Links for Keyword: Alzheimers

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By Daniela Kaufer, Alon Friedman It was the middle of the night in Jerusalem, and we were watching mice swim. The year was 1994, and the two of us were crouching over a pool of cold water in a laboratory at the Hebrew University. The room was chilly, our hunched backs ached, and we had been repeating this routine over many nights, so we were tired and uncomfortable. So were the mice. Mice really dislike swimming, especially in cold water—but we wanted to stress them out. We humans were on the night shift because both of us had other things to do during the day. Kaufer was working on a doctorate in molecular neurobiology, and Friedman was an Israel Defense Forces physician and was often on call. What brought us together with the mice every evening was an attempt to understand a medical mystery: Gulf War syndrome. After the conflict ended in 1991, there were an increasing number of reports of soldiers from the U.S.-led coalition who were afflicted with chronic fatigue, muscle pain, sleep problems and cognitive deterioration, and those soldiers were hospitalized at higher rates than nondeployed veterans. Some doctors suspected that pyridostigmine, a drug that had been given to soldiers to protect them from chemical weapons, could cause these ailments if it made it into their brains. There was a big problem with this theory, however: pyridostigmine in the bloodstream was not supposed to reach the brain. Blood vessels that course through this vital organ have walls made of specialized cells, packed very closely and with abilities to control what can get in and out. They form a shield that keeps toxins, pathogens such as bacteria, and most drugs safely within the vessels. This structure is called the blood-brain barrier, or BBB for short, and the drug should not have been able to pass through it. © 2021 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27816 - Posted: 05.12.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27803 - Posted: 05.05.2021

Jon Hamilton An experimental drug intended for Alzheimer's patients seems to improve both language and learning in adults with Fragile X syndrome. The drug, called BPN14770, increased cognitive scores by about 10% in 30 adult males after 12 weeks, a team reports in the journal Nature Medicine. That is enough to change the lives of many people with Fragile X, says Mark Gurney, CEO of Tetra Therapeutics, developer of the medicine. "People with Fragile X with an IQ of 40 are typically living with their parents or in an institutional setting," Gurney says. "With an IQ of 50, in some cases they're able to ride the bus, they're able to hold a job with some assistance and they're able to function better in their community." But it will take a much larger study to know whether the drug is as good as it seems, says Mark Bear, Picower professor of neuroscience at the Massachusetts Institute of Technology. "This study is certainly not definitive, but it's encouraging," he says. Fragile X syndrome is a genetic disorder that affects about 1 in 4,000 males and a smaller proportion of females. It is the most common inherited cause of intellectual disabilities and autism. The idea of treating Fragile X with an Alzheimer's drug came from Gurney after he learned that both conditions affect a substance called cyclic AMP that helps transmit messages inside cells. © 2021 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27796 - Posted: 05.01.2021

Enhancing the brain’s lymphatic system when administering immunotherapies may lead to better clinical outcomes for Alzheimer’s disease patients, according to a new study in mice. Results published April 28 in Nature suggest that treatments such as the immunotherapies BAN2401 or aducanumab might be more effective when the brain’s lymphatic system can better drain the amyloid-beta protein that accumulates in the brains of those living with Alzheimer’s. Major funding for the research was provided by the National Institute on Aging (NIA), part of the National Institutes of Health, and all study data is now freely available to the broader scientific community. “A broad range of research on immunotherapies in development to treat Alzheimer’s by targeting amyloid-beta has not to date demonstrated consistent results,” said NIA Director Richard J. Hodes, M.D. “While this study’s findings require further confirmation, the link it has identified between a well-functioning lymphatic system in the brain and the ability to reduce amyloid-beta accumulation may be a significant step forward in pursuing this class of therapeutics.” Abnormal buildup of amyloid-beta is one hallmark of Alzheimer’s disease. The brain’s lymphatic drainage system, which removes cellular debris and other waste, plays an important part in that accumulation. A 2018 NIA-supported study showed a link between impaired lymphatic vessels and increased amyloid-beta deposits in the brains of aging mice, suggesting these vessels could play a role in age-related cognitive decline and Alzheimer’s. The lymphatic system is made up of vessels which run alongside blood vessels and which carry immune cells and waste to lymph nodes. Lymphatic vessels extend into the brain’s meninges, which are membranes that surround the brain and spinal cord.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27795 - Posted: 05.01.2021

