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By Miryam Naddaf An analysis of around 1,500 blood proteins has identified biomarkers that can be used to predict the risk of developing dementia up to 15 years before diagnosis. The findings, reported today in Nature Aging1, are a step towards a tool that scientists have been in search of for decades: blood tests that can detect Alzheimer’s disease and other forms of dementia at a very early, pre-symptomatic stage. Researchers screened blood samples from more than 50,000 healthy adults in the UK Biobank, 1,417 of whom developed dementia in a 14-year period. They found that high blood levels of four proteins — GFAP, NEFL, GDF15 and LTBP2 — were strongly associated with dementia. “Studies such as this are required if we are to intervene with disease-modifying therapies at the very earliest stage of dementia,” said Amanda Heslegrave, a neuroscientist at University College London, in a statement to the Science Media Centre in London. According to the World Health Organization, more than 55 million people worldwide currently live with dementia. People are often diagnosed only when they notice memory problems or other symptoms. At that point, the disease might have been progressing for years. “Once we diagnose it, it’s almost too late,” says study co-author Jian-Feng Feng, a computational biologist at Fudan University in Shanghai, China. “And it’s impossible to reverse it.” By screening 1,463 proteins in blood samples from 52,645 people, the authors found that increased levels of GFAP, NEFL, GDF15 and LTBP2 were associated with dementia and Alzheimer’s disease. For some participants who developed dementia, blood levels of these proteins were outside normal ranges more than ten years before symptom onset. © 2024 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: 29146 - Posted: 02.13.2024

Ian Sample Science editor After a decades-long and largely fruitless hunt for drugs to combat Alzheimer’s disease, an unlikely candidate has raised its head: the erectile dysfunction pill Viagra. Researchers found that men who were prescribed Viagra and similar medications were 18% less likely to develop the most common form of dementia years later than those who went without the drugs. The effect was strongest in men with the most prescriptions, with scientists finding a 44% lower risk of Alzheimer’s in those who received 21 to 50 prescriptions of the erectile dysfunction pills over the course of their study. While the findings are striking, the observational study cannot determine whether Viagra and similar pills protect against Alzheimer’s or whether men who are already less prone to the condition are simply more likely to use the tablets. “We can’t say that the drugs are responsible, but this does give us food for thought on how we move into the future,” said the lead author Dr Ruth Brauer at University College London. “We now need a proper clinical trial to look at the effects of these drugs on Alzheimer’s in women as well as men.” Brauer and her colleagues analysed medical records for more than 260,000 men who were diagnosed with erectile dysfunction but had no evidence of memory or thinking problems. Just over half were taking PDE5 inhibitor drugs, including sildenafil (sold as Viagra), avanafil, vardenafil and tadalafil. The men were followed for an average of five years to record any new cases of Alzheimer’s. © 2024 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: 29138 - Posted: 02.08.2024

By Laura Sanders Under extremely rare circumstances, it appears that Alzheimer’s disease can be transmitted between people. Five people who received contaminated injections of a growth hormone as children went on to develop Alzheimer’s unusually early, researchers report January 29 in Nature Medicine. The findings represent “the first time iatrogenic Alzheimer’s disease has been described,” neurologist John Collinge said January 25 in a news briefing, referring to a disease caused by a medical procedure. That sounds alarming, but researchers are quick to emphasize that Alzheimer’s disease is not contagious in everyday life, including caretaking and most medical settings. Support Science Today. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. Donate Now “We are not suggesting for a moment that you can catch Alzheimer’s disease,” said Collinge, of the University College London’s Institute of Prion Diseases. “This is not transmissible in the sense of a viral or bacterial infection.” The reassurance is echoed by Carlo Condello, a neurobiologist at the University of California, San Francisco who wasn’t involved in the study. “In no way do we believe sporadic Alzheimer’s disease is a communicable disease,” he says. “Only under incredibly artificial, now out-of-date, medical practices is this appearing. It’s no longer an issue.” © Society for Science & the Public 2000–202

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: 29126 - Posted: 01.31.2024

