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By Robert Martone Neurological conditions can release a torrent of new creativity in a few people as if opening some mysterious floodgate. Auras of migraine and epilepsy may have influenced a long list of artists, including Pablo Picasso, Vincent van Gogh, Edvard Munch, Giorgio de Chirico, Claude Monet and Georges Seurat. Traumatic brain injury (TBI) can result in original thinking and newfound artistic drive. Emergent creativity is also a rare feature of Parkinson’s disease. But this burst of creative ability is especially true of frontotemporal dementia (FTD). Although a few rare cases of FTD are linked to improvements in verbal creativity, such as greater poetic gifts and increased wordplay and punning, enhanced creativity in the visual arts is an especially notable feature of the condition. Fascinatingly, this burst of creativity indicates that the potential to create may rest dormant in some of us, only to be unleashed by a disease that also causes a loss of verbal abilities. The emergence of a vibrant creative spark in the face of devastating neurological disease speaks to the human brain’s remarkable potential and resilience. A new study published in JAMA Neurology examines the roots of this phenomenon and provides insight into a possible cause. As specific brain areas diminish in FTD, the researchers find, they release their inhibition, or control, of other regions that support artistic expression. Frontotemporal dementia is relatively rare—affecting about 60,000 people in the U. S.—and distinct from the far more common Alzheimer’s disease, a form of dementia in which memory deficits predominate. FTD is named for the two brain regions that can degenerate in this disease, specifically the frontal and temporal lobes.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 14: Attention and Higher Cognition
Link ID: 28797 - Posted: 05.27.2023

Sara Reardon Researchers have identified a man with a rare genetic mutation that protected him from developing dementia at an early age. The finding, published on 15 May in Nature Medicine1, could help researchers to better understand the causes of Alzheimer’s disease and potentially lead to new treatments. For nearly 40 years, neurologist Francisco Lopera at the University of Antioquia in Medellín, Colombia, has been following an extended family whose members develop Alzheimer’s in their forties or earlier. Many of the approximately 6,000 family members carry a genetic variant called the paisa mutation that inevitably leads to early-onset dementia. But now, Lopera and his collaborators have identified a family member with a second genetic mutation — one that protected him from dementia until age 67. “Reading that paper made the hair on my arms stand up,” says neuroscientist Catherine Kaczorowski at the University of Michigan in Ann Arbor. “It’s just such an important new avenue to pursue new therapies for Alzheimer’s disease.” Lopera and his colleagues analysed the genomes and medical histories of 1,200 Colombians with the paisa mutation, which causes dementia around ages 45—50. They identified the man with the second mutation when he was 67 and had only mild cognitive impairment. When the researchers scanned his brain, they found high levels of the sticky protein complexes known as amyloid plaques, which are thought to kill neurons and cause dementia, as well as a protein called tau that accumulates as the disease progresses. The brain looked like that of a person with severe dementia, says study co-author Joseph Arboleda, an ophthalmologist at Harvard Medical School in Boston, Massachusetts. But a small brain area called the entorhinal cortex, which coordinates skills such as memory and navigation, had low levels of tau. © 2023 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: 28786 - Posted: 05.18.2023

Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer’s dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH. Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study. “If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place,” said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study. By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls. A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson’s disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer’s disease, which could mean that this structural variant plays a role in the broader dementia population.

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: 28775 - Posted: 05.10.2023

