Links for Keyword: Alzheimers

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By Emily Underwood One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia. Although this evidence won’t itself resolve the amyloid-tau debate, the finding could spur more research into new, tau-targeting treatments and lead to better diagnostic tools, researchers say. Scientists have long used an imaging technique called positron emission tomography (PET) to visualize ß-amyloid deposits marked by radioactive chemical tags in the brains of people with AD. Combined with postmortem analyses of brain tissue, these studies have demonstrated that people with AD have far more ß-amyloid plaques in their brains than healthy people, at least as a general rule. But they have also revealed a puzzle: Roughly 30% of people without any signs of dementia have brains “chock-full” of ß-amyloid at autopsy, says neurologist Beau Ances at Washington University in St. Louis in Missouri. That mystery has inspired many in the AD field to ask whether a second misfolded protein, tau, is the real driver of the condition’s neurodegeneration and symptoms, or at least an important accomplice. Until recently, the only ways to test that hypothesis were to measure tau in brain tissue after a person died, or in a sample of cerebrospinal fluid (CSF) extracted from a living person by needle. But in the past several years, researchers have developed PET imaging agents that can harmlessly bind to tau in the living brain. The more tau deposits found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team reports today in Science Translational Medicine. © 2016 American Association for the Advancement of Science.

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: 22210 - Posted: 05.12.2016

Patricia Neighmond Hoping to keep your mental edge as you get older? Look after your heart, a recent analysis suggests, and your brain will benefit, too. A research team led by Hannah Gardener, an epidemiologist at the University of Miami, analyzed a subset of data from the Northern Manhattan Study, a large, ongoing study of risk factors for stroke among whites, blacks and Hispanics living in the Washington Heights neighborhood of New York City. The scientists wanted to see how people in their 60s and 70s would do on repeated tests of memory and mental acuity six years later — and, specifically, what sort of subtle differences a heart-healthy lifestyle might make to the brain, beyond the prevention of strokes. Their findings appear in a recent issue of the Journal of the American Heart Association. In this particular study, the researchers started with more than a thousand people who'd had their cardiovascular health assessed using measures that the American Heart Association has dubbed Life's Simple 7. These seven factors known to benefit the heart and blood vessels include maintaining a normal body weight and good nutrition, not smoking, getting exercise regularly and keeping blood pressure, cholesterol and blood sugar levels under control. To measure thinking skills, Gardener's team used a variety of tests of memory, judgement, the ability to plan, mental quickness and other sorts of problem solving. The results were striking: Across all demographic groups, the people who had higher scores on the measures of cardiovascular health did better on the mental tests than those who scored low. © 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: 22167 - Posted: 05.02.2016

By n. r. kleinfield IT BEGAN WITH what she saw in the bathroom mirror. On a dull morning, Geri Taylor padded into the shiny bathroom of her Manhattan apartment. She casually checked her reflection in the mirror, doing her daily inventory. Immediately, she stiffened with fright. Huh? What? She didn’t recognize herself. She gazed saucer-eyed at her image, thinking: Oh, is this what I look like? No, that’s not me. Who’s that in my mirror? This was in late 2012. She was 69, in her early months getting familiar with retirement. For some time she had experienced the sensation of clouds coming over her, mantling thought. There had been a few hiccups at her job. She had been a nurse who climbed the rungs to health care executive. Once, she was leading a staff meeting when she had no idea what she was talking about, her mind like a stalled engine that wouldn’t turn over. “Fortunately I was the boss and I just said, ‘Enough of that; Sally, tell me what you’re up to,’” she would say of the episode. Certain mundane tasks stumped her. She told her husband, Jim Taylor, that the blind in the bedroom was broken. He showed her she was pulling the wrong cord. Kept happening. Finally, nothing else working, he scribbled on the adjacent wall which cord was which. Then there was the day she got off the subway at 14th Street and Seventh Avenue unable to figure out why she was there. So, yes, she had had inklings that something was going wrong with her mind. She held tight to these thoughts. She even hid her suspicions from Mr. Taylor, who chalked up her thinning memory to the infirmities of age. “I thought she was getting like me,” he said. “I had been forgetful for 10 years.”