By Laura Sanders For more than a year now, scientists have been racing to understand how the mysterious new virus that causes COVID-19 damages not only our bodies, but also our brains. Early in the pandemic, some infected people noticed a curious symptom: the loss of smell. Reports of other brain-related symptoms followed: headaches, confusion, hallucinations and delirium. Some infections were accompanied by depression, anxiety and sleep problems. Recent studies suggest that leaky blood vessels and inflammation are somehow involved in these symptoms. But many basic questions remain unanswered about the virus, which has infected more than 145 million people worldwide. Researchers are still trying to figure out how many people experience these psychiatric or neurological problems, who is most at risk, and how long such symptoms might last. And details remain unclear about how the pandemic-causing virus, called SARS-CoV-2, exerts its effects. “We still haven’t established what this virus does in the brain,” says Elyse Singer, a neurologist at the University of California, Los Angeles. There are probably many answers, she says. “It’s going to take us years to tease this apart.” Getting the numbers For now, some scientists are focusing on the basics, including how many people experience these sorts of brain-related problems after COVID-19. © Society for Science & the Public 2000–2021.

Related chapters from BN: 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 and Learning; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27792 - Posted: 04.28.2021

The government of New Brunswick says there are now 47 cases of a mysterious neurological disease, for which experts are still trying to figure out a source. As of last Thursday, there have been 37 confirmed and 10 suspected cases of "a neurological syndrome of unknown cause," Bruce Macfarlane, spokesperson for the Department of Health, said in an email Monday. That brings the number of cases up from 44. The province last reported a new case in early April. There have been six deaths caused by the disease, with no new deaths reported Monday. Macfarlane said the province is collaborating with local and national subject matter experts and health-care providers to investigate the individuals showing signs and symptoms of the syndrome. "At this time, the investigation is active and ongoing to determine if there are similarities among the reported cases that can identify potential causes for this syndrome, and to help identify possible strategies for prevention. "The investigation team is exploring all potential causes including food, environmental and animal exposures." Macfarlane said most of the cases are in people who were living in areas around Moncton and on the Acadian Peninsula. "However, it is unknown at this stage of our investigation whether geographic area is linked to the neurological condition and related symptoms" he said. The disease cluster was first reported on in March, when Radio-Canada obtained a memo from Public Health to medical professionals. ©2021 CBC/Radio-Canada.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 27788 - Posted: 04.28.2021

David Cox When John Abraham began to lose his mind in late 2019, his family immediately feared the worst. Abraham had enjoyed robust health throughout retirement, but now at 80 he suddenly found himself struggling to finish sentences. “I would be talking to people, and all of a sudden the final word wouldn’t come to mind,” he remembers. “I assumed this was simply a feature of ageing, and I was finding ways of getting around it.” But within weeks, further erratic behaviours started to develop. Abraham’s family recall him often falling asleep mid-conversation, he would sometimes shout out bizarre comments in public, and during the night he would wake up every 15 minutes, sometimes hallucinating. Patients can go from being in a nursing home, unable to communicate, to returning to work To his son Steve, the diagnosis seemed inevitable, one which all families dread. “I was convinced my dad had dementia,” he says. “What I couldn’t believe was the speed at which it was all happening. It was like dementia on steroids.” Dementia is not just one disease – it has more than 200 different subtypes. Over the past decade neurologists have become increasingly interested in one particular subtype, known as autoimmune dementia. In this condition, the symptoms of memory loss and confusion are the result of brain inflammation caused by rogue antibodies – known as autoantibodies – binding to the neuronal tissue, rather than an underlying neurodegenerative disease. Crucially this means that unlike almost all other forms of dementia, in some cases it can be cured, andspecialist neurologists have become increasingly adept at both spotting and treating it. © 2021 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27780 - Posted: 04.21.2021

