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By Esther Landhuis Among hundreds of genes that might nudge your risk of Alzheimer's up or down, Apolipoprotein E (APOE) has the strongest effect. Scientists discovered a quarter century ago that people with the APOE ε4 version of this gene are four to 15 times more likely to develop Alzheimer’s, a deadly brain disorder that afflicts more than five million Americans. Yet how APOE actually sets off dementia has been somewhat of a mystery—and efforts to use it as a drug target have floundered. The field’s attention has focused on another “A” word—amyloid beta (Aβ). This protein can unwittingly accrue in the brain for years, disrupting nerve connections essential for thinking and memory. APOE has been thought of as a co-conspirator in this process, but finding ways to undermine its collusion have proved challenging. Anti-amyloid drugs have consumed the labors of pharmaceutical companies. If a drug could break those insidious clumps of protein or keep them from forming, drug developers reasoned, it could in theory halt the progression of the disease. But billions of dollars have poured into large-scale clinical trials of amyloid-lowering therapies that so far have failed. Advertisement APOE has hovered on the periphery as far as drug development, but this could soon change. Connections have emerged between the functioning of APOE and Aβ. In 2012 Boston scientists studying autopsy tissue from Alzheimer’s patients found APOE ε4 individuals had unusually high levels of brain Aβ. And they noticed Aβ clumped more readily in test tubes if mixed with ApoE proteins, especially ApoE4. Mouse data from teams at Washington University in Saint Louis and the University of California, San Francisco—suggested a similar relationship. Each lab worked with existing Alzheimer’s mouse models and further modified their genomes to make different types and amounts of ApoE proteins. In both studies animals with less ApoE had fewer Aβ plaques in their brains. © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24176 - Posted: 10.12.2017

By NICHOLAS BAKALAR Women with high blood pressure in their 40s are at increased risk for dementia in later years, researchers report. But the finding does not hold for men. Beginning in 1964, investigators collected health and lifestyle information on 5,646 men and women when they were 30 to 35 years old, and again when they were in their 40s. From 1996 to 2015, 532 of them were found to have Alzheimer’s or other forms of dementia. The study is in Neurology. Hypertension in women in their 30s was not associated with dementia. But women who were hypertensive at an average age of 44 had a 68 percent higher risk for dementia than those who had normal blood pressure at that age, even after adjusting for B.M.I., smoking and other risk factors. High blood pressure in men in their 30s or 40s was not associated with later dementia, but the study’s senior author, Rachel A. Whitmer, said that studies have tied hypertension in men in their 50s to later dementia. Dr. Whitmer, a senior research scientist at Kaiser Permanente in Oakland, Calif., added that hypertension is more common in men, and the hypertensive men in the study tended to die at a younger age than the women. “The big picture here is that brain health is a lifelong issue,” she said. “What you do in young adulthood matters for your brain in old age.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24175 - Posted: 10.12.2017

Jon Hamilton Fresh evidence that the body's immune system interacts directly with the brain could lead to a new understanding of diseases from multiple sclerosis to Alzheimer's. A study of human and monkey brains found lymphatic vessels — a key part of the body's immune system — in a membrane that surrounds the brain and nervous system, a team reported Tuesday in the online journal eLife. Lymphatic vessels are a part of the lymphatic system, which extends throughout the body much like our network of veins and arteries. Instead of carrying blood, though, these vessels carry a clear fluid called lymph, which contains both immune cells and waste products. The new finding bolsters recent evidence in rodents that the brain interacts with the body's lymphatic system to help fend off diseases and remove waste. Until a few years ago, scientists believed that the brain's immune and waste removal systems operated independently. The discovery of lymphatic vessels near the surface of the brain could lead to a better understanding of multiple sclerosis, which seems to be triggered by a glitch in the immune system, says Dr. Daniel Reich, an author of the study and a senior investigator at the National Institute of Neurological Disorders and Stroke. © 2017 npr

Related chapters from BN8e: 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: 24146 - Posted: 10.04.2017