By Laurie McGinley ABINGTON, Pa. — Wrapped in a purple blanket, Robert Williford settles into a quiet corner of a bustling neurology clinic, an IV line delivering a colorless liquid into his left arm. The 67-year-old, who has early Alzheimer’s disease, is getting his initial dose of Leqembi. The drug is the first to clearly slow the fatal neurodegenerative ailment that afflicts 6.7 million older Americans, though the benefits may be modest. The retired social worker, one of the first African Americans to receive the treatment, hopes it will ease his forgetfulness so “I drive my wife less crazy.” But as Williford and his doctors embark on this treatment, they are doing so with scant scientific data about how the medication might work in people of color. In the pivotal clinical trial for the drug, Black patients globally accounted for only 47 of the 1,795 participants — about 2.6 percent. For U.S. trial sites, the percentage was 4.5 percent. The proportion of Black enrollees was similarly low for Eli Lilly Alzheimer’s drug, called donanemab, expected to be cleared by the Food and Drug Administration in coming months. Black people make up more than 13 percent of the U.S. population. The paltry data for the new class of groundbreaking drugs, which strip a sticky substance called amyloid beta from the brain, has ignited an intense debate among researchers and clinicians. Will the medications — the first glimmer of hope after years of failure — be as beneficial for African Americans as for White patients? “Are these drugs going to work in non-Whites? And particularly in Blacks? We just don’t have enough data, I don’t think,” said Suzanne E. Schindler, a clinical neurologist and dementia specialist at Washington University in St. Louis.

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: 29122 - Posted: 01.31.2024

By Mark Johnson There had been early clues, but it was a family game of dominoes around Christmas 2021 that convinced Susan Stewart that something was wrong with her husband. Charlie Stewart, then 75 and retired, struggled to match the dots on different domino tiles. Susan assumed it was a vision problem. Charlie’s memory was fine, and he had no family history of dementia. But months later the Marin County, Calif., couple were shocked to learn that his domino confusion was a sign he had a lesser-known variant of Alzheimer’s disease. For patients with this variant, called posterior cortical atrophy, the disease begins with problems affecting vision rather than memory. The unusual early symptoms mean that thousands of people may go years before receiving the correct diagnosis, experts said. That may change with the first large-scale international study of the condition, published Monday in the journal Lancet Neurology. An international team led by researchers at the University of California at San Francisco studied records of 1,092 PCA patients from 16 countries and found that, on average, the syndrome begins affecting patients at age 59 ― about five to six years earlier than most patients with the more common form of Alzheimer’s. Although the number of patients with PCA has not been established, researchers say that the variant may account for as many as 10 percent of all Alzheimer’s cases; that would put the number of Americans with the condition close to 700,000. “We have a lot of work to do to raise awareness about the syndrome,” said Gil D. Rabinovici, one of the study’s authors and director of the UCSF Alzheimer’s Disease Research Center. “One thing that we found in our large study is that by the time people are diagnosed, they’ve had [the disease] for quite a few years.” The study authors said they hope greater awareness of the syndrome will help doctors diagnose it earlier and will encourage researchers to include patients with PCA in future Alzheimer’s clinical trials. Unusual symptoms delay diagnosis

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 29107 - Posted: 01.23.2024

Jon Hamilton A new generation of blood tests is poised to change the way doctors determine whether patients with memory loss also have Alzheimer's disease. The tests detect substances in the blood that indicate the presence of sticky amyloid plaques in the brain — a hallmark of Alzheimer's. So these tests have the potential to replace current diagnostic procedures, like costly PET scans and uncomfortable spinal taps. Blood tests also promise to provide doctors with a quick way to identify patients who could benefit from new drugs that remove amyloid from the brain. But the accuracy of the tests still varies widely. "Some of them are really good, and some of them are really bad," says Dr. Suzanne Schindler, a dementia specialist at Washington University School of Medicine in St. Louis. Blood tests represent the latest advance in efforts to detect the buildup of amyloid plaques and fibrous tangles in the brain. "It used to be that the only way you could definitively diagnose someone with Alzheimer disease is by doing an autopsy," Schindler says. Then, starting in the early 2000s, scientists found ways to detect plaques and tangles using PET scans and tests of spinal fluid. There are now versions of both approaches that are approved by the Food and Drug Administration. But the scans are costly, and spinal taps are unpopular with many doctors and patients. Both also require expertise that is in short supply. So Schindler and her colleagues got a lot of attention in 2019 when they published a paper showing that amyloid plaques could be revealed by a blood test. © 2024 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: 29088 - Posted: 01.11.2024