Sara Reardon For the second time, an experimental drug has been shown to reduce the cognitive decline associated with Alzheimer’s disease. On 3 May, pharmaceutical company Eli Lilly announced in a press release that its monoclonal antibody donanemab slowed mental decline by 35% for some participants in a 1,736-person trial — a rate comparable to that for competitor drug lecanemab. But researchers warn that until the full results are published, questions remain as to the drug’s clinical usefulness, as well as whether the modest benefit outweighs the risk of harmful side effects. Like lecanemab, donanemab targets amyloid protein, which is thought to cause dementia by accumulating in the brain and damaging neurons. The trial results provide strong evidence that amyloid is a key driver of Alzheimer’s, says Jeffrey Cummings, a neuroscientist at the University of Nevada, Las Vegas. “These are transformative in an enormously important way from a scientific point of view,” he adds. “They’re terrific.” But Marsel Mesulam, a neurologist at Northwestern University in Chicago, is more cautious. “The results that are described are extremely significant and impressive, but clinically their significance is doubtful,” he says, adding that the modest effect suggests that factors other than amyloid contribute to Alzheimer’s disease progression. “We’re heading to a new era — there’s room to cheer, but it’s an era that should make us all very sober, realizing that there will be no single magic bullet.” In the press release, Eli Lilly said that people with mild Alzheimer’s who received donanemab showed 35% less clinical decline over 18 months than did those who received a placebo, and 40% less decline in their ability to perform daily tasks. The company, based in Indianapolis, Indiana, says that it will present the full results at a conference in July and publish them in a peer-reviewed journal. It plans to apply for approval by the US Food and Drug Administration (FDA) in the next two months. Promising treatments © 2023 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: 28773 - Posted: 05.06.2023

By Jaya Padmanabhan Speaking two languages provides the enviable ability to make friends in unusual places. A new study suggests that bilingualism may also come with another benefit: improved memory in later life. Studying hundreds of older patients, researchers in Germany found that those who reported using two languages daily from a young age scored higher on tests of learning, memory, language and self-control than patients who spoke only one language. The findings, published in the April issue of the journal Neurobiology of Aging, add to two decades of work suggesting that bilingualism protects against dementia and cognitive decline in older people. “It’s promising that they report that early and middle-life bilingualism has a beneficial effect on cognitive health in later life,” said Miguel Arce Rentería, a neuropsychologist at Columbia University who was not involved in the study. “This would line up with the existing literature.” In recent years, scientists have gained a greater understanding of bilingualism and the aging brain, though not all their findings have aligned. Some have found that if people who have fluency in two languages develop dementia, they’ll develop it at a later age than people who speak one language. But other research has shown no clear benefit from bilingualism. Neuroscientists hypothesize that because bilingual people switch fluidly between two languages, they may be able to deploy similar strategies in other skills — such as multitasking, managing emotions and self-control — that help delay dementia later on. The new study tested 746 people age 59 to 76. Roughly 40 percent of the volunteers had no memory problems, while the others were patients at memory clinics and had experienced confusion or memory loss. © 2023 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 13: Memory and Learning
Link ID: 28761 - Posted: 04.29.2023

Nicola Davis Science correspondent From loud snores to twitching paws, dogs often appear to have a penchant for a good snooze. But researchers have said elderly canines with dementia appear to spend less time slumbering than those with healthy brains – mirroring patterns seen in humans. It has long been known that people with dementia can experience sleep problems, including finding it harder to get to sleep. Researchers have also found changes in the brainwaves of people with dementia during sleep – including decreased slow brain waves that occur during non-rapid eye movement deep sleep. These are important in memory consolidation and appear to be linked to the activity of the brain’s system for clearing away waste. Now it seems sleep impairment may occur in dogs experiencing a condition similar to dementia in humans. “Changes in sleep habits should be expected in older dogs, and could be a harbinger of decline in cognition,” said Prof Natasha Olby, senior author of a study at North Carolina State University. Writing in the journal Frontiers in Veterinary Science, Olby and colleagues reported on their study of 28 dogs aged between 10 and 16 years old. The canines’ brainwaves were recorded by electroencephalogram (EEG) while the dogs took a two-hour afternoon nap. The researchers also assessed owners’ answers to a questionnaire and each dog’s performance on a range of problem-solving, memory and attention tasks, to provide a score indicating whether the dog had, or was at risk of, canine dementia. Twenty of the dogs were deemed to have cognitive impairment, with this judged to be severe in eight of them. Combining their data, the team found dogs with higher dementia scores took longer to fall asleep and spent less time sleeping. © 2023 Guardian News & Media Limited

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: 28760 - Posted: 04.29.2023