Tina Hesman Saey A genetic risk factor for Alzheimer’s disease is a double, make that triple, whammy. In addition to speeding up the development of brain plaques associated with Alzheimer’s, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature. APOE4 protein also ramps up brain inflammation that kills brain cells, neuroscientist David Holtzman of Washington University School of Medicine in St. Louis and colleagues have discovered. “This paper is a tour de force,” says Robert Vassar, a neuroscientist at Northwestern University Feinberg School of Medicine in Chicago. “It’s a seminal study that’s going to be a landmark in the field” of Alzheimer’s research, Vassar predicts. For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood. But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24103 - Posted: 09.23.2017

By Anil Ananthaswamy Artificial intelligence can identify changes in the brains of people likely to get Alzheimer’s disease almost a decade before doctors can diagnose the disease from symptoms alone. The technique uses non-invasive MRI scans to identify alterations in how regions of the brain are connected. Alzheimer’s is a neurodegenerative disease that is the leading cause of dementia for the elderly, eventually leading to loss of memory and cognitive functions. The race is on to diagnose the disease as early as possible. Although there is no cure, drugs in development are likely to work better the earlier they are given. An early diagnosis can also allow people to start making lifestyle changes to help slow the progression of the disease. When will we cure Alzheimer’s? Learn more at New Scientist Live In an effort to enable earlier diagnosis, Nicola Amoroso and Marianna La Rocca at the University of Bari in Italy and their colleagues developed a machine-learning algorithm to discern structural changes in the brain caused by Alzheimer’s disease. First, they trained the algorithm using 67 MRI scans, 38 of which were from people who had Alzheimer’s and 29 from healthy controls. The scans came from the Alzheimer’s Disease Neuroimaging Initiative database at the University of Southern California in Los Angeles. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24067 - Posted: 09.15.2017

By Michael Le Page We are still evolving – very slowly. In the 20th century, people in the UK evolved to be less likely to smoke heavily, but the effect was tiny. So claims a study of 200,000 genomes. A population can be described as evolving when the frequency of gene variants changes over time. Because most people in rich countries now live well beyond reproductive age, some argue that we have stopped evolving because natural selection has been weakened. But several recent studies claim we are still evolving, albeit slowly. Now Joseph Pickrell at Columbia University in New York and his team have analysed human genome sequences to spot gene variants that are becoming rarer. One variant, of a gene called CHRNA3, is associated with heavier smoking in those that smoke, raising their risk of a smoking-related death. Comparing people over the age of 80 with people over the age of 60, Pickrell estimates that the variant has declined by 1 per cent between generations. However, his team was not able to prove this, as they did not have any genomic data from people under the age of 40. A variant of the ApoE4 gene that is known to increase the risk of late-onset Alzheimer’s disease, as well as cardiovascular disease, may also be getting rarer. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24038 - Posted: 09.06.2017

Anna VlasitsAnna Vlasits A sheen is starting to appear on Rocky Blumhagen’s forehead, just below his gray hair. He’s marching in place in a starkly lit room decked out with two large flatscreens. On both of the TVs, a volcano lets off steam through wide cracks glowing with lava, their roar muffling the Andean percussion and flutes on the soundtrack. Golden coins slide across the screen. Rocky reaches out his left hand, as if to grasp a coin from midair, and one of them disappears with a brrring. “I don’t know if I can do it,” he says to a guy named Josh sitting nearby in a felt-covered lounge chair. He looks up from his iPad, watching Rocky, age 66, grab, jog, kick, and reach his way through the videogame. “Keep it up,” Josh says as the heart monitor in the corner of the screen reads 129. Rocky and research assistant Josh Volponi are technically in a lab clinic at the University of California, San Francisco, but aside from the mannequin heads studded with electrodes, the room looks more like a man cave. But here, the videogames could halt the mental decay of aging. This is the premise that the university’s new research institute, named Neuroscape, was built to test. This is Rocky’s 18th training session at Neuroscape, founded by neuroscientist Adam Gazzaley. Rocky is fit for his age—he works as a substitute yoga instructor, after retiring from careers producing radio and performing Cole Porter songs—but as he makes it to the end of the level, he looks exhausted. The game cuts to an animation of a jungle, birds chirping and light playing through the canopy as a list of his past scores pops up. This round wasn’t his best. “I haven’t been here for a week,” he says. Volponi asks him to rate his physical exertion level. Rocky gives it a 15 out of 20; Volponi marks it on the iPad. “I feel rusty,” he says, wiping his hands on his orange exercise shorts.