By Mark Johnson In the first study of its kind in humans, researchers have discovered that it is safe to use sound waves fired into specific areas of the brain to open a protective barrier and clear the way for Alzheimer’s medications. The study, reported in the New England Journal of Medicine, involved just three patients, but it raises hope about the long-term potential of the treatment strategy known as focused ultrasound. “We want to be very cautious. This is the first three people in the world that have had this [treatment]. What we’ve learned from this, I think, can help us,” said Ali Rezai, lead author of the study and executive chair and director of the Rockefeller Neuroscience Institute at West Virginia University. Rezai stressed that the goal of the research is not to replace pharmaceutical treatments but to improve their benefits by helping more of the drug penetrate the brain. Nature has provided humans with a barrier made of tightly packed cells that blocks harmful toxins, such as viruses, bacteria and fungi, from reaching the brain. Known as the blood-brain barrier, this shield has for decades presented a major challenge to scientists trying to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s, which afflict at least 7 million Americans. The barrier is a locked door that stops about 98 percent of treatments from reaching the brain. With focused ultrasound, Rezai explained, “what we want to do is push individuals toward the milder stages of Alzheimer’s with less plaques to give them a fighting chance.” Two men and a woman suffering from mild loss of memory, learning, concentration and decision-making skills due to Alzheimer’s took part in the study. The patients, who ranged in age from 59 to 77, were given six monthly doses of the federally approved — if somewhat controversial — lab-made antibody aducanumab, sold under the brand name Aduhelm. The antibody, which is administered directly into a patient’s vein, reduces a sticky substance in the brain called amyloid beta, which clumps between neurons and disrupts their function.

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: 29085 - Posted: 01.09.2024

Robin McKie, Science Editor People in Britain could benefit from a key medical breakthrough next year. They may be given access to the first drugs ever developed to slow the impact of Alzheimer’s disease. The first of these medicines – lecanemab – was recently approved in the US and Japan, where treatments using it have already been launched. A second drug, donanemab, is expected to follow soon, and next year it is anticipated that the UK medical authorities will consider both of them for approval in Britain. The prospect has raised hopes that, after years of effort, scientists may be closing in on ways to directly tackle the UK’s dementia crisis. About a million people are living with the condition in this country, and this is expected to rise to about 1.7 million by 2040 – with potentially grim consequences. Last year dementia took the lives of 66,000 people in England and Wales, and it is now the leading cause of death in Britain, with Alzheimer’s accounting for two-thirds of cases. Until now doctors have only been able to prescribe medicines that help patients manage their symptoms, so the arrival of the first drugs that treat the actual cause of the condition has been welcomed – although experts have warned that their use should be treated with some caution. “The new drugs slow down the development of Alzheimer’s by six months to a year and are useful only for those in the early stages of the condition, so they are certainly not miracle medicines,” said David Thomas, head of policy at Alzheimer’s Research UK. “However, after decades of research, they are the first to improve patients’ lives directly, and that is a justifiable cause for excitement. If nothing else, they suggest we are probably on the right road to tackling Alzheimer’s.” © 2023 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: 29056 - Posted: 12.19.2023