By Laurie McGinley — When Rebecca Chopp was diagnosed with early-stage Alzheimer’s disease, she and her husband did the only thing that seemed to make sense: They went to their favorite Mexican restaurant, held each other in a back booth and drank margaritas. And cried. After a while, they helped each other back across the street to their home. Chopp, at 67, was chancellor of the University of Denver, at the pinnacle of a career powered by a daunting intellect and relentless work. She was also an ordained minister, prolific author and former president of Swarthmore College and Colgate University. Sometimes, Chopp thought of herself as a brain with a body attached. The changes were subtle: Chopp was sleeping more. She got lost on the way to the doctor. Then came the diagnosis. (Joanna Kulesza/For The Washington Post ) Now, she was crushed, facing the loss of that beautiful mind. She worried she would soon be an empty shell, drooling and unkempt, a burden to the people she loved. “There is a sense that when you are diagnosed, you are immediately going to descend into madness,” Chopp said. When she relinquished the job she loved, Chopp fell into deep despair, confounded by the prescription given to her by an empathetic doctor: “Live with joy!” She had nightmares about going insane. But, eventually, she began to push back against the darkness. Chopp has mild cognitive impairment, a condition that involves subtle changes in thinking and memory and that, in most cases, leads to Alzheimer’s dementia, a fatal neurodegenerative disease that affects more than 6.7 million Americans. Using diet, exercise and joy to slow Alzheimer’s For years, there was little doctors could do for people with Alzheimer’s, even at a very early stage. Now, changes are coming in how the disease is diagnosed and treated, and patients with mild cognitive impairment are at the center of the efforts. Lacking a cure, scientists are trying desperately to delay the worst phase of the illness.

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: 28752 - Posted: 04.26.2023

Alison Abbott When neurologist Reisa Sperling stepped up to receive her lifetime achievement award at an international Alzheimer’s conference last December, she was more excited about the future than about celebrating the past. What thrilled Sperling, who won the award for her work on clinical trials of Alzheimer’s treatments, was a sense of hope, which has been conspicuously missing from research into the disease for many years. Most other attendees felt the same. Just a few months before the meeting, researchers had announced that an antibody drug called lecanemab clearly lowered the amount of amyloid protein plaques — a tell-tale sign of the disease — in the brains of participants in a clinical trial, and slowed their cognitive decline. Sperling, who runs a laboratory at Harvard Medical School in Boston, Massachusetts, was buoyant as she gripped the microphone tightly. After spending more than 30 frustrating years in Alzheimer’s research, she said, there was finally proof that she and her colleagues were on the right track. “But still, it isn’t enough,” she said. In the trial, treatment led to a 25% slowing of decline, enough to give participants a few extra months of independent living1. “But actually conquering a destructive disease that affects tens of millions of people worldwide is a different story,” she says. What’s more, lecanemab, marketed in the United States as Leqembi, makes for a tough treatment regime. It has to be infused through a vein by a nursing professional. And because the drug can cause potentially life-threatening brain swelling and bleeds, people taking it have to be monitored regularly.

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: 28736 - Posted: 04.12.2023

By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
Link ID: 28731 - Posted: 04.09.2023

Visual: Andrew Bret Wallis/The Image Bank via Getty Images By Lina Tran At 25, Dasha Kiper moved in with a 98-year-old man. She’d just left a graduate program in clinical psychology; Mr. Kessler was a Holocaust survivor in the early stages of Alzheimer’s disease, whose son had hired Kiper as a live-in caregiver. One day, Mr. Kessler clambers onto a chair to replace the battery in a smoke detector. When he ignores her instructions to come down, Kiper loses her cool. She shouts that he’s incapable of changing the battery and doing much of anything for himself. Later, Kiper is filled with remorse. She should have known better than to yell at a nonagenarian with dementia. This is the focus of Kiper’s “Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain” — not the mind of the patient, but the caregiver. Often, the spouses, children, and loved ones of people living with dementia succumb to arguing or pleading with their patients, despite reason. “We want to reestablish a shared reality,” Kiper writes. “It’s not cruelty but desperation that drives us to confront them with the truth.” Caregivers aren’t mere observers to cognitive decline but the “invisible victims” of dementia disorders, Kiper writes. They traverse warped realities that operate under different rules of time and memory. One caregiver says, referring to a famous case study by neurologist and author Oliver Sacks, it’s “like being an anthropologist on Mars.” But a caregiver’s slip-up isn’t necessarily the result of character flaws or a lapse in compassion. Rather, Kiper shows the healthy brain is riddled with cognitive biases that impede the work of caring for a person with an impaired mind. This takes a heavy toll. “People always ask about the patient,” one exasperated woman tells Kiper, after recounting how her husband, who doesn’t recognize her, takes to locking her out of their apartment each night. She starts carrying a spare key to let herself in after he falls asleep. “Let me tell you something, the patient is fine; it’s the caregiver who’s going crazy.”