Related chapters from BN8e: 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: 24033 - Posted: 09.04.2017

Robin McKie Science Editor People who use genetic tests to trace their ancestry only to discover that they are at risk of succumbing to an incurable illness are being left to suffer serious psychological problems. Dementia researchers say the problem is particularly acute for those found to be at risk of Alzheimer’s disease, which has no cure or effective treatment. Yet these people are stumbling upon their status inadvertently after trying to find their Viking, Asian or ancient Greek roots. “These tests have the potential to cause great distress,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. “Companies should make counselling available, before and after people take tests.” The issue is raised in a paper by Middleton and others in the journal Future Medicine. A similar warning was sounded by Louise Walker, research officer at the Alzheimer’s Society. “Everyone has a right to know about their risk if they want to, but these companies have a moral responsibility to make sure people understand the meaning and consequences of this information. Anyone considering getting genetic test results should do so with their eyes open.” Alzheimer’s is linked to the build-up in the brain of clumps of a protein called amyloid. This triggers severe memory loss, confusion and disorientation. One gene, known as ApoE, affects this process and exists in three variants: E2, E3 and E4. Those possessing the last of these face an increased chance of getting the disease in late life. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24031 - Posted: 09.04.2017

By Meghana Keshavan, Inflammation has become one of the hottest buzzwords in medical science, pointed to as a culprit in causing or aggravating conditions ranging from allergy to autism to Alzheimer’s disease. But it’s far from clear that standard anti-inflammatory drugs, which have been around for decades, will help patients with those conditions, especially since they often come with dangerous side effects. So in labs across the country, scientists are trying to puzzle through the basic biology, understanding how inflammation leads to disease — and whether it’s possible to develop drugs that could interrupt that process. The latest evidence of inflammation’s broad role in disease came this past week, when a global clinical trial of 10,000 patients who had previous heart attacks showed that an anti-inflammatory drug from Novartis reduced their risk of further heart attacks or strokes. A surprise side effect: The drug also sharply cut the risk of lung cancer. That finding still needs to be confirmed with more research. But lead investigator Dr. Paul Ridker, a cardiologist at Brigham and Women’s Hospital, said he saw the trial as a clear indication of inflammation’s role in spurring cancer growth. The results, he said, turn “the way people look at oncology upside down.” Although inflammation has been studied for decades, there’s still a lot left to learn about this complex physiological condition. It’s basically an unnecessary state of hyperactivity in the body, in which the immune system’s reserve capacity is thrown into overdrive. This excess immune activation sends the wrong cellular signals to various parts of the body — and can wind up worsening conditions like diabetes, Alzheimer’s, and potentially even cancer. © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24028 - Posted: 09.02.2017

By James Gallagher People with higher levels of lithium in their drinking water appear to have a lower risk of developing dementia, say researchers in Denmark. Lithium is naturally found in tap water, although the amount varies. The findings, based on a study of 800,000 people, are not clear-cut. The highest levels cut risk, but moderate levels were worse than low ones. Experts said it was an intriguing and encouraging study that hinted at a way of preventing the disease. The study, at the University of Copenhagen, looked at the medical records of 73,731 Danish people with dementia and 733,653 without the disease. Tap water was then tested in 151 areas of the country. The results, published in JAMA Psychiatry, showed moderate lithium levels (between 5.1 and 10 micrograms per litre) increased the risk of dementia by 22% compared with low levels (below five micrograms per litre). However, those drinking water with the highest lithium levels (above 15 micrograms per litre) had a 17% reduction in risk. The researchers said: "This is the first study, to our knowledge, to investigate the association between lithium in drinking water and the incidence of dementia. "Higher long-term lithium exposure from drinking water may be associated with a lower incidence of dementia." Lithium is known to have an effect on the brain and is used as a treatment in bipolar disorder. However, the lithium in tap water is at much lower levels than is used medicinally. Experiments have shown the element alters a wide range of biological processes in the brain. © 2017 BBC.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23990 - Posted: 08.24.2017