By Tosin Thompson Last month saw the first-ever approval of a gene therapy that uses the CRISPR–Cas9 gene-editing tool, a treatment for the blood conditions sickle-cell disease and β-thalassaemia that works by precisely cutting out a faulty gene in people’s stem cells. Now, researchers in search of new treatments for Alzheimer’s disease are hoping to deploy similar strategies against forms of the disease that are caused by genetic mutations. Although there are now some treatments that slow the progression of Alzheimer’s, these often don’t benefit people who are in the later stages or who have mutations that raise the risk of the disease. “CRISPR therapies could potentially be a one-and-done cure, which no other drug can match,” says Subhojit Roy, a neuroscientist at the University of California, San Diego. But he adds that there is a long way to go before these therapies could be deployed against such a complex condition. “Cutting and pasting a gene is much harder to do in the brain using current technology.” Alzheimer’s is the most common form of dementia, a health issue of global concern. More than 55 million people are affected by dementia, and this figure is projected to nearly triple by 2050. “We do not fully understand how the brain works, which makes the challenge of understanding and treating brain diseases like Alzheimer’s very difficult,” says Tara Spires-Jones, who studies neurodegeneration at the University of Edinburgh, UK. Much of Alzheimer’s research is driven by the amyloid hypothesis, the idea that the build-up of amyloid-β proteins in the brain, which eventually form clumps called plaques, is the main cause of the disease. Amyloid plaques trigger another brain protein, called tau, to clump together and spread inside neurons. It is usually well into this process that symptoms such as memory loss start to appear. Usually, the more tau is present, the more severe the symptoms are. © 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: 29046 - Posted: 12.13.2023

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

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: 29032 - Posted: 12.06.2023

Max Kozlov Researchers have sifted through genomes from thousands of individuals in an effort to identify genes linked to Alzheimer’s disease. But these scientists have faced a serious obstacle: it’s hard to know for certain which of those people have Alzheimer’s. There’s no foolproof blood test for the disease, and dementia, a key symptom of Alzheimer’s, is also caused by other disorders. Early-stage Alzheimer’s might cause no symptoms at all. Now, researchers have developed artificial intelligence (AI)-based approaches that could help. One algorithm efficiently sorts through large numbers of brain images and picks out those that include characteristics of Alzheimer’s. A second machine-learning method identifies important structural features of the brain — an effort that could eventually help scientists to spot new signs of Alzheimer’s in brain scans. The goal is to use people’s brain images as visual ‘biomarkers’ of Alzheimer’s. Applying the method to large databases that also include medical information and genetic data, such as the UK Biobank, could allow scientists to pinpoint genes that contribute to the disease. In turn, this work could aid the creation of treatments and of models that predict who’s at risk of developing the disease. Combining genomics, brain imaging and AI is allowing researchers to “find brain measures that are tightly linked to a genomic driver”, says Paul Thompson, a neuroscientist at the University of Southern California in Los Angeles, who is spearheading efforts to develop these algorithms. Thompson and others described the new AI techniques on 4 November at the annual conference of the American Society of Human Genetics in Washington DC. Overwhelmed with data © 2023 Springer Nature Limited

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: 29004 - Posted: 11.13.2023

Sara Reardon Scientists have identified two types of brain cell linked to a reduced risk of dementia in older people — even those who have brain abnormalities that are hallmarks of Alzheimer’s disease1. The finding could eventually lead to new ways to protect these cells before they die. The results were published in Cell on 28 September. The most widely held theory about Alzheimer’s attributes the disease to a build-up of sticky amyloid proteins in the brain. This leads to clump-like ‘plaques’ of amyloid that slowly kill neurons and eventually destroy memory and cognitive ability. But not everyone who develops cognitive impairment late in life has amyloid clumps in their brain, and not everyone with amyloid accumulation develops Alzheimer’s. Neurobiologist Hansruedi Mathys at the University of Pittsburgh School of Medicine in Pennsylvania and neuroscientist Li-Huei Tsai and computer scientist Manolis Kellis at the Massachusetts Institute of Technology in Cambridge and their colleagues decided to investigate this disconnect. To do so, they used data from a massive study that tracks cognitive and motor skills in thousands of people throughout old age. The researchers examined tissue samples from 427 brains from participants who had died. Some of those participants had dementia typical of advanced Alzheimer’s disease, some had mild cognitive impairment and the remainder had no sign of impairment. The researchers isolated cells from each participant’s prefrontal cortex, the region involved in higher brain function. To classify the cells, they sequenced all the active genes in each one. This allowed them to create an atlas of the brain showing where the different cell types occur. The scientists identified two key cell types that had a specific genetic marker. One had active genes coding for reelin, a protein associated with brain disorders such as schizophrenia, and the other had active genes that code for somatostatin, a hormone that regulates processes throughout the body. © 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: 28938 - Posted: 09.29.2023

