By Deborah Blum Back in the year 2000, sitting in his small home office in California’s Mill Valley, surrounded by stacks of spreadsheets, Jay Rosner hit one of those dizzying moments of dismay. An attorney and the executive director of The Princeton Review Foundation, the philanthropic arm of the private test-preparation and tutoring company, The Princeton Review, Rosner was scheduled to give testimony in a highly charged affirmative action lawsuit against the University of Michigan. He knew the case, Grutter v. Bollinger, was eventually headed to the U.S. Supreme Court, but as he reviewed the paperwork, he discovered a daunting gap in his argument.  Rosner had been asked to explore potential racial and cultural biases baked into standardized testing. He believed such biases, which critics had been surfacing for years prior, were real, but in that moment, he felt himself coming up short. “I suddenly realized that I would be deposed on this issue,” he recalled, “and I had no data to support my hypothesis, only deductive reasoning.”   The punch of that realization still resonates. Rosner is the kind of guy who really likes data to stand behind his points, and he recalls an anxiety-infused hunt for some solid facts. Rosner was testifying about an entrance exam for law school, the LSAT, for which he could find no particulars. But he knew that a colleague had data on how students of different racial backgrounds answered specific questions on another powerful standardized test, the SAT, long used to help decide undergraduate admission to colleges — given in New York state. He decided he could use that information to make a case by analogy. The two scholars agreed to crunch some numbers.  Based on past history of test results, he knew that White students would overall have higher scores than Black students. Still, Rosner expected Black students to perform better on some questions. To his shock, he found no trace of such balance. The results were “incredibly uniform,” he said, skewing almost entirely in favor of White students. “Every single question except one in the New York state data on four SATs favored Whites over Blacks,” Rosner recalled.

Keyword: Intelligence; Genes & Behavior
Link ID: 28611 - Posted: 12.24.2022

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.

Keyword: Alzheimers; Learning & Memory
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.

Keyword: Alzheimers
Link ID: 28604 - Posted: 12.21.2022

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Keyword: Depression; Schizophrenia
Link ID: 28603 - 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

Keyword: Alzheimers
Link ID: 28595 - Posted: 12.15.2022

Kristine Zengeler Many neurodegenerative diseases, or conditions that result from the loss of function or death of brain cells, remain largely untreatable. Most available treatments target just one of the multiple processes that can lead to neurodegeneration, which may not be effective in completely addressing disease symptoms or progress, if at all. But what if researchers harnessed the brain’s inherent capabilities to cleanse and heal itself? My colleagues and I in the Lukens Lab at the University of Virginia believe that the brain’s own immune system may hold the key to neurodegenerative disease treatment. In our research, we found a protein that could possibly be leveraged to help the brain’s immune cells, or microglia, stave off Alzheimer’s disease. No available treatments for neurodegenerative diseases stop ongoing neurodegeneration while also helping affected areas in the body heal and recuperate. In terms of failed treatments, Alzheimer’s disease is perhaps the most infamous of neurodegenerative diseases. Affecting more than 1 in 9 U.S. adults 65 and older, Alzheimer’s results from brain atrophy with the death of neurons and loss of the connections between them. These casualties contribute to memory and cognitive decline. Billions of dollars have been funneled into researching treatments for Alzheimer’s, but nearly every drug tested to date has failed in clinical trials.