/ By Steven Lubet There is a memorable episode in the now-classic sitcom Scrubs in which the conniving Dr. Kelso unveils a plan to peddle useless “full body scans” as a new revenue stream for the perpetually cash-strapped Sacred Heart Hospital. The irascible but ultimately patient-protecting Dr. Cox objects loudly. “I think showing perfectly healthy people every harmless imperfection in their body just to scare them into taking invasive and often pointless tests is an unholy sin,” he says. Undeterred, Kelso launches an advertising campaign that promotes the scans in a tear-jerking television commercial and a billboard screaming “YOU may already be DYING.” Alarmist medical advertising is pretty funny on television, but it can be far more troubling in real life. Although I’ve never been alerted to impending death, I recently received an advertisement from my own trusted health care provider warning that I may have Alzheimer’s disease, although I have no known symptoms and no complaints. As long-time patients at NorthShore University Health System, which is affiliated with the University of Chicago, my wife and I received two solicitations from its Center for Brain Health touting the development of “ways to slow brain aging and even prevent the onset of Alzheimer’s.” According to the ads, which arrived in both postcard and email form, there is “new hope for delaying — even preventing — aging brain diseases” through “genetic testing, advanced diagnostics, and lifestyle factors.” Copyright 2017 Undark

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23978 - Posted: 08.19.2017

By Andy Coghlan Can exercise during childhood protect you against memory loss many decades later? Exercise early in life seems to have lifelong benefits for the brain, in rats at least. “This is an animal study, but it indicates that physical activity at a young age is very important – not just for development, but for the whole lifelong trajectory of cognitive development during ageing,” says Martin Wojtowicz of the University of Toronto, Canada. “In humans, it may compensate for and delay the appearance of Alzheimer’s symptoms, possibly to the point of preventing them.” Wojtowicz’s team spilt 80 young male rats into two equal groups, and placed running wheels in the cages of one group for a period of six weeks. Around four months later – when the rats had reached middle age – the team taught all the rats to associate an electric shock with being in a specific box. When placed in the box, they froze with fear. Two weeks later, the team tested the rats in three scenarios: exactly the same box in the same room, the same box with the room arranged and lit differently, and a completely different box in a different room. The rats without access to a running wheel when they were young now froze the same proportion of times in each of these situations, suggesting they couldn’t remember which one was hazardous. But those that had been able to run in their youth froze 40 to 50 per cent less in both altered box settings. © Copyright New Scientist Ltd

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23959 - Posted: 08.15.2017

By Aggie Mika Individuals who possess an innate resilience to age-related brain pathologies may offer molecular clues to unexplored therapeutics for neurodegenerative disease. After having accidentally discovered rapid aging and disease in mice with mutations in the gene that encodes the protein klotho—named after the Greek Fate Clotho, daughter of Zeus and spinner of the thread of life—independent researchers have shown that some people with genetic variants that promote elevated klotho levels live longer and tend to stave off age-related cognitive decline. In a paper published today (August 8) in Cell Reports, scientists report that a fragment of klotho, similar to what winds up in circulation after cleavage from the cell membrane, boosted spatial and short-term memory in young and aging mice and improved both memory and mobility in a transgenic mouse model of neurodegenerative disease. Notably, in each type of mouse, the protein fragment was injected into the animals’ bodies either a day or a few hours before cognitive testing took place. Previously, neurologist and researcher Dena Dubal of the University of California, San Francisco, and others have demonstrated that transgenic overexpression of klotho throughout an organism’s lifespan produces similar cognitive improvements. Dubal’s current work, she says, provides a promising answer to a “big, burning question” of klotho’s therapeutic utility: “could you give it acutely, and would it increase cognition in a rapid way?” © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23942 - Posted: 08.10.2017

Shirley S. Wang Efforts to develop a treatment that stalls the memory-robbing devastation of Alzheimer's disease have so far been unsuccessful, but scientists are making strides in another important area: the development of better tests to tell who has the condition. Their aim is to develop more accurate, cheaper and less invasive tests to detect the biological markers of Alzheimer's-induced changes in the brain. At the recent Alzheimer's Association International Conference in London, scientists presented early but promising data on a new blood test and a novel brain imaging technique. They also unveiled preliminary data on a study to investigate the potential clinical usefulness of a test that's already on the market but isn't widely reimbursed by insurance. Alzheimer's is characterized by changes to the brain involving clumping of a protein called amyloid and another called tau — pathologies that until the last decade or so could only be seen upon autopsy. The biomarker tests available to date focus primarily on detecting amyloid. These tests are generally used only for research purposes because they can be expensive or require special technology. They are meant to be used for ruling out Alzheimer's in patients who already have memory problems. Less invasive, easier to use and cheaper technologies may mean that more people could have access to testing. For public health, this could mean being able to more broadly screen the population to identify people who are at high-risk for getting the illness and then focusing more expensive, involved efforts for testing, prevention and treatment on them. © 2017 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23914 - Posted: 08.05.2017