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: 22160 - Posted: 04.30.2016

By PAM BELLUCK Alzheimer’s disease can seem frightening, mysterious and daunting. There are still a lot of unknowns about the disease, which afflicts more than five million Americans. Here are answers to some common questions: Sometimes I forget what day it is or where I put my glasses. Is this normal aging, or am I developing Alzheimer’s? Just because you forgot an item on your grocery list doesn’t mean you are developing dementia. Most people have occasional memory lapses, which increase with age. The memory problems that characterize warning signs of Alzheimer’s are usually more frequent, and they begin to interfere with safe or competent daily functioning: forgetting to turn off the stove, leaving home without being properly dressed or forgetting important appointments. Beyond that, the disease usually involves a decline in other cognitive abilities: planning a schedule, following multistep directions, carrying out familiar logistical tasks like balancing a checkbook or cooking a meal. It can also involve mood changes, agitation, social withdrawal and feelings of confusion, and can even affect or slow a person’s gait. How is Alzheimer’s diagnosed? Diagnosing Alzheimer’s usually involves a series of assessments, including memory and cognitive tests. Clinicians will also do a thorough medical work-up to determine whether the thinking and memory problems can be explained by other diagnoses, such as another type of dementia, a physical illness or side effects from a medication. Brain scans and spinal taps may also be conducted to check for corroborating evidence like the accumulation of amyloid, the hallmark protein of Alzheimer’s, in the brain or spinal fluid. The cause is unknown for most cases. Fewer than 5 percent of cases are linked to specific, rare gene mutations. Those are usually early-onset cases that develop in middle age. © 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: 22159 - Posted: 04.30.2016

By Esther Landhuis Peer inside the brain of someone with Alzheimer’s disease, and you’ll see some striking features: shriveled nerve cells and strange protein clumps. According to a leading theory, proteins called amyloid beta and tau build up in the brain and choke nerve cell communication, setting the disease in motion years before people suspect anything is wrong with their recall. Yet the Alzheimer’s brain has another curious aspect. Some of the clusters of toxic amyloid proteins are entangled with octopus-like immune cells called microglia, cells that live in the brain to clear unwanted clutter. By munching on amyloid plaques, microglia are thought to help keep the disease at bay. But these housekeeping cells have an additional role—they switch on inflammatory pathways. Inflammation is critically important when the immune system encounters infection or needs to repair tissue. If left unchecked, however, the inflammatory process churns out toxic substances that can kill surrounding cells, whose death triggers more inflammation and creates a vicious cycle. For years scientists have probed how neuroinflammation contributes to Alzheimer’s disease and other neurodegenerative ailments. Researchers face a number of immediate questions: Is neuroinflammation a driving force? Does it kick in when the disease is already underway and worsen the process? Could it be harnessed for good in the early stages? Those questions are far from settled, but research is starting to reveal a clearer picture. “It may not be the amyloid plaques themselves that directly damage neurons and the connections between them. Rather, it may be the immune reaction to the plaques that does the damage,” says Cynthia Lemere, a neuroscientist at Brigham and Women’s Hospital. Still, it is hard to say if microglia are good guys or bad, making it challenging to create therapeutics that target these cells. © 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: 22124 - Posted: 04.21.2016

Nicola Davis The proportion of older people suffering from dementia has fallen by a fifth over the past two decades with the most likely explanation being because men are smoking less and living healthier lives, according to new scientific research. A team from three British universities concluded that as a result the number of new cases of dementia is lower than had been predicted in the 1990s, estimated at around 210,000 a year in the UK as opposed to 250,000. The findings are potentially significant because they suggest that it is possible to take preventative action, such as stopping smoking and reducing cholesterol, that could help avoid the condition. “Physical health and brain health are clearly highly linked,” said Carol Brayne of Cambridge University, who co-authored the study. Nick Fox, professor of neurology at University College, London, who was not involved in the study, agrees: “This does suggest that our risk, in any particular age in later life, can be reduced probably by what we do 10, 20 or 30 years before.” The scientists found that new cases of dementia had dropped from 20.1 in every 1,000 people per year in the first study conducted in the early 1990s to 17.7 in the second, which looked at new cases between 2008 and 2013. When sex and age differences were taken into account, the dementia rates were found to have dropped by 20%. The trend emerges from a dramatic drop in new cases for men across all age groups. In the 1990s study, for every 1,000 men aged 70-74, 12.9 went on to develop dementia within a year. In the second study, 20 years later, that figure had dropped to only 8.7 men. For men aged 65-69 the rate of new cases had more than halved between the two studies. © 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: 22122 - Posted: 04.20.2016