Keyword: Alzheimers; Neuroimmunology
Link ID: 28590 - Posted: 12.13.2022

By Emily Anthes In creating modern dog breeds, humans sculpted canines into physical specimens perfectly suited for a wide variety of tasks. Bernese mountain dogs have solid, muscular bodies capable of pulling heavy loads, while greyhounds have lean, aerodynamic frames, ideal for chasing down deer. The compact Jack Russell terrier can easily shimmy into fox or badger dens. Now, a large study, published in Cell on Thursday, suggests that behavior, not just appearance, has helped qualify these dogs for their jobs. Breeds that were created for similar roles — whether rounding up sheep or flushing birds into the air — tend to cluster into distinct genetic lineages, which can be characterized by different combinations of behavioral tendencies, the researchers found. “Much of modern breeding has been focused predominantly on what dogs look like,” Evan MacLean, an expert on canine cognition at the University of Arizona who was not involved in the study, said in an email. But, he emphasized, “Long before we were breeding dogs for their appearances, we were breeding them for behavioral traits.” The study also found that many of the genetic variants that set these lineages apart from each other appear to regulate brain development, and many seem to predate modern breeds. Together, the results suggest that people may have created today’s stunning assortment of breeds, in part, by harnessing and preserving desirable behavioral traits that already existed in ancient dogs, the researchers said. “Dogs have fundamentally the same blueprint, but now you’ve got to emphasize certain things to get particular tasks done,” said Elaine Ostrander, a dog genomics expert at the National Human Genome Research Institute and the senior author of the study. “You’re going to tweak a gene up, you’re going to tweak it down.” In an email, Bridgett vonHoldt, an evolutionary biologist at Princeton University who was not involved in the research, called the new paper “a major landmark in the field of dog genomics and behavior. We know it is complicated. This study not only gives us hope, it will be viewed as an inspiration for all in the field.” © 2022 The New York Times Company

Keyword: Genes & Behavior; Evolution
Link ID: 28589 - Posted: 12.10.2022

Heidi Ledford Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples1. The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19. The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.” Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper2, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects. She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects. The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28584 - Posted: 12.06.2022

Nicola Davis Science correspondent The brains of teenagers who lived through Covid lockdowns show signs of premature ageing, research suggests. The researchers compared MRI scans of 81 teens in the US taken before the pandemic, between November 2016 and November 2019, with those of 82 teens collected between October 2020 and March 2022, during the pandemic but after lockdowns were lifted. After matching 64 participants in each group for factors including age and sex, the team found that physical changes in the brain that occurred during adolescence – such as thinning of the cortex and growth of the hippocampus and the amygdala – were greater in the post-lockdown group than in the pre-pandemic group, suggesting such processes had sped up. In other words, their brains had aged faster. “Brain age difference was about three years – we hadn’t expected that large an increase given that the lockdown was less than a year [long],” said Ian Gotlib, a professor of psychology at Stanford University and first author of the study. Writing in the journal Biological Psychiatry: Global Open Science, the team report that the participants – a representative sample of adolescents in the Bay Area in California – originally agreed to take part in a study looking at the impact of early life stress on mental health across puberty. As a result, participants were also assessed for symptoms of depression and anxiety. The post-lockdown group self-reported greater mental health difficulties, including more severe symptoms of anxiety, depression and internalising problems. © 2022 Guardian News & Media

Keyword: Stress; Development of the Brain
Link ID: 28578 - Posted: 12.03.2022

By Gina Kolata In a bold attempt to stop the progress of some cases of Alzheimer’s disease, a group of researchers is trying something new — injecting a protective gene into patients’ brains. The trial involved just five patients with a particular genetic risk for Alzheimer’s. They received a very low dose of the gene therapy — a test of safety, which the treatment passed. But the preliminary results, announced Friday during the Clinical Trials on Alzheimer’s Disease conference, showed that proteins from the added gene appeared in the patients’ spinal fluid, and levels in the brain of two markers of Alzheimer’s disease, tau and amyloid, fell. Those findings were promising enough to advance the clinical trial into its next phase. Treatment of another five patients at a higher dose is underway, and the work, initially funded by the nonprofit Alzheimer’s Drug Discovery Foundation, is supported by Lexeo Therapeutics, a fledgling company founded by Dr. Ronald Crystal, who is also chairman of the department of genetic medicine at Weill Cornell Medicine in New York. The hope is to get a stronger response, eventually leading to a treatment that might slow the disease in whom it has started or, even better, protect people at high risk who have no symptoms. “It’s a very provocative, very intriguing approach,” said Dr. Eliezer Masliah, director of the neuroscience division at the National Institute on Aging. Participants in the study are among the approximately 2 percent of people who have inherited a pair of copies of a gene, APOE4, which markedly increases their risk of Alzheimer’s. For the study subjects, the first symptoms of Alzheimer’s had already emerged — their genetic risk had played out, and they had few options. There is no treatment that is directed specifically at APOE4-driven Alzheimer’s, nor is one on the near horizon. © 2022 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 28575 - Posted: 12.03.2022