By Ryan Cross Researchers have discovered tell-tale signs of Alzheimer’s disease in 20 elderly chimpanzee brains, rekindling a decades-old debate over whether humans are the only species that develop the debilitating condition. Whether chimps actually succumb to Alzheimer’s or are immune from symptoms despite having the key brain abnormalities is not clear. But either way, the work suggests that chimps could help scientists better understand the disease and how to fight it—if they could get permission to do such studies on these now-endangered animals. A definitive diagnosis of Alzheimer’s includes dementia and two distortions in the brain: amyloid plaques, sticky accumulations of misfolded pieces of protein known as amyloid beta peptides; and neurofibrillary tangles, formed when proteins called tau clump into long filaments that twist around each other like ribbons. Many other primates including rhesus monkeys, baboons, and gorillas also acquire plaques with aging, but tau tangles are either absent in those species or don’t fully resemble those seen in humans. In the new study, researchers led by biological anthropologist Mary Ann Raghanti at Kent State University in Ohio turned to our closest relative, chimpanzees. In 2015, the U.S. Fish and Wildlife Service declared all U.S. chimps endangered, effectively ending all invasive research on them. But thanks to a newly founded center that collects brains from chimps that die at zoos or research centers, the team was able to examine the brains of 20 chimps aged 37 to 62—the oldest recorded age for a chimp, roughly equivalent to a human at the age of 120. Of these chimps, 13 had amyloid plaques, and four also had the neurofibrillary tangles typical of more advanced stages of Alzheimer’s in humans, the team writes [DATE TK] in Neurobiology of Aging. © 2017 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23906 - Posted: 08.01.2017

By Tara Bahrampour Older patients who become disoriented or confused after surgery are more than three times more likely to develop dementia later, a new study has found. The report, published Friday by the British Journal of Anaesthesia, assesses the effects of post-operative delirium (POD) on people 65 and older who were cognitively normal before their operations. Of 1,152 such patients, 9.5 percent met criteria for mild cognitive impairment or dementia a median of nine months after surgery. The frequency of being diagnosed with MCI or dementia after surgery was much higher – 33.3 percent – among those who had experienced post-operative delirium, compared with 9 percent among those who had not. While earlier studies have showed a relationship between POD and dementia, this is the first to look entirely at subjects who showed no cognitive decline in pre-surgery assessments, said David Warner, an anesthesiologist at Mayo Clinic in Rochester, Minnesota and the study’s senior author. Delirium is defined by an acute state of confusion, inattention, disorganized thinking, and a fluctuating mental state. Older patients are more likely than younger ones to develop it after surgery, as are people with lower education levels and those who undergo vascular procedures. Further study is needed to determine whether delirium contributes to later cognitive decline or is an indicator of some underlying factor that made people more likely to develop dementia, Warner said. © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 23888 - Posted: 07.28.2017

Joseph Jebelli The terror of Alzheimer’s is that it acts by degrees, and can therefore bewilder family members as much as its victims. Those who first notice the onset of Alzheimer’s in a loved one tell of forgotten names and unsettling behaviour, of car keys found in the fridge and clothing in the kitchen cabinet, of aimless wanderings. Naturally, they want to understand the boundaries of normal ageing and whether these are being crossed. Often, the answer arrives when they’re greeted as complete strangers, when the patient’s mind becomes irrevocably unmoored from its past. The disease is terrifying for its insidiousness as well as its long-term manifestations. Fear partly explains why Alzheimer’s has been ignored for so long. Yet it is now the leading cause of death among the oldest people, and according to Professor Sir Michael Marmot, an expert in health inequalities, it could be an “important part” of the stagnation in increases in life expectancy since 2010 that he has identified. As a researcher, I have been struck by how many patients speak openly about their condition only after receiving a diagnosis. “I knew something wasn’t right. Sometimes I don’t know what day of the week it is or what I have to do,” one newly diagnosed patient told me. “I look in my calendar but then I think: why am I looking at this? My husband was the one who made me see a GP. I was too frightened. I thought I might have it but I didn’t want to hear it.” © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23862 - Posted: 07.22.2017