By Gretchen Reynolds Brisk walking improves brain health and thinking in aging people with memory impairments, according to a new, yearlong study of mild cognitive impairment and exercise. In the study, middle-aged and older people with early signs of memory loss raised their cognitive scores after they started walking frequently. Regular exercise also amplified the healthy flow of blood to their brains. The changes in their brains and minds were subtle but consequential, the study concludes, and could have implications not just for those with serious memory problems, but for any of us whose memories are starting to fade with age. Most of us, as we get older, will find that our ability to remember and think dulls a bit. This is considered normal, if annoying. But if the memory loss intensifies, it may become mild cognitive impairment, a medical condition in which the loss of thinking skills grows obvious enough that it becomes worrisome to you and others around you. Mild cognitive impairment is not dementia, but people with the condition are at heightened risk of developing Alzheimer’s disease later. Scientists have not yet pinpointed the underlying causes of mild cognitive impairment, but there is some evidence that changes in blood flow to the brain can contribute. Blood carries oxygen and nutrients to brain cells and if that stream sputters, so can the vitality of neurons. Unfortunately, many people experience declines in the flow of blood to their brains with age, when their arteries stiffen and hearts weaken. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27751 - Posted: 03.31.2021

By Elizabeth Anne Brown Forget the soul — it turns out the eyes may be the best window to the brain. Changes to the retina may foreshadow Alzheimer’s and Parkinson’s diseases, and researchers say a picture of your eye could assess your future risk of neurodegenerative disease. Pinched off from the brain during embryonic development, the retina contains layers of neurons that seem to experience neurodegenerative disease along with their cousins inside the skull. The key difference is that these retinal neurons, right against the jellylike vitreous of the eyeball, live and die where scientists can see them. Early detection “is sort of the holy grail,” said Ron Petersen, director of Mayo Clinic’s Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. By the time a patient complains of memory problems or tremors, the machinery of neurodegenerative disease has been at work probably for years or decades. Experts liken it to a cancer that only manifests symptoms at Stage 3 or 4. When patients begin to feel neurodegenerative disease’s impact on their daily life, it’s almost too late for treatment. Catching the warning signs of neurodegenerative disease earlier could give patients more time to plan for the future — whether that’s making caregiving arrangements, spending more time with family or writing the Great American novel. In the longer term, researchers hope the ability to notice brain changes before symptoms begin could eventually lead to early treatments more successful at slowing or stopping the progress of Parkinson’s and Alzheimer’s, since no such treatment is currently available. The hope is that “the sooner we intervene, the better we will be” at preventing cognitive impairment, Petersen said © 1996-2021 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27713 - Posted: 02.28.2021

In a study led by National Institutes of Health researchers, scientists found that five genes may play a critical role in determining whether a person will suffer from Lewy body dementia, a devastating disorder that riddles the brain with clumps of abnormal protein deposits called Lewy bodies. Lewy bodies are also a hallmark of Parkinson’s disease. The results, published in Nature Genetics, not only supported the disease’s ties to Parkinson’s disease but also suggested that people who have Lewy body dementia may share similar genetic profiles to those who have Alzheimer’s disease. “Lewy body dementia is a devastating brain disorder for which we have no effective treatments. Patients often appear to suffer the worst of both Alzheimer’s and Parkinson’s diseases. Our results support the idea that this may be because Lewy body dementia is caused by a spectrum of problems that can be seen in both disorders,” said Sonja Scholz, M.D., Ph.D., investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope that these results will act as a blueprint for understanding the disease and developing new treatments.” The study was led by Dr. Scholz’s team and researchers in the lab of Bryan J. Traynor, M.D., Ph.D., senior investigator at the NIH’s National Institute on Aging (NIA). Lewy body dementia usually affects people over 65 years old. Early signs of the disease include hallucinations, mood swings, and problems with thinking, movements, and sleep. Patients who initially have cognitive and behavioral problems are usually diagnosed as having dementia with Lewy bodies, but are sometimes mistakenly diagnosed with Alzheimer’s disease. Alternatively, many patients, that are initially diagnosed with Parkinson’s disease, may eventually have difficulties with thinking and mood caused by Lewy body dementia. In both cases, as the disease worsens, patients become severely disabled and may die within eight years of diagnosis.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27694 - Posted: 02.17.2021