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: 28728 - Posted: 04.09.2023

ByJennifer Couzin-Frankel A class of Alzheimer’s drugs that aims to slow cognitive decline, including the antibody lecanemab that was granted accelerated approval in the United States in January, can cause brain shrinkage, researchers report in a new analysis. Although scientists and drug developers have documented this loss of brain volume in clinical trial participants for years, the scientific review, published yesterday in Neurology, is the first to look at data across numerous studies. It also links the brain shrinkage to a better known side effect of the drugs, brain swelling, which often presents without symptoms. “We don’t fully know what these changes might imply,” says Jonathan Jackson, a cognitive neuroscientist at Massachusetts General Hospital. But, “These data are extremely concerning, and it’s likely these changes are detrimental.” The analysis, which found that trial participants taking these Alzheimer’s drugs often developed more brain shrinkage than when they were on a placebo, alarmed Scott Ayton, a neuroscientist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, who led the work. “We’re talking about the possibility of brain damage” from treatment, says Ayton, who was invited by Eisai to join an advisory board on lecanemab’s rollout in Australia if the drug is approved there. “I find it very peculiar that these data, which are very important, have been completely ignored by the field.” A spokesperson for Eisai suggested there are benign theories for the brain shrinkage, too. The company said that although participants in its pivotal trial did experience “greater cortical volume loss on lecanemab relative to placebo,” those reductions may be due to antibody clearing the protein beta amyloid from the brain, and reducing inflammation. © 2023 American Association for the Advancement of Science.

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: 28721 - Posted: 03.29.2023

By Dani Blum The family of Bruce Willis announced that the actor has frontotemporal dementia, known as FTD, a form of dementia that occurs most commonly when nerve cells in the frontal and temporal lobes of the brain decrease in number. Mr. Willis, 67, was previously diagnosed with aphasia, which prompted him to retire from acting. “FTD is a cruel disease that many of us have never heard of and can strike anyone,” the family wrote in a statement. There are two main variants of FTD: primary progressive aphasia, which hampers a patient’s ability to communicate, and behavioral variant frontotemporal dementia, which manifests as personality and behavioral changes. “It hits the parts of the brain that make us the most human,” said Dr. Bruce Miller, a professor of neurology at the University of California, San Francisco. FTD is the most common cause of dementia for people under the age of 60, said Susan Dickinson, the chief executive of the Association for Frontotemporal Degeneration. There are roughly 50,000 people in the United States with a diagnosis of FTD, she added, although many experts consider that number to be a vast undercount, because of how challenging it can be to diagnose. There is no blood test or single biomarker to diagnose the condition — doctors instead identify it based on symptoms and neuroimaging. On average, it takes patients more than three years to get an accurate diagnosis, Ms. Dickinson said. People with primary progressive aphasia may struggle to speak in full sentences or have difficulty comprehending conversations. They may have a hard time writing or reading. Those with the behavioral variant of FTD may act out of character, said Dr. Ian Grant, an assistant professor of neurology at the Northwestern University Feinberg School of Medicine. Families will say that patients “seem like they’ve lost a little bit of their filter,” he said. Someone who is typically quiet and reserved may start spewing profanities, for example, or loudly comment on a stranger’s appearance. The person may act apathetic, Dr. Miller said, losing motivation. Some may also display a lack of empathy for those around them. © 2023 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: 28675 - Posted: 02.18.2023