By Pam Belluck The hotly anticipated results of a clinical trial of an experimental Alzheimer’s drug suggest that the treatment slowed cognitive decline somewhat for people in the early stages of the disease but also caused some patients to experience brain swelling or brain bleeding. The new data, released Tuesday evening, offered the first detailed look at the effects of the drug, lecanemab, and comes two months after its manufacturers, Eisai and Biogen, stoked excitement by announcing that the drug had shown positive results. Alzheimer’s experts said the new information showed reason for both optimism and caution. “The benefit is real; so too are the risks,” said Dr. Jason Karlawish, a co-director of the University of Pennsylvania’s Penn Memory Center, who was not involved in the research. A report of the findings published in the New England Journal of Medicine said that over 18 months, lecanemab “resulted in moderately less decline on measures of cognition and function,” compared with patients receiving a placebo. Still, the study of nearly 1,800 patients with mild symptoms, which was funded by the companies and co-written by scientists at Eisai, concluded that “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.” The companies’ initial announcement in September had sent their stock prices soaring because the field of Alzheimer’s drug development has been marked by years of failures. © 2022 The New York Times Company

Keyword: Alzheimers
Link ID: 28572 - Posted: 11.30.2022

Cephalopods like octopuses, squids and cuttlefish are highly intelligent animals with complex nervous systems. In “Science Advances”, a team led by Nikolaus Rajewsky of the Max Delbrück Center has now shown that their evolution is linked to a dramatic expansion of their microRNA repertoire. If we go far enough back in evolutionary history, we encounter the last known common ancestor of humans and cephalopods: a primitive wormlike animal with minimal intelligence and simple eyespots. Later, the animal kingdom can be divided into two groups of organisms – those with backbones and those without. While vertebrates, particularly primates and other mammals, went on to develop large and complex brains with diverse cognitive abilities, invertebrates did not. With one exception: the cephalopods. Scientists have long wondered why such a complex nervous system was only able to develop in these mollusks. Now, an international team led by researchers from the Max Delbrück Center and Dartmouth College in the United States has put forth a possible reason. In a paper published in “Science Advances”, they explain that octopuses possess a massively expanded repertoire of microRNAs (miRNAs) in their neural tissue – reflecting similar developments that occurred in vertebrates. “So, this is what connects us to the octopus!” says Professor Nikolaus Rajewsky, Scientific Director of the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB), head of the Systems Biology of Gene Regulatory Elements Lab, and the paper’s last author. He explains that this finding probably means miRNAs play a fundamental role in the development of complex brains.

Keyword: Evolution; Epigenetics
Link ID: 28571 - Posted: 11.30.2022

Ian Sample Science editor At the end of November, thousands of researchers from around the world will descend on San Francisco for the annual Clinical Trials on Alzheimer’s Disease meeting. The conference is a mainstay of the dementia research calendar, the place where the latest progress – and all too often, setbacks – in the quest for Alzheimer’s treatments are made public for the first time. This year’s meeting is poised to be a landmark event. After more than a century of research into Alzheimer’s, scientists expect to hear details of the first treatment that can unambiguously alter the course of the disease. Until now, nothing has reversed, halted or even slowed the grim deterioration of patients’ brains. Given that dementia and Alzheimer’s are the No 1 killer in the UK, and the seventh largest killer worldwide, there is talk of a historic moment. The optimism comes from a press statement released in September from Eisai, a Japanese pharmaceutical firm, and Biogen, a US biotech. It gave top-line results from a major clinical trial of an antibody treatment, lecanemab, given to nearly 2,000 people with early Alzheimer’s disease. The therapy slowed cognitive decline, the statement said, raising hopes that a drug might finally apply the brakes to Alzheimer’s and provide “a clinically meaningful impact on cognition and function”. The announcement was greeted, broadly, with delight and relief from researchers who have endured failure after failure in the long search for Alzheimer’s drugs. But even the most enthusiastic conceded that significant questions remained. With only a press release to go on, it was hard to be sure the claims stood up. The answer will come on 29 November when researchers leading the trial, named Clarity AD, present their results at the San Francisco meeting. © 2022 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 28562 - Posted: 11.23.2022