By Leslie Nemo Ironically, this tangle of brain cells is helping scientists tease apart a larger problem: how to help people with Alzheimer’s disease. Matheus Victor, a researcher at the Massachusetts Institute of Technology, photographed these neurons after coaxing them to life in a petri dish in the hope that the rudimentary brain tissue will reveal why a new therapy might alleviate Alzheimer’s symptoms. In humans and mice, a healthy memory is associated with a high level of synced neurons that turn on and off simultaneously. Those with neurological conditions such as Alzheimer’s and Parkinson’s disease often have fewer brain cells blinking unanimously. A couple of years ago Victor’s lab leader Li-Huei Tsai and her team at M.I.T. found that when they surrounded mice genetically predisposed to Alzheimer’s with sound pulses beating 40 times a second, the rodents performed better on memory-related tasks. The animals also lost some amyloid plaques, protein deposits in the brain that are characteristic of the disease. The researchers had previously performed a similar study with light flickering at the same rate, and the mice were found to experience additional improvements when the sound and light pulses were combined. Astoundingly, the mouse neurons synced up to the 40-beats-per-second rhythm of the audio pulses, though the mechanism behind this result and the reason the shift improves symptoms remain a mystery. To help solve it, the researchers want to watch how brain tissue responds to the stimulants at the cellular level. The goal is to one day understand how this exposure treatment might work for people, so the team is growing human brain cells in the lab and engineering them to respond to sound and light without eyes and ears. “We are trying to mimic the sensory stimulation in mice but missing a lot of the hardware that makes it possible. So this is a bit of a hack,” Victor says. © 2021 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27690 - Posted: 02.15.2021

By Gina Kolata Is it possible to predict who will develop Alzheimer’s disease simply by looking at writing patterns years before there are symptoms? According to a new study by IBM researchers, the answer is yes. And, they and others say that Alzheimer’s is just the beginning. People with a wide variety of neurological illnesses have distinctive language patterns that, investigators suspect, may serve as early warning signs of their diseases. For the Alzheimer’s study, the researchers looked at a group of 80 men and women in their 80s — half had Alzheimer’s and the others did not. But, seven and a half years earlier, all had been cognitively normal. The men and women were participants in the Framingham Heart Study, a long-running federal research effort that requires regular physical and cognitive tests. As part of it, they took a writing test before any of them had developed Alzheimer’s that asks subjects to describe a drawing of a boy standing on an unsteady stool and reaching for a cookie jar on a high shelf while a woman, her back to him, is oblivious to an overflowing sink. The researchers examined the subjects’ word usage with an artificial intelligence program that looked for subtle differences in language. It identified one group of subjects who were more repetitive in their word usage at that earlier time when all of them were cognitively normal. These subjects also made errors, such as spelling words wrongly or inappropriately capitalizing them, and they used telegraphic language, meaning language that has a simple grammatical structure and is missing subjects and words like “the,” “is” and “are.” The members of that group turned out to be the people who developed Alzheimer’s disease. The A.I. program predicted, with 75 percent accuracy, who would get Alzheimer’s disease, according to results published recently in The Lancet journal EClinicalMedicine. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 27677 - Posted: 02.03.2021