By Janet Lee Doing puzzles, playing memory-boosting games, taking classes and reading are activities that we often turn to for help keeping our brains sharp. But research is showing that what you eat, how often you exercise and the type of exercise you do can help lower your risk of dementia to a greater extent than previously thought. Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. Although more studies are needed, “there’s a lot of data that suggests exercise and diet are good for the brain and can prevent or help slow down” cognitive changes, says Jeffrey Burns, co-director of the University of Kansas Alzheimer’s Disease Research Center in Fairway. And living a healthy lifestyle can produce brain benefits no matter what your age. The big diet picture If you’re already eating in a way that protects your heart — plenty of whole grains, vegetables, and fruit, and little saturated fat, sodium and ultra-processed “junk” foods — there’s good news: You’re also protecting your brain. A healthy cardiovascular system keeps blood vessels open, allowing good blood flow to the brain and reducing the risk of high blood pressure, stroke and dementia. Research suggests that two specific dietary approaches — the Mediterranean diet and the MIND diet (the Mediterranean-DASH Intervention for Neurodegenerative Delay, essentially a combo of two heart-healthy eating plans) — may help stave off cognitive decline. Both diets rely on eating mostly plant foods (fruits, vegetables, whole grains, beans, nuts), olive oil, fish and poultry. The main difference between the two is that the MIND diet emphasizes specific fruits and vegetables, such as berries and leafy greens. Studies show that people who most closely follow either diet have a reduced risk of dementia compared with those who don’t. For example, people eating the Mediterranean way had a 23 percent lower risk of dementia in a nine-year study of more than 60,000 men and women published this year in BMC Medicine.

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: 28915 - Posted: 09.21.2023

By Claudia López Lloreda Cells hidden in the skull may point to a way to detect, diagnose and treat inflamed brains. A detailed look at the skull reveals that bone marrow cells there change and are recruited to the brain after injury, possibly traveling through tiny channels connecting the skull and the outer protective layer of the brain. Paired with the discovery that inflammation in the skull is disease-specific, these new findings collectively suggest the skull’s marrow could serve as a target to track and potentially treat neurological disorders involving brain inflammation, researchers report August 9 in Cell. Immune cells that infiltrate the central nervous system during many diseases and neuronal injury can wreak havoc by flooding the brain with damaging molecules. This influx of immune cells causes inflammation in the brain and spinal cord and can contribute to diseases like multiple sclerosis (SN: 11/26/19). Detecting and dampening this reaction has been an extensive field of research. With this new work, the skull, “something that has been considered as just protective, suddenly becomes a very active site of interaction with the brain, not only responding to brain diseases, but also changing itself in response to brain diseases,” says Gerd Meyer zu Hörste, a neurologist at University of Münster in Germany who was not involved in the study. Ali Ertürk of the Helmholtz Center in Munich and colleagues discovered this potential role for the skull while probing the idea that the cells in skull marrow might behave differently from those in other bones. Ertürk’s team compared the genetic activity of cells in mice skull marrow, and the proteins those cells made, with those in the rodent’s humerus, femur and four other bones, along with the meninges, the protective membranes between the skull and the brain. © Society for Science & the Public 2000–2023.