Scientists believe injections of a natural protein may lessen the symptoms and progress of Alzheimer's dementia after promising early trials in mice. The treatment - IL 33 - appeared to improve memory and help clear and prevent brain deposits similar to those seen in people with Alzheimer's. Tentative human studies of the treatment will soon begin, but experts say it will take many years to know if it could help patients in real life. The work is published in PNAS journal. Interleukin 33, or IL 33 for short, is made by the body as part of its immune defence against infection and disease, particularly within the brain and spinal cord. And patients with Alzheimer's have been found to have lower amounts of IL 33 in their brains than healthy adults. The researchers from the University of Glasgow and the Hong Kong University of Science and Technology tested what effect a boost of IL 33 might have on mice bred to have brain changes akin to Alzheimer's. The rodents rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week of having the injections. Prof Eddy Liew, who led the work at the University of Glasgow, is excited but cautious about his findings. "Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done." © 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: 22115 - Posted: 04.19.2016

By Jordana Cepelewicz The brain relies on a system of chemical messengers, known as neurotransmitters, to carry missives from cell to cell. When all is well, these communications enable the brain to coordinate various functions, from complex thought to quick, knee-jerk reactions—but when the system is out of whack, serious disease or disorder can ensue. A team of researchers at the Technical University of Denmark (D.T.U.) and University of Oxford have for the first time identified the molecular structure of dopamine beta-hydroxylase (DBH), the enzyme that controls the conversion between dopamine and norepinephrine, two major neurotransmitters. Understanding the crystal structure of the enzyme could provide an ideal target for drug development. Dopamine and norepinephrine play key roles in many brain functions such as learning, memory, movement and the fight-or-flight response. Imbalances in the levels of these neurotransmitters—and the role DBH plays in regulating them—have been implicated in a wide range of disorders, including hypertension, congestive heart failure, anxiety, depression, post-traumatic stress disorder, Alzheimer’s, schizophrenia, Parkinson’s and even cocaine addiction. DBH has long intrigued biochemists but it has been challenging to perform the analyses needed to determine the protein’s structure. “This enzyme has been particularly difficult,” says Hans Christensen, a chemist at D.T.U. and the study’s lead researcher. “We tried many different expression systems before we finally succeeded. Now that we have the structure it is clear why—[it] is very intricate, with different parts of the enzyme interacting very tightly.” © 2016 Scientific American,

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: 22087 - Posted: 04.09.2016

By Roni Caryn Rabin Alzheimer’s disease is a progressive brain disorder that causes dementia, destroying memory, cognitive skills, the ability to care for oneself, speak and walk, said Ruth Drew, director of family and information services at the Alzheimer’s Association. “And since the brain affects everything, Alzheimer’s ultimately affects everything,” she said, “including the ability to swallow, cough and breathe.” Once patients reach the advanced stages of Alzheimer’s, they may stop eating and become weak and susceptible to infections, said Dr. Jason Karlawish, a professor of medicine at the University of Pennsylvania. Unable to swallow or cough, they are at high risk of choking, aspirating food particles or water into the lungs and developing pneumonia, which is often the immediate cause of death, he said. “You see a general decline in the contribution the brain makes, not just in thinking, but in maintaining the body’s homeostasis,” Dr. Karlawish said. Using a feeding tube to nourish patients and hospitalizing them for infections does not significantly extend life at the advanced stages of the disease and is discouraged because it can prolong suffering with no hope of recovery, he said. Alzheimer's is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention, but that figure may underestimate the actual number of cases, Dr. Karlawish said, since some deaths may be attributed to other causes like pneumonia. © 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: 22071 - Posted: 04.06.2016

The mystery is starting to untangle. It has long been known that twisted fibres of a protein called tau collect in the brain cells of people with Alzheimer’s, but their exact role in the disease is unclear. Now a study in mice has shown how tau interferes with the strengthening of connections between neurons – the key mechanism by which we form memories. In healthy cells, the tau protein helps to stabilise microtubules that act as rails for transporting materials around the cell. In people with Alzheimer’s, these proteins become toxic, but an important unanswered question is what forms of tau are toxic: the tangles may not be the whole story. In the new study, Li Gan and her colleagues at the Gladstone Institute of Neurological Disease in San Francisco found that the brains of those with Alzheimer’s have high levels of tau with a particular modification, called acetylated tau. They then looked at what acetylated tau does in a mouse model of Alzheimer’s, finding that it accumulates at synapses – the connections between neurons. When we form memories, synapses become strengthened through extra receptors inserted into the cell membranes, and this heightens their response. But acetylated tau depletes another protein called KIBRA, which is essential for this synapse-strengthening mechanism. “We’re excited because we think we now have a handle on the link between tau and memory,” says Gan. “We’re also cautious because we know this may not be the only link. It’s still early days in understanding the mechanism.” © Copyright Reed Business Information Ltd.

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: 22064 - Posted: 04.04.2016

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