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By Esther Landhuis In January 2023, the US Food and Drug Administration (FDA) approved lecanemab — an antibody medication that decreases β-amyloid protein build-up in the brain — as a treatment for Alzheimer’s disease. Pivotal evidence came from a large, randomized trial of people with early-stage Alzheimer’s, which afflicts around 32 million people worldwide. By the end of that 18-month study1, patients in the placebo group scored on average 1.66 points worse than their performance at baseline on a standard dementia test, which assesses cognitive and functional changes over time through interviews with a patient and their caregiver. The mean score of treated participants, by comparison, worsened by 1.21 points — a 27% slowing of cognitive decline. But is this improvement meaningful for patients and their families? There are two major categories of drugs used to treat Alzheimer’s disease and other progressive conditions: symptomatic drugs, which treat the symptoms, and disease-modifying drugs, which target the root cause. Donepezil and rivastigmine, for example, are symptomatic drugs that boost the activity of chemicals in the brain to compensate for declines in cognitive and memory function caused by Alzheimer’s disease, but they cannot stop its progression. Lecanemab, developed jointly by Japanese pharmaceutical company Eisai and American biotechnology firm Biogen, targets the underlying issue of amyloid build-up in the brain, and in doing so, could fundamentally change the course of the disease. An important feature of disease-modifying drugs is that their benefits are cumulative. Studies of patients with multiple sclerosis, for example, have shown the benefits of starting disease-modifying drugs earlier in the course of the disease compared with later, including improved mortality rates and reduced disability in the long term. Being able to quantify how long a disease-modifying drug can delay or halt the progression of Alzheimer’s disease could change how researchers understand — and communicate — its benefits. © 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: 29193 - Posted: 03.16.2024

By Katherine Ellison Jonel Dershem first noticed problems with her memory in 2016 after her breast cancer surgery. She was only 50 and at first blamed the lapses on chemotherapy, and then on her busy, stressful life. So did her husband and friends — and doctor. “I kept blowing it off,” said Dershem, an obstetrician from Voorhees, N.J., whose challenges began with little things like leaving a faucet running and progressed to trouble finishing routine tasks. “I was our family’s primary breadwinner. I didn’t want there to be any serious problems.” In December 2022, nearly seven years after her memory loss began, Dershem was diagnosed with mild cognitive impairment (MCI). Her delayed diagnosis wasn’t unusual, but experts say that needs to change. More than occasional forgetfulness, MCI causes problems that disrupt daily life but don’t make it impossible to function, said Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. It is often but not always a precursor to dementia, he added. “It’s a subtle condition,” said Petersen, who in 1999 led the first study differentiating patients with MCI from healthy subjects and those with dementia. If you miss a golf date once, no worries, he said, but if “that happened a couple of times last week and people in your family are starting to worry about you — well, that may be MCI.” “With MCI, people can still drive, pay their bills and do their taxes — they just do so less efficiently,” Petersen said. A 2022 study in the journal Alzheimer’s & Dementia projected that 14.4 million people in the United States would have MCI in 2025, and 19.3 million in 2050. An American Academy of Neurology subcommittee estimated that about 1 in 10 people ages 70 to 74 had MCI, and 1 in 4 ages 80 to 84 in 2018.

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: 29178 - Posted: 03.05.2024