By Gina Kolata In a small clinical trial, an experimental Alzheimer’s drug slowed the rate at which patients lost the ability to think and care for themselves, the drug maker Eli Lilly announced on Monday. The findings have not been published in any form, and not been widely reviewed by other researchers. If accurate, it is the first time a positive result has been found in a so-called Phase 2 study, said Dr. Lon S. Schneider, professor of psychiatry, neurology and gerontology at the University of Southern California. Other experimental drugs against Alzheimer’s were never tested in Phase 2 trials, moving straight to larger Phase 3 trials, or failed to produce positive results. The Phase 3 studies themselves have repeatedly had disappointing results. The two-year study involved 272 patients with brain scans indicative of Alzheimer’s disease. Their symptoms ranged from mild to moderate. The drug, donanemab, a monoclonal antibody, binds to a small part of the hard plaques in the brain made of a protein, amyloid, that are hallmarks of Alzheimer’s disease. Patients received the drug by infusion every four weeks. Participants who received the drug had a 32 percent deceleration in the rate of decline, compared with those who got a placebo. In six to 12 months, plaques were gone and stayed gone, said Dr. Daniel Skovronsky, the company’s chief scientific officer. At that point, patients stopped getting the drug — they got a placebo instead — for the duration of the study. The small study needs to be replicated, noted Dr. Michael Weiner, a leading Alzheimer’s researcher at the University of California, San Francisco. Still, “this is big news,” he said. “This holds out hope for patients and their families.” Eli Lilly did not release the sort of pertinent data needed for a thorough analysis, Dr. Schneider said. For example, the company provided only percentages describing declines in function among the participants, not the actual numbers. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27648 - Posted: 01.15.2021

By Jennie Erin Smith MEDELLÍN, Colombia — Aliria Rosa Piedrahita de Villegas carried a rare genetic mutation that had all but guaranteed she would develop Alzheimer’s disease in her 40s. But only at age 72 did she experience the first symptoms of it. Her dementia was not terribly advanced when she died from cancer on Nov. 10, a month shy of her 78th birthday, in her daughter’s home on a hillside that overlooks the city. Neurology investigators at the University of Antioquia in Medellín, led by Dr. Francisco Lopera, have followed members of Ms. Piedrahita de Villegas’s vast extended family for more than 30 years, hoping to unlock the secrets of early-onset Alzheimer’s disease. In that time they encountered several outliers, people whose disease developed later than expected, in their 50s or even 60s. But none were as medically remarkable as the woman they all knew as doña Aliria. In recent years Aliria traveled to Boston, where investigators at Massachusetts General Hospital conducted nuclear imaging studies of her brain as part of an ongoing study of this Colombian family, the largest in the world with genetic early-onset Alzheimer’s. In Boston it was discovered that Aliria had exceptionally large quantities of one protein seen in Alzheimer’s — amyloid beta — without much tau, the toxic protein that spreads later in the disease cascade. Something had interrupted the usual degenerative process, leaving her day-to-day functioning relatively preserved. Last year, researchers at Harvard Medical School and the University of Antioquia published the surprise finding that while Aliria carried a well-known mutation, unique to Colombia, that causes early Alzheimer’s, she also carried two copies of another rare mutation that appear to have thwarted the activity of the first one. Since then, investigators worldwide have been studying what is known as the Christchurch mutation, a variant on a gene, APOE, that can affect a person’s risk of developing Alzheimer’s. Thus far, drugs targeting amyloid beta have disappointed in clinical trials. If the protective effect of Aliria’s double Christchurch mutation can be replicated, a new avenue for desperately needed therapies could open. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27620 - Posted: 12.12.2020

