s type.” That’s more than just a long-winded way of saying “Alzheimer’s.” By using five words instead of one, journalists were trying to point a big, flashing neon arrow at the complex realities of dementia. Dementia is more of a symptom than a diagnosis, and it can be caused by a number of different diseases. Even Alzheimer’s, the most common type of dementia, doesn’t seem to have a single cause. Instead, what ties Summitt to millions of other Alzheimer’s patients all over the world is the physical damage it wrought in her brain. Worldwide, 47.5 million people are living with some kind of dementia. Alzheimer’s represents 60 percent to 70 percent of those cases. Imagine a map of a city — roads branching out, intersecting with other roads, creating a network that allows mail to be delivered, food to be sold and brought home, people to get to their jobs. What would happen to that town if random intersections were suddenly barricaded and impassible? That’s the dystopian chaos Alzheimer’s causes, as damaged proteins clog the neurons and inhibit the flow of information from one neuron to another. Cut off from food, as well as data, the cells die. The brain shrinks. Eventually, the person dies, too. Afterward, doctors can cut into their brain and see the barriers, which are called plaques.

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: 22426 - Posted: 07.12.2016

By Edd Gent, The devastating neurodegenerative condition Alzheimer's disease is incurable, but with early detection, patients can seek treatments to slow the disease's progression, before some major symptoms appear. Now, by applying artificial intelligence algorithms to MRI brain scans, researchers have developed a way to automatically distinguish between patients with Alzheimer's and two early forms of dementia that can be precursors to the memory-robbing disease. The researchers, from the VU University Medical Center in Amsterdam, suggest the approach could eventually allow automated screening and assisted diagnosis of various forms of dementia, particularly in centers that lack experienced neuroradiologists. Additionally, the results, published online July 6 in the journal Radiology, show that the new system was able to classify the form of dementia that patients were suffering from, using previously unseen scans, with up to 90 percent accuracy. [10 Things You Didn't Know About the Brain] "The potential is the possibility of screening with these techniques so people at risk can be intercepted before the disease becomes apparent," said Alle Meije Wink, a senior investigator in the center's radiology and nuclear medicine department. "I think very few patients at the moment will trust an outcome predicted by a machine," Wink told Live Science. "What I envisage is a doctor getting a new scan, and as it is loaded, software would be able to say with a certain amount of confidence [that] this is going to be an Alzheimer's patient or [someone with] another form of dementia." © 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: 22425 - Posted: 07.12.2016

By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.

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: 22420 - Posted: 07.11.2016

By Nancy Stearns Bercaw In her memoir “Aliceheimer’s: Alzheimer’s Through the Looking Glass,” Dana Walrath uses drawings and stories to chronicle three years of caregiving for her mother, Alice, who was in the middle stages of Alzheimer’s disease. The experience turned out to be a magical trip down the rabbit hole of memory loss, an outcome that inspired Dr. Walrath, a medical anthropologist who taught at the University of Vermont College of Medicine and who also studied art and writing, to share their tale. Refusing to accept the dominant narrative of Alzheimer’s disease as a horror story, Dr. Walrath used the techniques of graphic medicine to create “Aliceheimer’s,” an 80-page, 35-picture tribute to her mother’s animated mind. Graphic medicine uses text and graphics to, as she writes in the book’s introduction, “let us better understand those who are hurting, feel their stories, and redraw and renegotiate those social boundaries.” We spoke with Dr. Walrath to learn more about graphic medicine, how the book came into being, and what it can teach others about caring for someone with Alzheimer’s disease. Here’s an edited excerpt of our conversation. Q. You say that “Aliceheimer’s” found you, not the other way around. What’s the backstory of your story? A. After a lifetime of mutually abrasive interaction, my mother moved into my home when a lock-down memory-care unit was her only other option. The years of living together not only brought us closure, but it also integrated my disparate career threads. Medical anthropology, creative writing, visual art — who knew they were connected? I sure didn’t. But Alice must have. During dementia, she said to me, “You should quit your job and make art full time.” © 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: 22350 - Posted: 06.23.2016

By Aleszu Bajak Can the various puzzles and quizzes associated with commercial brain-training games really improve cognitive function — or better yet, stave off cognitive decline? To date, the scientific evidence is murky, but that hasn’t kept companies from trying to cash-in on consumers’ native desire for quick fixes to complex health problems. The most famous among such companies is probably Lumosity, a product of San Francisco-based Lumos Labs, which once marketed its suite of web-based games and mobile apps as being “built on proven neuroscience,” and by encouraging users to “harness your brain’s neuroplasticity and train your way to a brighter life.” Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Those claims were among several that attracted the attention of the Federal Trade Commission, which earlier this year filed a complaint against the company. Lumosity was ultimately slapped with $50 million in fines for deceiving consumers — although $48 million of that was reportedly suspended by a district court, because the company was financially unable to pay the full amount. “Lumosity preyed on consumers’ fears about age-related cognitive decline, suggesting their games could stave off memory loss, dementia, and even Alzheimer’s disease,” said Jessica Rich, Director of the FTC’s Bureau of Consumer Protection, in a statement accompanying the settlement. “But Lumosity simply did not have the science to back up its ads.” Copyright 2016 Undark

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: 22328 - Posted: 06.16.2016

By Sandra G. Boodman Richard McGhee and his family believed the worst was behind them. McGhee, a retired case officer at the Defense Intelligence Agency who lives near Annapolis, had spent six months battling leukemia as part of a clinical trial at MD Anderson Cancer Center in Houston. The experimental chemotherapy regimen he was given had worked spectacularly, driving his blood cancer into a complete remission. But less than nine months after his treatment ended, McGhee abruptly fell apart. He became moody, confused and delusional — even childish — a jarring contrast with the even-keeled, highly competent person he had been. He developed tremors in his arms, had trouble walking and became incontinent. “I was really a mess,” he recalled. Doctors suspected he had developed a rapidly progressive and fatal dementia, possibly a particularly aggressive form of Alzheimer’s disease. If that was the case, his family was told, his life span would be measured in months. Luckily, the cause of McGhee’s precipitous decline proved to be much more treatable — and prosaic — than doctors initially feared. “It’s really a pleasure to see somebody get better so rapidly,” said Michael A. Williams, a professor of neurology and neurosurgery at the University of Washington School of Medicine in Seattle. Until recently, Williams was affiliated with Baltimore’s Sinai Hospital, where he treated McGhee in 2010. “This was a diagnosis waiting to be found.”

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: 22293 - Posted: 06.07.2016

By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.

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: 22265 - Posted: 05.31.2016

By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,

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: 22257 - Posted: 05.28.2016

By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company

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: 22255 - Posted: 05.26.2016