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: 28898 - Posted: 09.07.2023

Lilly Tozer A study that followed thousands of people over 25 years has identified proteins linked to the development of dementia if their levels are unbalanced during middle age. The findings, published in Science Translational Medicine on 19 July1, could contribute to the development of new diagnostic tests, or even treatments, for dementia-causing diseases. Most of the proteins have functions unrelated to the brain. “We’re seeing so much involvement of the peripheral biology decades before the typical onset of dementia,” says study author Keenan Walker, a neuroscientist at the US National Institute on Aging in Bethesda, Maryland. Equipped with blood samples from more than 10,000 participants, Walker and his colleagues questioned whether they could find predictors of dementia years before its onset by looking at a person’s proteome — the collection of all the proteins expressed throughout the body. They searched for any signs of dysregulation — when proteins are at levels much higher or lower than normal. The samples were collected as part of an ongoing study that began in 1987. Participants returned for examination six times over three decades, and during this time, around 1 in 5 of them developed dementia. The researchers found 32 proteins that, if dysregulated in people aged 45 to 60, were strongly associated with an elevated chance of developing dementia in later life. It is unclear how exactly these proteins might be involved in the disease, but the link is “highly unlikely to be due to just chance alone”, says Walker © 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: 28856 - Posted: 07.22.2023

By Robert Kolker Barb was the youngest in her large Irish Catholic family — a surprise baby, the ninth child, born 10 years after the eighth. Living in the suburbs of Pittsburgh, her family followed the football schedule: high school games on Friday night, college games on Saturday, the Steelers on Sunday. Dad was an engineer, mom was a homemaker and Barb was the family mascot, blond and adorable, watching her brothers and sisters finish school and go on to their careers. Barb was the only child left at home in the 1980s to witness the seams of her parents’ marriage come apart. Her father all but left, and her mother turned inward, sitting quietly in front of the television, always smoking, often with a cocktail. Something had overtaken her, though it wasn’t clear what. Barb observed it all with a measure of detachment; her parents had been older than most, and her sisters and brothers supplied more than enough parental energy to make up the difference. And so in 1990, when Barb was 14 and her mother learned she had breast cancer and died within months at the age of 62, Barb was shattered and bewildered but also protected. Her siblings had already stepped in, three of them living back home. Together they arrived at a shared understanding of the tragedy. Their mother could have lived longer if she had cut back on her drinking sooner or gone to see a doctor or hadn’t smoked. Six years later, Barb was 20 and in college when someone else in the family needed help. Her sister Christy was the second-born, 24 years older than Barb and the star of the family in many ways. She had traveled extensively as a pharmaceutical-company executive while raising two children with her husband in a nice house in a New Jersey suburb. But where once Christy was capable and professionally ambitious and socially conscious, now, at 44, she was alone, her clothes unkempt and ripped, her hair unwashed, her marriage over. Again, the family came together: Susan, the third-born, volunteered to take care of Christy full time, and Jenny, the eighth, searched for a specialist (the family members asked to be identified by their first names to protect their privacy). Depression was the first suspected diagnosis, then schizophrenia, though neither seemed quite right. Christy wasn’t sad or delusional; she wasn’t even upset. It was more as if she were reverting to a childlike state, losing her knack for self-regulation. Her personality was diluting — on its way out, with seemingly nothing to replace it. © 2023 The New York Times Company

Related chapters from BN: Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 28855 - Posted: 07.22.2023

By Pam Belluck Treating Alzheimer’s patients as early as possible — when symptoms and brain pathology are mildest — provides a better chance of slowing cognitive decline, a large study of an experimental Alzheimer’s drug presented Monday suggests. The study of 1,736 patients reported that the drug, donanemab, made by Eli Lilly, can modestly slow the progression of memory and thinking problems in early stages of Alzheimer’s, and that the slowing was greatest for early-stage patients when they had less of a protein that creates tangles in the brain. For people at that earlier stage, donanemab appeared to slow decline in memory and thinking by about four and a half to seven and a half months over an 18-month period compared with those taking a placebo, according to the study, published in the journal JAMA. Among people with less of the protein, called tau, slowing was most pronounced in those younger than 75 and those who did not yet have Alzheimer’s but had a pre-Alzheimer’s condition called mild cognitive impairment, according to data presented Monday at the Alzheimer’s Association International Conference in Amsterdam. “The earlier you can get in there, the more you can impact it before they’ve already declined and they’re on this fast slope,” Dr. Daniel Skovronsky, Eli Lilly’s chief medical and scientific officer, said in an interview. “No matter how you cut the data — earlier, younger, milder, less pathology — every time, it just looks like early diagnosis and early intervention are the key to managing this disease,” he added. The findings and the recent approval of another drug that modestly slows decline in the early stages of Alzheimer’s, Leqembi, signal a potentially promising turn in the long, rocky path toward finding effective medications for Alzheimer’s, a brutal disease that plagues more than six million Americans. Donanemab is currently being considered for approval by the Food and Drug Administration. © 2023 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: 28852 - Posted: 07.19.2023