By Fergus Walsh Medical correspondent One in three cases of dementia could be prevented if more people looked after their brain health throughout life, according to an international study in the Lancet. It lists nine key risk factors including lack of education, hearing loss, smoking and physical inactivity. The study is being presented at the Alzheimer's Association International Conference in London. By 2050, 131 million people could be living with dementia globally. There are estimated to be 47 million people with the condition at the moment. Nine factors that contribute to the risk of dementia Mid-life hearing loss - responsible for 9% of the risk Failing to complete secondary education - 8% Smoking - 5% Failing to seek early treatment for depression - 4% Physical inactivity - 3% Social isolation - 2% High blood pressure - 2% Obesity - 1% Type 2 diabetes - 1% These risk factors - which are described as potentially modifiable - add up to 35%. The other 65% of dementia risk is thought to be potentially non-modifiable. Source: Lancet Commission on dementia prevention, intervention and care "Although dementia is diagnosed in later life, the brain changes usually begin to develop years before," said lead author Prof Gill Livingston, from University College London. "Acting now will vastly improve life for people with dementia and their families and, in doing so, will transform the future of society." The report, which combines the work of 24 international experts, says lifestyle factors can play a major role in increasing or reducing an individual's dementia risk. It examines the benefits of building a "cognitive reserve", which means strengthening the brain's networks so it can continue to function in later life despite damage. Image caption Eve Laird is taking part in a study on how to prevent dementia © 2017 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23856 - Posted: 07.21.2017

By Tara Bahrampour A significant portion of people with mild cognitive impairment or dementia who are taking medication for Alzheimer’s may not actually have the disease, according to interim results of a major study currently underway to see how PET scans could change the nature of Alzheimer’s diagnosis and treatment. The findings, presented Wednesday at the Alzheimer’s Association International Conference in London, come from a four-year study launched in 2016 that is testing over 18,000 Medicare beneficiaries with MCI or dementia to see if their brains contain the amyloid plaques that are one of the two hallmarks of the disease. So far, the results have been dramatic. Among 4,000 people tested so far in the Imaging Dementia-Evidence for Amyloid Scanning (IDEAS) study, researchers from the Memory and Aging Center at the University of California, San Francisco found that just 54.3 percent of MCI patients and 70.5 percent of dementia patients had the plaques. A positive test for amyloid does not mean someone has Alzheimer’s, though its presence precedes the disease and increases the risk of progression. But a negative test definitively means a person does not have it. The findings could change the way doctors treat people in these hard-to-diagnose groups and save money currently being spent on inappropriate medication. “If someone had a putative diagnosis of Alzheimer’s Disease, they might be on an Alzheimer’s drug like Aricept or Namenda,” said James Hendrix, the Alzheimer Association’s director of global science initiatives who co-presented the findings. “What if they had a PET scan and it showed that they didn’t have amyloid in their brain? Their physician would take them off that drug and look for something else.” © 1996-2017 The Washington Post

Related chapters from BN8e: 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: 23848 - Posted: 07.19.2017

Shirley S. Wang In nursing homes and residential facilities around the world, health care workers are increasingly asking dementia patients questions: What are your interests? How do you want to address us? What should we do to celebrate the life of a friend who has passed away? The questions are part of an approach to care aimed at giving people with memory loss and other cognitive problems a greater sense of control and independence. At its core is the idea that an individual with dementia should be treated as a whole person and not "just" a patient. Scientists sometimes call this approach an ecopsychosocial intervention. The goal is to create environments that better meet patients' psychological and emotional needs through strategies other than medication. At the Alzheimer's Association International Conference this week in London, researchers from the U.S., the U.K. and Israel presented data from four trials demonstrating that such interventions significantly improve residents' mood and quality of life. The interventions can also reduce their use of antipsychotic drugs and improve their ability to care for themselves. Taken together, these studies and others suggest that relatively simple and potentially cost-effective interventions can yield significant benefits for people with dementia, even those in residential facilities in the later stages of disease. Behavioral Therapy Helps More Than Drugs For Dementia Patients As the population continues to age, and the number of people with dementia continues to rise, these interventions are likely to increase in importance as well. © 2017 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23847 - Posted: 07.19.2017