By Annabelle Timsit A new study of more than 29,000 older adults has identified six habits — from eating a variety of foods to regularly reading or playing cards — that are linked with a lower risk of dementia and a slower rate of memory decline. Eating a balanced diet, exercising the mind and body regularly, having regular contact with others, and not drinking or smoking — these six “healthy lifestyle factors” were associated with better cognitive outcomes in older adults, in a large Chinese study conducted over a decade and published in the BMJ on Wednesday. While researchers have long known that there is a link between dementia and factors such as social isolation and obesity, the size and scope of the new study adds substantial evidence to a global body of research that suggests a healthy lifestyle may help brains age better. It also suggests that the effects of a healthy lifestyle are beneficial even for people who are genetically more susceptible to memory decline — a “very hope-giving” finding for the millions of individuals around the world who carry the APOEε4 gene, a major risk factor for Alzheimer’s disease, said Eef Hogervorst, chair of biological psychology at Loughborough University, who was not involved in the study. Memory naturally declines gradually as people age. Some older people may develop dementia, an umbrella term that can include Alzheimer’s, and generally describes a deterioration in cognitive function that goes beyond the normal effects of aging. But for many, “memory loss can merely be senescent forgetfulness,” write the authors of the BMJ study — like forgetting the name of that TV program you used to love, or that pesky fact you wanted to look up. Memory loss is no less damaging for being gradual, and age-related memory decline can in some cases be an early symptom of dementia. But the good news, the researchers say, is that it “can be reversed or become stable rather than progress to a pathological state.” How do you live to be 100? Good genes, getting outside and friends.

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: 28644 - Posted: 01.27.2023

ByMeredith Wadman A massive data mining study has found numerous associations between common viruses like the flu and devastating neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). The findings expand on previous research linking individual viruses to neurological diseases. But experts caution that the study, which relied on electronic medical records rather than biological samples, merely describes correlations and doesn’t prove causation. Still, it’s “really exciting,” says Kristen Funk, a neuroimmunologist who studies Alzheimer’s at the University of North Carolina, Charlotte. Rather than homing in on, say, the relationship between herpes simplex infections and Alzheimer’s—a recent focus in her own field—“this research broadens that scope to look at different viruses and more neurodegenerative diseases.” Scientists have found connections between viruses and neurodegenerative diseases before. Previous studies uncovered ties between the influenza virus and Parkinson’s, for example, and between genital warts (caused by human papillomavirus) and dementia. A landmark project published in Science last year cemented another connection: Epidemiologists who analyzed 2 decades of data from the blood tests of 10 million U.S. soldiers reported that it’s nearly impossible to develop multiple sclerosis without first being infected with the Epstein-Barr virus—a ubiquitous pathogen long suspected of causing MS. Inspired by that paper, National Institutes of Health (NIH) researchers wondered whether they could mine other large databases to tease out more associations. They focused on viral links to six neurodegenerative diseases: Alzheimer’s, Parkinson’s, dementia, ALS, MS, and vascular dementia. (Some scientists dispute that MS and vascular dementia are neurodegenerative diseases.)

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
Link ID: 28638 - Posted: 01.25.2023

Kaitlyn Radde Socially isolated older adults have a 27% higher chance of developing dementia than older adults who aren't, a new study by Johns Hopkins researchers found. "Social connections matter for our cognitive health, and it is potentially easily modifiable for older adults without the use of medication," Dr. Thomas Cudjoe, an assistant professor of medicine at Johns Hopkins and a senior author of the study, said in a news release. Published in the Journal of the American Geriatrics Society, the study tracked 5,022 dementia-free U.S. adults who were 65 or older – with an average age of 76 – and not living in a residential care facility. About 23% of participants were socially isolated. Social isolation is defined as having few relationships and few people to interact with regularly. The study measured this based on whether or not participants lived alone, talked about "important matters" with two or more people in the past year, attended religious services or participated in social events. Participants were assigned one point for each item, and those who scored a zero or one were classified as socially isolated. Over the course of nine years, researchers periodically administered cognitive tests. Overall, about 21% of the study participants developed dementia. But among those were who were socially isolated, about 26% developed dementia – compared to slightly less than 20% for those who were not socially isolated. The study did not find significant differences by race or ethnicity. However, more than 70% of the participants in the study were white – with particularly small sample sizes of Hispanic, Asian and Native participants – and the authors call for further research on the topic. © 2023 npr