Nicola Davis Science correspondent Taking part in activities such as chess, writing a journal, or educational classes in older age may help to reduce the risk of dementia, a study has suggested. According to the World Health Organization, more than 55 million people have the disease worldwide, most of them older people. However experts have long emphasised that dementia is not an inevitable part of ageing, with being active, eating well and avoiding smoking among the lifestyle choices that can reduce risk. Now researchers have revealed fresh evidence that challenging the brain could also be beneficial. Writing in the journal Jama Network Open, researchers in the US and Australia report how they used data from the Australian Aspree Longitudinal Study of Older Persons covering the period from 1 March 2010 to 30 November 2020. Participants in the study were over the age of 70, did not have a major cognitive impairment or cardiovascular disease when recruited between 2010 and 2014, and were assessed for dementia through regular study visits. In the first year, participants were asked about their social networks. They were also questioned on whether they undertook certain leisure activities or trips out to venues such as galleries or restaurants, and how frequently: never, rarely, sometimes, often or always. The team analysed data from 10,318 participants, taking into account factors such as age, sex, smoking status, education, socioeconomic status, and whether participants had other diseases such as diabetes. The results reveal that for activities such as writing letters or journals, taking educational classes or using a computer, increasing the frequency of participation by one category, for example from “sometimes” to “often”, was associated with an 11% drop in the risk of developing dementia over a 10-year period. Similarly, increased frequency of activities such as card games, chess or puzzle-solving was associated with a 9% reduction in dementia risk. © 2023 Guardian News & Media Limited

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: 28851 - Posted: 07.19.2023

Sara Reardon Vaccination against shingles might also prevent dementia, such as that caused by Alzheimer’s disease, according to a study of health records from around 300,000 people in Wales. The analysis found that getting the vaccine lowers the risk of dementia by 20%. But some puzzling aspects of the analysis have stirred debate about the work’s robustness. The study was published on the medRxiv preprint server on 25 May and has not yet been peer reviewed. “If it is true, it’s huge,” says Alberto Ascherio, an epidemiologist at Harvard University in Cambridge, Massachusetts, who was not involved in the study. “Even a modest reduction in risk is a tremendous impact.” Dementia–infection link The idea that viral infection can play a part in at least some dementia cases dates back to the 1990s, when biophysicist Ruth Itzhaki at the University of Manchester, UK, and her colleagues found herpesviruses in the brains of deceased people with dementia2. The theory has been controversial among Alzheimer’s researchers. But recent work has suggested that people infected with viruses that affect the brain have higher rates of neurodegenerative diseases3. Research has also suggested that those vaccinated against certain viral diseases are less likely to develop dementia4. But all these epidemiological studies have shared a key problem: people who get any type of vaccination tend to have healthier lifestyles than those who don’t5, meaning that other factors could account for their lowered risk of diseases such as Alzheimer’s. With that in mind, epidemiologist Pascal Geldsetzer at Stanford University in California and his colleagues turned to a natural experiment: a shingles vaccination programme in Wales, which began on 1 September 2013. Shingles is caused by the reawakening of inactive varicella zoster virus (VZV), the herpesvirus that causes chickenpox and which is present in most people. Shingles is most common in older adults and can cause severe pain and rashes. © 2023 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 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28814 - Posted: 06.07.2023

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