By Paula Span Determining whether someone has Alzheimer’s disease usually requires an extended diagnostic process. A doctor takes a patient’s medical history, discusses symptoms, administers verbal and visual cognitive tests. The patient may undergo a PET scan, an M.R.I. or a spinal tap — tests that detect the presence of two proteins in the brain, amyloid plaques and tau tangles, both associated with Alzheimer’s. All of that could change dramatically if new criteria proposed by an Alzheimer’s Association working group are widely adopted. Its final recommendations, expected later this year, will accelerate a shift that is already underway: from defining the disease by symptoms and behavior to defining it purely biologically — with biomarkers, substances in the body that indicate disease. The draft guidelines, Revised Criteria for Diagnosis and Staging of Alzheimer’s Disease, call for a simpler approach. That could mean a blood test to indicate the presence of amyloid. Such tests are already available in some clinics and doctors’ offices. “Someone who has biomarker evidence of amyloid in the brain has the disease, whether they’re symptomatic or not,” said Dr. Clifford R. Jack Jr., the chair of the working group and an Alzheimer’s researcher at the Mayo Clinic. “The pathology exists for years before symptom onset,” he added. “That’s the science. It’s irrefutable.” He and his colleagues on the panel do not recommend testing people who have no symptoms of cognitive decline. But skeptics predict that’s likely to happen nonetheless. If so, a sizable proportion would test positive for amyloid and would therefore be diagnosed with Alzheimer’s. A 2015 Dutch study estimated that more than 10 percent of cognitively normal 50-year-olds would test positive, as would almost 16 percent of 60-year-olds and 23 percent of 70-year-olds. Most of those individuals would never develop dementia. © 2024 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: 29177 - Posted: 03.05.2024

Fen-Biao Gao Around 55 million people worldwide suffer from dementia such as Alzheimer’s disease. On Feb. 22, 2024, it was revealed that former talk show host Wendy Williams had been diagnosed with frontotemporal dementia, or FTD, a rare type of dementia that typically affects people ages 45 to 64. Bruce Willis is another celebrity who was diagnosed with the syndrome, according to his family. In contrast to Alzheimer’s, in which the major initial symptom is memory loss, FTD typically involves changes in behavior. The initial symptoms of FTD may include changes in personality, behavior and language production. For instance, some FTD patients exhibit inappropriate social behavior, impulsivity and loss of empathy. Others struggle to find words and to express themselves. This insidious disease can be especially hard for families and loved ones to deal with. There is no cure for FTD, and there are no effective treatments. Up to 40% of FTD cases have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, more than a dozen genes have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment. I am a researcher who studies the development of FTD and related disorders, including the motor neuron disease amyotrophic lateral sclerosis, or ALS. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases. Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic. © 2010–2024, The Conversation US, Inc.

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: 29161 - Posted: 02.25.2024

David Robson Scientific discoveries can emerge from the strangest places. In early 1900s France, the doctor Albert Calmette and the veterinarian Camille Guérin aimed to discover how bovine tuberculosis was transmitted. To do so, they first had to find a way of cultivating the bacteria. Sliced potatoes – cooked with ox bile and glycerine – proved to be the perfect medium. As the bacteria grew, however, Calmette and Guérin were surprised to find that each generation lost some of its virulence. Animals infected with the microbe (grown through many generations of their culture) no longer became sick but were protected from wild TB. In 1921, the pair tested this potential vaccine on their first human patient – a baby whose mother had just died of the disease. It worked, and the result was the Bacille Calmette-Guérin (BCG) vaccine that has saved millions of lives. A black and white image pf Camille Guérin and physician Albert Calmette side by side. French veterinarian Camille Guérin and physician Albert Calmette developed the BCG jab in 1921 using sliced potatoes cooked with ox bile and glycerine. Photograph: Musée Pasteur Calmette and Guérin could have never imagined that their research would inspire scientists investigating an entirely different kind of disease more than a century later. Yet that is exactly what is happening, with a string of intriguing studies suggesting that BCG can protect people from developing Alzheimer’s disease. If these preliminary results bear out in clinical trials, it could be one of the cheapest and most effective weapons in our fight against dementia. According to the World Health Organization, 55 million people now have dementia, with about 10 million new cases each year. Alzheimer’s disease is by far the most common form, accounting for about 60%-70% of cases. It is characterised by clumps of a protein called amyloid beta that accumulate within the brain, killing neurons and destroying the synaptic connections between the cells. © 2024 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: 29160 - Posted: 02.25.2024

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