Links for Keyword: Alzheimers

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By Pam Belluck, Sheila Kaplan and Rebecca Robbins Two months before the Food and Drug Administration’s deadline to decide whether to approve Biogen’s controversial Alzheimer’s drug, aducanumab, a council of senior agency officials resoundingly agreed that there wasn’t enough evidence it worked. The council, a group of 15 officials who review complex issues, concluded that another clinical trial was necessary before approving the drug. Otherwise, one council member noted, approval could “result in millions of patients taking aducanumab without any indication of actually receiving any benefit, or worse, cause harm,” according to minutes of the meeting, obtained by The New York Times. “It is critical that the decision be made from a place of certainty,” the minutes said. The session, whose details have not been reported before, represented at least the third time that proponents of approving aducanumab in the F.D.A. had received a clear message that the evidence did not convincingly show the drug could slow cognitive decline. On June 7, the F.D.A. greenlighted the drug anyway — a decision that has been met with scathing rebuke from many Alzheimer’s experts and other scientists and calls for investigations into how the agency approved a treatment that has little evidence it helps patients. How and why the F.D.A. went ahead and approved the drug — an intravenous infusion, marketed as Aduhelm, that the company has since priced at $56,000 a year — has become the subject of intense scrutiny. Two congressional committees are investigating the approval and the price. Much is still unknown, but an examination by The Times has found that the process leading to approval took several unusual turns, including a decision for the F.D.A. to work far more closely with Biogen than is typical in a regulatory review. Allegations about the collaboration prompted the F.D.A. to conduct an internal inquiry after a consumer advocacy group called for an inspector general’s investigation, according to documents reviewed by The Times. The agency has not disclosed the inquiry. © 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: 27919 - Posted: 07.21.2021

By Linda Searing Keeping your brain active later in life may delay by as much as five years the onset of Alzheimer’s disease, the most common type of dementia. Research published in the journal Neurology found that cognitively stimulating activities that involve seeking or processing information — such as reading books, magazines or newspapers, writing letters, playing card games, board games or checkers, and doing puzzles — seemed to add dementia-free time to older people’s lives. The research involved 1,903 people (average age was 80), none of whom had dementia at the start of the study and who were tracked and tested for up to 22 years. In that time, 457 participants developed Alzheimer’s. That occurred on average at age 94 for people who did the most brain-stimulating activities later in life, compared with developing Alzheimer’s at age 89 for those with the least amount of cognitive activity. Alzheimer’s, considered a degenerative brain disease, affects memory, thinking and behavior, with symptoms eventually becoming severe enough to interfere with once-routine daily tasks. Today, about 6.2 million Americans 65 and older have the disease, two-thirds of them women, according to the Alzheimer’s Association. That number is expected to reach nearly 13 million by 2050, unless ways are discovered to prevent, cure or slow the disease. The researchers found that neither education nor cognitive activity early in life were associated with the age at which a person developed Alzheimer’s. Rather, it’s what you do later in life that seems to make a difference. And, as the lead author of the story said, “It’s never too late to start doing the kinds of inexpensive, accessible activities” tracked in the study, “even in your 80s.”

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 27914 - Posted: 07.21.2021

By Rebecca Robbins The Food and Drug Administration on Friday called for a federal investigation of the process that led to the approval of a new drug for Alzheimer’s disease that has spurred sharp criticism from lawmakers and the medical community. In a letter to the Department of Health and Human Services’ independent Office of the Inspector General, the F.D.A.’s acting commissioner, Dr. Janet Woodcock, acknowledged the scrutiny the agency has faced about the approval process for the drug, which is known as Aduhelm and has a $56,000 annual price tag. She pointed to interactions between representatives from the drug’s developer, Biogen, and the agency, saying some “may have occurred outside of the formal correspondence process.” “To the extent these concerns could undermine the public’s confidence in F.D.A.’s decision, I believe it is critical that the events at issue be reviewed by an independent body,” Dr. Woodcock wrote. She noted that the review should look at whether any of the communication between the agency’s staff and Biogen’s representatives violated F.D.A. rules. Dana Conti, a spokesman for Biogen, said the company “will, of course, cooperate with any inquiry in connection with a possible review of the regulatory process.” It is unusual for the agency to request an investigation into its own staff’s decision-making process for an individual drug approval. The move is likely to intensify the controversy that has surrounded Aduhelm. The F.D.A. approved it a month ago, overriding the fierce objections of its own independent advisers and many other scientists, who said there was insufficient evidence to know whether the drug was effective. On Thursday, the F.D.A. moved to narrow its recommendation about who should receive the drug. After originally recommending it for all Alzheimer’s patients, the agency’s new guidelines say it should be prescribed only to people with mild cognitive problems. © 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: 27900 - Posted: 07.10.2021