By Laurie McGinley Few illnesses instill as much fear as Alzheimer’s, a fatal neurodegenerative disease that destroys memory and identity. The dread is compounded by the uncertainty that often surrounds the diagnosis of the most common form of dementia. Brain autopsies remain the only way to know for sure whether someone had the disease, which the Centers for Disease Control and Prevention estimates affects 6.5 million people in the United States. Over the past several years, sophisticated tests such as spinal taps and specialized PET scans have become available — but they are invasive and costly and not routinely used. As a result, Alzheimer’s is frequently misdiagnosed, especially in the early stages. Other illnesses, including depression, can have similar symptoms and require other treatments. But simple blood tests designed to help doctors diagnose Alzheimer’s now are on the market. More are on the way. The tests are seen as an important scientific advance, but have ignited debate about how and when they should be used. Some experts say much more research is needed before the new tests can be widely deployed, especially in primary-care settings. Others say there already is sufficient information on the accuracy of some tests. All agree that no single test is perfect and physicians still should perform a complete clinical assessment. Widespread use of the tests may be some time off in the future — after insurance coverage improves and even more accurate next-generation tests become available. For now, none is covered by Medicare, and private insurance coverage is patchy. In the past few years, scientific and technological advances have made it possible to detect in the blood tiny fragments of brain proteins implicated in Alzheimer’s. That has prompted experts in academia and industry to develop blood tests for the disease. Some of the tests detect a sticky protein called amyloid beta, while others look for another protein called tau. Some search for both or other markers of disease. The abnormal accretions of amyloid plaques and tau tangles are the defining characteristics of Alzheimer’s. washingtonpost.com © 1996-2022

Keyword: Alzheimers
Link ID: 28560 - Posted: 11.19.2022

Researchers at the National Institutes of Health have successfully identified differences in gene activity in the brains of people with attention deficit hyperactivity disorder (ADHD). The study, led by scientists at the National Human Genome Research Institute (NHGRI), part of NIH, found that individuals diagnosed with ADHD had differences in genes that code for known chemicals that brain cells use to communicate. The results of the findings, published in Molecular Psychiatry(link is external), show how genomic differences might contribute to symptoms. To date, this is the first study to use postmortem human brain tissue to investigate ADHD. Other approaches to studying mental health conditions include non-invasively scanning the brain, which allows researchers to examine the structure and activation of brain areas. However, these studies lack information at the level of genes and how they might influence cell function and give rise to symptoms. The researchers used a genomic technique called RNA sequencing to probe how specific genes are turned on or off, also known as gene expression. They studied two connected brain regions associated with ADHD: the caudate and the frontal cortex. These regions are known to be critical in controlling a person’s attention. Previous research found differences in the structure and activity of these brain regions in individuals with ADHD. As one of the most common mental health conditions, ADHD affects about 1 in 10 children in the United States. Diagnosis often occurs during childhood, and symptoms may persist into adulthood. Individuals with ADHD may be hyperactive and have difficulty concentrating and controlling impulses, which may affect their ability to complete daily tasks and their ability to focus at school or work. With technological advances, researchers have been able to identify genes associated with ADHD, but they had not been able to determine how genomic differences in these genes act in the brain to contribute to symptoms until now.