Carrie Arnold In her job as a physician at the Boston Medical Center in Massachusetts, Sondra Crosby treated some of the first people in her region to get COVID-19. So when she began feeling sick in April, Crosby wasn’t surprised to learn that she, too, had been infected. At first, her symptoms felt like those of a bad cold, but by the next day, she was too sick to get out of bed. She struggled to eat and depended on her husband to bring her sports drinks and fever-reducing medicine. Then she lost track of time completely. For five days, Crosby lay in a confused haze, unable to remember the simplest things, such as how to turn on her phone or what her address was. She began hallucinating, seeing lizards on her walls and smelling a repugnant reptilian odour. Only later did Crosby realize that she had had delirium, the formal medical term for her abrupt, severe disorientation. “I didn’t really start processing it until later when I started to come out of it,” she says. “I didn’t have the presence of mind to think that I was anything more than just sick and dehydrated.” Physicians treating people hospitalized with COVID-19 report that a large number experience delirium, and that the condition disproportionately affects older adults. An April 2020 study in Strasbourg, France, found that 65% of people who were severely ill with coronavirus had acute confusion — a symptom of delirium1. Data presented last month at the annual meeting of the American College of Chest Physicians by scientists at the Vanderbilt University Medical Center in Nashville, Tennessee, showed that 55% of the 2,000 people they tracked who were treated for COVID-19 in intensive-care units (ICUs) around the world had developed delirium. These numbers are much higher than doctors are used to: usually, about one-third of people who are critically ill develop delirium, according to a 2015 meta-analysis2 (see ‘How common is delirium?’). © 2020 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27613 - Posted: 12.07.2020

By Jamie Talan After 20 years of marriage, after raising two kids, after building a farm in Kentucky and tending horses and dogs, Laura Prewitt knew this much about her husband: He was tenderhearted, fun-loving and never let stress land too long on his shoulders. But in 2014, old Ted somehow morphed into a new guy, one who is not so communicative. A guy who lost his social edge and seemed unable to read faces or feelings. Who is tired and withdrawn. “He’s just not the same guy,” she says. “I want him back.” At 59, the old Ted, the sensitive husband who cried during sad movies, is gone. A scan of Ted’s brain helps explain it: Discrete regions of the right temporal lobe that regulate emotion are getting smaller; the tissue is shrinking. Ted can still do some of the things he has done for decades. Until a few years ago, he was the president at a construction company. Lately, he’ll see someone he is supposed to know but forgets who they are. He sleeps a lot. And he can’t be left alone for too long or his wife may find him trying to eat a battery or a hammer. He’s agitated. He’s always putting things in his mouth. Ted Prewitt, who has behavioral variant frontotemporal dementia (bvFTD), is one of a growing number of people in midlife diagnosed with an atypical form of dementia. Unlike Alzheimer’s, which generally occurs in older people, these are rarer dementias — including bvFTD; another frontotemporal variant that leads to language disturbances called primary progressive aphasia; a visual and spatial dementia called posterior cortical atrophy; Lewy body dementia; and early-onset Alzheimer’s in people with no family history. These conditions show up in people in their 50s and 60s, sometimes even earlier and sometimes a bit later. No one knows whether these conditions are becoming more common or doctors are better at diagnosing them. © 1996-2020 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27612 - Posted: 12.07.2020

Alison Abbott Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ. The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. Norins wanted to reward work that would make the infection idea more persuasive. The amyloid hypothesis has become “the one acceptable and supportable belief of the Established Church of Conventional Wisdom”, says Norins. “The few pioneers who did look at microbes and published papers were ridiculed or ignored.” In large part, this was because some early proponents of the infection theory saw it as a replacement for the amyloid hypothesis. But some recent research has provided intriguing hints that the two ideas could fit together — that infection could seed some cases of Alzheimer’s disease by triggering the production of amyloid clumps. The data hint at a radical role for amyloid in neurons. Instead of just being a toxic waste product, amyloid might have an important job of its own: helping to protect the brain from infection. But age or genetics can interrupt the checks and balances in the system, turning amyloid from defender into villain. And that idea suggests new avenues to explore for potential therapies. To test the theory further, scientists are now developing animal models that mimic Alzheimer’s disease more closely. “We are taking the ideas seriously,” says neuroscientist Bart de Strooper, director of the UK Dementia Research Institute at University College London. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27571 - Posted: 11.07.2020