By Paula Span Dr. Kenneth Koncilja, a geriatrician at the Cleveland Clinic, saw the announcement from the Food and Drug Administration on June 7, on Twitter: The agency had approved Aduhelm (aducanumab), the first drug to treat Alzheimer’s disease to be approved in nearly 20 years. The calls from patients’ spouses and family members began within the hour, and have not stopped. “I was shocked at how fast the word spread — ‘Hey, is this something we can use? When can we get it?’” Dr. Koncilja recalled. “There’s a mix of excitement, anxiety and desperation.” His first call that morning came from Joan Morehouse, 78, who has been caring for her 71-year-old husband, James, in their home in North Perry, Ohio, since his Alzheimer’s diagnosis four years ago. She has watched him get lost on familiar drives and forget their grandchildren’s names. When her brother and her son both emailed her a news article about the F.D.A. action, she recalled, “I said, ‘Oh, my God, my prayers have been answered.’” It fell to Dr. Koncilja to explain the complexities: That Aduhelm is not yet widely available. That protocols determining which patients qualify have yet to be developed. That the clinical trial data was ambiguous and that the drug might bring no noticeable improvements in daily life. That its side effects include brain swelling and bleeding. And that its maker, Biogen, estimates the annual cost of monthly intravenous infusions at $56,000, plus expensive scans and tests. “It’s a more difficult question than I’ve ever had before,” Dr. Koncilja said. Patients ask him how their lives will change, “and I don’t know how to answer.” © 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: 27894 - Posted: 07.08.2021

By Laurie McGinley Neurologist Matthew S. Schrag was surprised when he heard the Food and Drug Administration had approved a controversial Alzheimer’s drug. There was scant evidence the treatment worked, in his view. Even more concerning to Schrag: the FDA’s apparent embrace of a long-debated theory about Alzheimer’s disease, which afflicts more than 6 million Americans. The amyloid hypothesis, which has dominated the field for decades, holds that toxic clumps in the brain, called amyloid beta, are the main driver of the disease and that removing them will slow cognitive decline. But years of testing drugs that target amyloid had yielded a string of failures, and Schrag and others had been pushing the field to focus on other possible factors, including inflammation in the brain or damage to tiny blood vessels. Anti-amyloid efforts, they said, had squeezed out other approaches that might be more promising. “We had been hoping for a recalibration of the field,” said Schrag, a researcher at Vanderbilt University Medical Center. Now, he’s worried drug companies will double down on an approach he thinks is a dead end. The role of the sticky clumps of protein in the brain has long divided researchers and is at the forefront again amid the FDA’s recent clearance of the first drug to treat the disease in almost two decades. It is one of many controversies that has erupted since the FDA approved the drug, called Aduhelm, on June 7. Members of Congress have vowed to conduct hearings on the relationship between the FDA and the drug’s maker, Massachusetts-based Biogen. Analysts worry the drug’s list price — $56,000 a year per patient — could wreck Medicare’s finances. Doctors are scrambling to decide who should take it, complaining that the FDA-approved label, which includes all Alzheimer’s patients, is far too broad.