Keyword: ADHD; Genes & Behavior
Link ID: 28559 - Posted: 11.19.2022

By Elie Dolgin, No gene variant is a bigger risk factor for Alzheimer’s disease than one called APOE4. But exactly how the gene spurs brain damage has been a mystery. A study has now linked APOE4 with faulty cholesterol processing in the brain, which in turn leads to defects in the insulating sheaths that surround nerve fibres and facilitate their electrical activity. Preliminary results hint that these changes could cause memory and learning deficits. And the work suggests that drugs that restore the brain’s cholesterol processing could treat the disease. “This fits in with the picture that cholesterol needs to be in the right place,” says Gregory Thatcher, a chemical biologist at the University of Arizona in Tucson. Inheriting a single copy of APOE4 raises the risk of developing Alzheimer’s around 3-fold; having two copies boosts the chances 8- to 12-fold. Interactions between the protein encoded by APOE4 and sticky plaques of amyloid—a substance tied to brain cell death—in the brain partially explain the connection. But those interactions are not the whole story. As neuroscientist Li-Huei Tsai at the Massachusetts Institute of Technology (MIT) in Cambridge and her colleagues report today in Nature, APOE4 triggers insulation-making brain cells known as oligodendrocytes to accumulate the fatty molecule cholesterol—a type of lipid—in all the wrong places. This interferes with the cells’ ability to cover nerve fibres in a protective wrapper made of a lipid-rich material called myelin. Electrical signalling in the brain then slows, and cognition usually suffers. Tsai’s team had previously linked lipid changes to malfunctions in other cell types, including some that offer structural support to neurons and others that provide immune protection for the brain. The latest findings add oligodendrocytes and their essential myelin function to the mix. © 2022 Scientific American

Keyword: Alzheimers; Genes & Behavior
Link ID: 28558 - Posted: 11.19.2022

By Laurie McGinley An experimental Alzheimer’s drug designed to slow cognitive decline failed to meet the goals of two closely watched clinical trials, a discouraging development that underscores the challenges of developing treatments for the memory-robbing disease. Genentech, a division of health-care giant Roche, said in a news release Monday that the treatment, called gantenerumab, slowed the pace of decline in patients with early-stage disease but not enough to be statistically significant. The therapy was tested in identical late-stage trials, each with 1,000 participants. Half received placebos and half got the treatment. The studies lasted 27 months. The drug, a monoclonal antibody, is designed to remove from the brain clumps of an abnormal version of a protein called amyloid beta, a hallmark of the disease. The company said Monday that the treatment removed less amyloid beta than expected. Some scientists have thought for years that amyloid-busting medicines could slow the fatal neurodegenerative disease, but there have been multiple failures, and just a few encouraging signs, involving amyloid-busting drugs. “So many of our families have been directly affected by Alzheimer’s, so this news is very disappointing to deliver,” Levi Garraway, Roche’s chief medical officer and head of global product development, said in a statement. He said the company looks forward to sharing more information about the results “as we continue to search for new treatments for this complex disease.” Genentech said that 25 percent of the patients who received gantenerumab experienced a side effect that can cause brain swelling and bleeding but that most did not have symptoms and few needed to stop taking the drug. The company said it planned to present more data from the trials at an Alzheimer’s conference this month. The company assessed the drug by measuring trial participants’ performance on an 18-point measure of memory and cognition, called the Clinical Dementia Rating scale — Sum of Boxes. The news on gantenerumab is a disappointment for patients, physicians and researchers desperate for effective treatments for a disease that affects 6.5 million Americans.