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: 28631 - Posted: 01.18.2023

By Laurie McGinley The Food and Drug Administration on Friday approved an Alzheimer’s drug that slowed cognitive decline in a major study, offering patients desperately needed hope — even as doctors sharply debated the safety of the drug and whether it provides a significant benefit. The FDA said the drug, called lecanemab, is for patients with mild cognitive impairment or early dementia because of Alzheimer’s. The accelerated approval was based on a mid-stage trial that showed the treatment effectively removed a sticky protein called amyloid beta — considered a hallmark of the illness — from the brain. A larger trial, conducted more recently, found the drug, which will be sold under the brand name Leqembi, slowed the progression of Alzheimer’s disease by 27 percent. “This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Billy Dunn, director of the FDA’s Office of Neuroscience, said in a statement. The approval followed a barrage of criticism endured by the FDA for its 2021 approval of Aduhelm, another amyloid-targeting drug that had been panned by the agency’s outside experts. Lecanemab is getting a warmer reception but disagreements remain. Many neurologists and advocates hailed lecanemab, given intravenously twice a month, as an important advance — one that follows years of failure involving Alzheimer’s drugs. They said the treatment will allow patients to stay longer in the milder stages of the fatal, neurodegenerative disorder, which afflicts more than 6 million people in the United States.

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: 28622 - Posted: 01.07.2023

Linda Geddes Science correspondent Scientists have developed a blood test to diagnose Alzheimer’s disease without the need for expensive brain imaging or a painful lumbar puncture, where a sample of cerebrospinal fluid (CSF) is drawn from the lower back. If validated, the test could enable faster diagnosis of the disease, meaning therapies could be initiated earlier. Alzheimer’s is the most common form of dementia, but diagnosis remains challenging – particularly during the earlier stages of the disease. Current guidelines recommend detection of three distinct markers: abnormal accumulations of amyloid and tau proteins, as well as neurodegeneration – the slow and progressive loss of neuronal cells in specified regions of the brain. This can be done through a combination of brain imaging and CSF analysis. However, a lumbar puncture can be painful and people may experience headaches or back pain after the procedure, while brain imaging is expensive and takes a long time to schedule. Prof Thomas Karikari at the University of Pittsburgh, in Pennsylvania, US, who was involved in the study, said: “A lot of patients, even in the US, don’t have access to MRI and PET scanners. Accessibility is a major issue.” The development of a reliable blood test would be an important step forwards. “A blood test is cheaper, safer and easier to administer, and it can improve clinical confidence in diagnosing Alzheimer’s and selecting participants for clinical trial and disease monitoring,” Karikari said. Although current blood tests can accurately detect abnormalities in amyloid and tau proteins, detecting markers of nerve cell damage that are specific to the brain has been harder. Karikari and his colleagues around the world focused on developing an antibody-based blood test that would detect a particular form of tau protein called brain-derived tau, which is specific to Alzheimer’s disease. © 2022 Guardian News & Media 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: 28616 - Posted: 12.28.2022