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: 27890 - Posted: 07.06.2021

Asher Mullard The recent controversial approval of the Alzheimer’s drug aducanumab by the US Food and Drug Administration (FDA) has raised the possibility that the agency could now be more willing to fast-track treatments for a swathe of neurodegenerative diseases — illnesses that have so far thwarted drug developers. But an independent advisory panel fiercely questioned the new drug’s effectiveness, and researchers are divided on whether the potentially smoother approval path that aducanumab has paved will really deliver useful therapies for people with conditions such as amyotrophic lateral sclerosis (ALS), Huntington’s disease and Parkinson’s disease. Drug developers including Amgen, in Thousand Oaks, California, and Pfizer, based in New York City, have shut down their neuroscience programmes in recent years because of the difficulties of finding successful treatments for brain diseases. So Eric Siemers, a drug-development consultant in Zionsville, Indiana, thinks aducanumab’s approval could bring renewed investment and innovation. On the basis of conversations he has had with investors and clients, he says the tide is already turning. “There’s a lot more interest now in research in neurodegenerative diseases,” says Siemers, who is also chief medical officer of the Alzheimer’s disease company Acumen Pharmaceuticals in Charlottesville, Virginia. Acumen filed paperwork for an initial public offering just days after the approval of aducanumab. Some advocacy groups are also encouraged, on behalf of desperate patients with few or no therapeutic options. “If the FDA can find a way to be flexible for Alzheimer’s, maybe they can find a way to be flexible for ALS,” says Neil Thakur, chief mission officer at the ALS Association. © 2021 Springer Nature Limited

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: 27884 - Posted: 07.03.2021

By Pam Belluck and Rebecca Robbins In a powerful statement of disagreement with the Food and Drug Administration’s approval of Biogen’s controversial Alzheimer’s drug, three scientists have resigned from the independent committee that advised the agency on the treatment. “This might be the worst approval decision that the F.D.A. has made that I can remember,” said Dr. Aaron Kesselheim, a professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, who submitted his resignation Thursday after six years on the committee. He said the agency’s approval of the drug, aducanumab, which is being marketed as Aduhelm, a monthly intravenous infusion that Biogen has priced at $56,000 per year, was wrong “because of so many different factors, starting from the fact that there’s no good evidence that the drug works.” Two other members of the committee resigned earlier this week, expressing dismay at the approval of the drug despite the committee’s overwhelming rejection of it after reviewing clinical trial data in November. The committee had found that the evidence did not convincingly show that Aduhelm could slow cognitive decline in people in the early stages of the disease — and that the drug could cause potentially serious side effects of brain swelling and brain bleeding. None of the 11 members of the committee considered the drug ready for approval: Ten voted against and one was uncertain. “Approval of a drug that is not effective has serious potential to impair future research into new treatments that may be effective,” said Dr. Joel Perlmutter, a neurologist at Washington University School of Medicine in St. Louis, who was the first to resign from the committee. © 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: 27849 - Posted: 06.11.2021

By Laurie McGinley The Food and Drug Administration on Monday approved the first Alzheimer’s treatment intended to slow cognitive decline, a move hailed by patients and advocates but sharply criticized by others who argued there was not sufficient evidence that the drug works. The medication, called aducanumab, is the first drug cleared for Alzheimer’s that is designed to alter the course of the disease by slowing the deterioration of brain function — not just to ease symptoms. No Alzheimer’s treatment has been approved since 2003, reflecting the extraordinarily high failure rate of drugs developed for the illness. But in an explicit acknowledgment of the uncertainties about the effectiveness of the drug, the FDA did not grant the medication full approval. Instead, the agency cleared the drug — its brand name will be Aduhelm — based on its ability to reduce clumps of amyloid beta in the brain, a hallmark of the disease. It ordered the drug’s maker, the biotech giant Biogen, to conduct a post-approval study confirming the medicine actually slows cognitive deterioration. If the medication does not provide such a clinical benefit, the FDA’s approval could be withdrawn. Patrizia Cavazzoni, director of the FDA’s Center for Drug Evaluation and Research, said officials believe it is “reasonably likely” that the reduction in amyloid clumps will confer “important benefits to patients.” Monday’s FDA decision was the most contentious in years and followed prolonged debate among researchers, doctors, patients and advocates about whether the medication works — a consequence of the drug’s complicated history. One of the biggest points of disagreement is whether a reduction in amyloid beta, a sticky compound that many scientists believe damages communication between brain cells and eventually kills them, results in a slowdown in cognitive decline. © 1996-2021 The Washington Post

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: 27846 - Posted: 06.08.2021