Keyword: Alzheimers
Link ID: 28554 - Posted: 11.16.2022

Linda Geddes Science correspondent Lead exposure during childhood may lead to reduced cognitive abilities in later life, meaning people experience symptoms of dementia sooner, data suggest. The study, one of the first to investigate the decades-long consequences of lead poisoning, suggests countries could face an explosion of people seeking support for dementia as individuals who were exposed to high lead levels during early life progress into old age. “In the US, and I would imagine the UK, the prime years when children were exposed to the most lead was in the 1960s and 70s. That’s when the most leaded gasoline was getting used, lead paint was still common, and municipal water systems hadn’t done much to clean up their lead,” said Prof John Robert Warren at the University of Minnesota in Minneapolis, who was involved in the research. “Those children who are now in their 40s, 50s and early 60s, will soon be entering the time of life when cognitive impairment and dementia are really common. So there’s this coming wave, potentially, of problems for the people who were most exposed.” Although scientists have long known that children and adults who are exposed to lead have poorer cognitive and educational outcomes, few studies have investigated the longer-term consequences. Warren and his colleagues combined data from the US-based longitudinal Health and Retirement Study (HRS), which has followed the brain health of thousands of adults over several decades, with census records to pinpoint where 1,089 of these individuals lived as children. They also mapped the locations of towns and cities that used lead pipes and had acidic or alkaline water – a proxy for high lead exposure. The research, published in Science Advances, revealed that people who lived in cities with lead-contaminated water as children had worse baseline cognitive functioning – a measure of their ability to learn, process information, and reason – at age 72, compared with those who did not. The difference was equivalent to being roughly eight years older. © 2022 Guardian News & Media Limited

Keyword: Neurotoxins; Alzheimers
Link ID: 28550 - Posted: 11.13.2022

by David Dobbs For 40 years, Leo Kanner and Hans Asperger have dominated virtually every story about the ‘pioneers of autism research.’ These two men published in 1943 and 1944, respectively, what were long accepted as the first descriptions of, as Kanner’s seminal paper claimed, ”children whose condition differs … markedly and uniquely from anything reported so far.” Both papers are absorbing, touching and authoritative. Both describe young people whose challenges defied the known diagnoses of the time but clearly fall into what we now call autism. And both offered a new diagnostic category for such people. Kanner’s 1943 paper, ”Autistic Disturbances of Affective Contact,” drew almost immediate attention. Within a year, he renamed the condition these children shared, dubbing it ‘early infantile autism,’ which soon became known as ‘autism’ or ‘Kanner’s syndrome.’ His articulation of the condition, based on observations of 11 children he and his associates treated in his Baltimore, Maryland, clinic, remained the standard well into the 1980s and involved three elements: Autism was a condition marked by: (1) emergence early in childhood, (2) deficits in communication and social interaction, and (3) restricted or repetitive behaviors and a desire for sameness. Even today, these three elements anchor the official diagnostic criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, as well as the widely used International Classification of Diseases and Related Health Problems. Asperger’s 1944 paper, which presented case studies on four children he and his colleagues had seen in his clinic in Vienna, Austria, made its impact far more slowly. In fact, because Asperger published in German (and in a German journal in the middle of a war that had essentially halted transatlantic scholarly exchange), the paper went largely unnoticed outside Europe for decades. Asperger’s descriptions resembled Kanner’s in many ways, although he outlined a wider apparent range of intelligence and capabilities than Kanner did, with some of his study participants reaching prominence in their fields. Asperger coined the diagnostic term ‘autistic psychopathy.’ © 2022 Simons Foundation

Keyword: Autism
Link ID: 28544 - Posted: 11.09.2022

Jon Hamilton An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning. Scientists are launching a study designed to make or break the hypothesis that Alzheimer's is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer's to appear in their 30s or 40s. The study comes after several experimental drugs have failed to prevent declines in memory and thinking even though they succeeded in removing amyloid from the brains of patients in the early stages of Alzheimer's. Those failures have eroded support for the idea that amyloid is responsible for a cascade of events that eventually lead to the death of brain cells. "Many of us think of that as the ultimate test of the amyloid hypothesis," says Dr. Randall Bateman, a professor of neurology at Washington University School of Medicine in St. Louis."If that doesn't work, nothing will work." The new experiment, called the DIAN-TU primary Prevention Trial, is scheduled to begin enrolling patients by the end of the year. The amyloid hypothesis can be traced to Dr. Alois Alzheimer, a pathologist who first described the disease that would bear his name in 1906. Alzheimer was working at a psychiatric clinic in Munich, where he had the chance to conduct an autopsy on a woman who died at 50 after experiencing memory loss, disorientation, and hallucinations. He observed that the woman's brain had an "unusual disease of the cerebral cortex," including "senile plaque" usually seen in much older people. © 2022 npr

Keyword: Alzheimers
Link ID: 28534 - Posted: 11.02.2022