By Laura Sanders The fate of a potential new Alzheimer’s drug is still uncertain. Evidence that the drug works isn’t convincing enough for it to be approved, outside experts told the U.S. Food and Drug Administration during a Nov. 6 virtual meeting that at times became contentious. The scientists and clinicians were convened at the request of the FDA to review the evidence for aducanumab, a drug that targets a protein called amyloid-beta that accumulates in the brains of people with Alzheimer’s. The drug is designed to stick to A-beta and stop it from forming larger, more dangerous clumps. That could slow the disease’s progression but not stop or reverse it. When asked whether a key clinical study provided strong evidence that the drug effectively treated Alzheimer’s, eight of 11 experts voted no. One expert voted yes, and two were uncertain. The FDA is not bound to follow the recommendations of the guidance committee, though it has historically done so. If ultimately approved, the drug would be a milestone, says neurologist and neuroscientist Arjun Masurkar of New York University Langone’s Alzheimer’s Disease Research Center. Aducanumab “would be the first therapy that actually targets the underlying disease itself and slows progression.” Developed by the pharmaceutical company Biogen, which is based in Cambridge, Mass., the drug is controversial. That’s because two large clinical trials of aducanumab have yielded different outcomes, one positive and one negative (SN: 12/5/19). The trials were also paused at one point, based on analyses that suggested the drug didn’t work. © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27570 - Posted: 11.07.2020

By Nicholas Bakalar Some studies have suggested that older people who consistently engage in leisure activities are less likely to develop dementia than those who do not, suggesting that failure to participate in such pastimes could spur cognitive deterioration. A new study suggests another explanation: Failure to participate in leisure activities may be a consequence of dementia, not a cause. Researchers studied 8,280 people, average age 56, who were free of dementia at the start of the analysis. Over the next 18 years, the participants underwent periodic physical and psychological examinations, while researchers tracked their involvement in 13 leisure activities — listening to music, gardening, attending cultural events, playing cards, using a home computer and others. By the end of the project, 360 had developed dementia. The study, in Neurology, controlled for smoking, physical activity, education, coronary heart disease and other health and behavioral characteristics that are tied to dementia risk. They found no association between engagement in leisure activities at age 56 and the incidence of dementia over the following 18 years. The researchers concluded that actively pursuing leisure activities may not provide protection against developing dementia. “Dementia develops over a long period of time, so it’s possible that some changes happen before the diagnosis of dementia,” said the lead author, Andrew Sommerlad, a researcher at University College London. “Elderly people withdrawing from activities that they previously enjoyed may be developing early signs of dementia.” © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27563 - Posted: 11.04.2020

By Nicholas Bakalar Long-term exposure to noise may be linked to an increased risk for Alzheimer’s disease and other forms of dementia. Researchers did periodic interviews with 5,227 people 65 and older participating in a study on aging. They assessed them with standard tests of orientation, memory and language, and tracked average daytime noise levels in their neighborhoods for the five years preceding the cognitive assessments. About 11 percent had Alzheimer’s disease, and 30 percent had mild cognitive impairment, which often progresses to full-blown dementia. Residential noise levels varied widely, from 51 to 78 decibels, or from the level of a relatively quiet suburban neighborhood to that of an urban setting near a busy highway. The study is in Alzheimer’s & Dementia. After controlling for education, race, smoking, alcohol consumption, neighborhood air pollution levels and other factors, they found that each 10 decibel increase in community noise level was associated with a 36 percent higher likelihood of mild cognitive impairment, and a 29 percent increased risk for Alzheimer’s disease. The associations were strongest in poorer neighborhoods, which also had higher noise levels. The reasons for the connection are unknown, but the lead author, Jennifer Weuve, an associate professor of epidemiology at Boston University, suggested that excessive noise can cause sleep deprivation, hearing loss, increased heart rate, constriction of the blood vessels and elevated blood pressure, all of which are associated with an increased risk for dementia. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 27551 - Posted: 10.28.2020