Laurie McGinley When Phil Gutis was diagnosed with early-stage Alzheimer’s disease at 54, he immediately enrolled in a clinical trial for an experimental drug but had little hope of being helped. Over time, though, he started feeling better, his brain less cloudy. “There was just a fogginess I remember having a couple of years ago that I don’t really feel I have now,” said Gutis, who has received monthly infusions of a medication called aducanumab for five years, except for a short interruption. Now, he is hoping others with the disease will have a chance to try the drug. But he is worried that the Food and Drug Administration, which is weighing whether to approve the drug, will reject it, derailing the medication and jeopardizing his ability to get the treatment. “Would my world become fuzzy again?” said Gutis, who lives in New Hope, Pa., with his husband and is a former reporter. “I don’t want to go backward.” By June 7, the FDA is expected to make one of its most important decisions in years: whether to approve the drug for mild cognitive impairment or early-stage dementia caused by Alzheimer’s. It would be the first treatment ever sold to slow the deterioration in brain function caused by the disease, not just to ease symptoms. And it would be the first new Alzheimer’s treatment since 2003. The medication is a monoclonal antibody, a protein made in the laboratory that can bind to substances — in this case, clumps of amyloid beta, a sticky plaque compound that many scientists believe damages communication between brain cells and eventually kills them. The treatment is designed to trigger an immune response that removes the plaques.

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: 27839 - Posted: 06.02.2021

Amanda Heidt A damaged drainage system in the brain might be behind the spotty performance of some Alzheimer’s therapies, according to a study published April 28 in Nature. Mice modeling the neurodegenerative disorder that received plaque-busting antibodies along with a treatment to stimulate the growth of lymphatic vessels in the brain saw many of their symptoms reversed. Mice with damaged lymphatics, on the other hand, didn’t respond as well to the antibodies. This suggests that dysfunctional lymphatics might hinder the performance of antibody-based immunotherapy, an approach that has had mixed results in clinical trials among Alzheimer’s patients. “Whenever a paper provides us with a novel way to look at Alzheimer’s, such as this one does . . . it opens up a world of possibilities,” says Gabrielle Britton, a neuroscientist at the Instituto de Investigaciones Científicas y Servicios de Alta Tecnología in Panama who was not involved in the research. “The methods are sound, and [the fact] that they use several different approaches that converge on the same findings suggests a very strong paper.” The buildup of amyloid-β plaques in the brain is a hallmark of the disease, and one of the most promising immunotherapies has been a monoclonal antibody called aducanumab that breaks them up. But two clinical trials were discontinued after they yielded contradictory results, and scientists have been working ever since to figure out why as the companies continue to move forward with new trials of the therapy. The working hypothesis, Britton tells The Scientist, is that the discrepancy stems from some unexplained variation among participants. © 1986–2021 The Scientist.

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: 27835 - Posted: 05.29.2021

By Mitch Leslie For the past 3 years, about 6000 middle-aged and elderly Australians have pumped iron, loaded up on greens and whole grains, strived to quell stress, and challenged their wits with computer exercises, all in an effort to preserve their cognition. They’re part of a clinical trial called Maintain Your Brain, one of about 30 current or planned studies that eschew pharmaceutical interventions and test whether altering multiple aspects of participants’ lives improves brain health. Such multidomain studies may finally reveal whether modifying diet, exercise, and other factors can slow cognitive decline as people age—or even prevent dementia. “There’s a lot of hope for multidomain trials,” says psychologist Kaarin Anstey of the University of New South Wales, Sydney, one of the principal investigators of the Maintain Your Brain trial, which will finish by the end of this year. Although people can’t escape some mental decline as they get older, lifestyle exerts a powerful influence over the risk of developing dementia—the type of severe cognitive impairment seen in conditions such as Alzheimer’s disease. Last year, an international committee of scientists and psychiatrists known as the Lancet Commission on dementia prevention, intervention, and care estimated that so-called modifiable factors account for 40% of dementia risk. Their report highlighted a dozen factors, including many familiar villains—diabetes, high blood pressure, smoking, obesity, and lack of exercise. Researchers are still probing exactly how these risk factors steal people’s faculties, but they’ve identified some likely mechanisms. Lack of physical activity may impair cognition, for instance, because exercise stimulates formation of new neurons and soothes brain inflammation. © 2021 American Association for the Advancement of Science.

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: 27834 - Posted: 05.29.2021

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