By Anthea Rowan To many, the word “hobby” signifies something lightweight or trivial. Yet taking on a new hobby as one ages might provide an important defense against dementia, some experts say. About 5.8 million adults over 65 in the United States live with Alzheimer’s disease or other dementia disorders, according to the Centers for Disease Control and Prevention. One in 9 Americans over 65 has Alzheimer’s, according to the Alzheimer’s Association. And although the rate of dementia may be falling thanks to lifestyle changes, more of us are living longer, which means the societal burden of dementia is rising. David Merrill, an adult and geriatric psychiatrist and director of the Pacific Brain Health Center in Santa Monica, Calif., suggests we use the word “pursuit” instead of “hobby,” as it elevates the concept of an activity to something demanding, something requiring concentration or collaboration. Something we ought to chase down. Activities that demand focus and industry are the whetstone to keeping cognition sharp, Merrill says. Our brains, he continues, are like any other part of our body. “‘Use it or lose it’ is not just a hypothesis, it’s a basic biologic fact that holds as true for our brains as our muscles or our bones.” While there is as yet no surefire way to prevent dementia or cure it, the Lancet in 2020 identified 12 potentially modifiable risk factors for the condition; they include physiological (blood pressure, diabetes, hearing loss), lifestyle choices (smoking, drinking, physical inactivity), environmental (air pollution) depression, social isolation and a lower level of education. The Alzheimer Society of Canada is also clear about what we can do to help minimize our dementia risk: keep cognitively engaged, learn new things, meet new people, keep a diary, remain curious and engage in conversations.

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: 28605 - Posted: 12.21.2022

Patrick Barkham Three species of cetacean stranded off the coast of Scotland, including a bottlenose dolphin and a long-finned pilot whale, have been found to have the classic markers of Alzheimer’s disease, according to a study. Although types of dementia have been fairly widely detected in other animals, Alzheimer’s disease has not been found to occur naturally in species other than humans. But researchers from the University of Glasgow, the universities of St Andrews and Edinburgh and the Moredun Research Institute in Scotland were surprised to find that postmortem tests of 22 toothed whales, or odontocetes, detected three key brain changes associated with human Alzheimer’s disease in three animals. Scientists do not know the cause of this brain degeneration but it could support one theory about why some groups or pods of whales and dolphins run aground in shallow water. Some mass strandings have been linked to increasing anthropogenic noise in the oceans, but Alzheimer’s-like signs in the brain could support a “sick leader” theory, whereby mostly healthy cetaceans are stranded because they follow a group leader that has become confused or lost. The researchers found signs of Alzheimer’s in three of 22 stranded odontocetes: a white-beaked dolphin, a bottlenose dolphin and a long-finned pilot whale, also a member of the dolphin family.

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: 28604 - Posted: 12.21.2022

By Yasemin Saplakoglu It’s often subtle at first. A lost phone. A forgotten word. A missed appointment. By the time a person walks into a doctor’s office, worried about signs of forgetfulness or failing cognition, the changes to their brain have been long underway — changes that we don’t yet know how to stop or reverse. Alzheimer’s disease, the most common form of dementia, has no cure. “There’s not much you can do. There are no effective treatments. There’s no medicine,” said Riddhi Patira, a behavioral neurologist in Pennsylvania who specializes in neurodegenerative diseases. That’s not how the story was supposed to go. Three decades ago, scientists thought they had cracked the medical mystery of what causes Alzheimer’s disease with an idea known as the amyloid cascade hypothesis. It accused a protein called amyloid-beta of forming sticky, toxic plaques between neurons, killing them and triggering a series of events that made the brain waste away. The amyloid cascade hypothesis was simple and “seductively compelling,” said Scott Small, the director of the Alzheimer’s Disease Research Center at Columbia University. And the idea of aiming drugs at the amyloid plaques to stop or prevent the progression of the disease took the field by storm. Decades of work and billions of dollars went into funding clinical trials of dozens of drug compounds that targeted amyloid plaques. Yet almost none of the trials showed meaningful benefits to patients with the disease. That is, until September, when the pharmaceutical giants Biogen and Eisai announced that in a phase 3 clinical trial, patients taking the anti-amyloid drug lecanemab showed 27% less decline in their cognitive health than patients taking a placebo did. Last week, the companies revealed the data, now published in the New England Journal of Medicine, to an excited audience at a meeting in San Francisco. Simons Foundation © 2022

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: 28595 - Posted: 12.15.2022