Chapter 13. Memory and Learning

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By William Wan If only Dan Goerke could hold his wife’s hand. Maybe she would talk again. Maybe she would look at him and smile as she used to. Maybe she would eat and stop wasting away. Since the pandemic began, Goerke’s wife, Denise — 63 years old and afflicted with Alzheimer’s disease — had declined dramatically. Left alone in her nursing home, she had lost 16 pounds, could not form the simplest words, no longer responded to the voices of her children. In recent weeks, she had stopped recognizing even the man she loved. Goerke, 61, could tell the isolation was killing his wife, and there was nothing he could do but watch. “Every day it gets a little worse,” he said. “We’ve lost months, maybe years of her already.” Beyond the staggering U.S. deaths caused directly by the novel coronavirus, more than 134,200 people have died from Alzheimer’s and other forms of dementia since March. That is 13,200 more U.S. deaths caused by dementia than expected, compared with previous years, according to an analysis of federal data by The Washington Post. Overlooked amid America’s war against the coronavirus is this reality: People with dementia are dying not just from the virus but from the very strategy of isolation that’s supposed to protect them. In recent months, doctors have reported increased falls, pulmonary infections, depression and sudden frailty in patients who had been stable for years. Social and mental stimulation are among the few tools that can slow the march of dementia. Yet even as U.S. leaders have rushed to reopen universities, bowling alleys and malls, nursing homes say they continue begging in vain for sufficient testing, protective equipment and help.

Keyword: Alzheimers
Link ID: 27478 - Posted: 09.19.2020

By Elizabeth Preston This is Panurgus banksianus, the large shaggy bee. It lives alone, burrowed into sandy grasslands across Europe. It prefers to feed on yellow-flowered members of the aster family. The large shaggy bee also has a very large brain. Just like mammals or birds, insect species of the same size may have different endowments inside their heads. Researchers have discovered some factors linked to brain size in back-boned animals. But in insects, the drivers of brain size have been more of a mystery. In a study published Wednesday in Proceedings of the Royal Society B, scientists scrutinized hundreds of bee brains for patterns. Bees with specialized diets seem to have larger brains, while social behavior appears unrelated to brain size. That means when it comes to insects, the rules that have guided brain evolution in other animals may not apply. “Most bee brains are smaller than a grain of rice,” said Elizabeth Tibbetts, an evolutionary biologist at the University of Michigan who was not involved in the research. But, she said, “Bees manage surprisingly complex behavior with tiny brains,” making the evolution of bee brains an especially interesting subject. Ferran Sayol, an evolutionary biologist at University College London, and his co-authors studied those tiny brains from 395 female bees belonging to 93 species from across the United States, Spain and the Netherlands. Researchers beheaded each insect and used forceps to remove its brain, a curled structure that’s widest in the center. “It reminds me a little bit of a croissant,” Dr. Sayol said. One pattern that emerged was a connection between brain size and how long each bee generation lasted. Bees that only go through one generation each year have larger brains, relative to their body size, than bees with multiple generations a year. © 2020 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 27476 - Posted: 09.16.2020

David Cox Gérard Karsenty was a young scientist trying to make a name for himself in the early 1990s when he first stumbled upon a finding that would go on to transform our understanding of bone, and the role it plays in our body. Karsenty had become interested in osteocalcin, one of the most abundant proteins in bone. He suspected that it played a crucial role in bone remodelling – the process by which our bones continuously remove and create new tissue – which enables us to grow during childhood and adolescence, and also recover from injuries. Intending to study this, he conducted a genetic knockout experiment, removing the gene responsible for osteocalcin from mice. However to his dismay, his mutant mice did not appear to have any obvious bone defects at all. “For him, it was initially a total failure,” says Mathieu Ferron, a former colleague of Karsenty who now heads a research lab studying bone biology at IRCM in Montreal. “In those days it was super-expensive to do modification in the mouse genome.” But then Karsenty noticed something unexpected. While their bones had developed normally, the mice appeared to be both noticeably fat and cognitively impaired. “Mice that don’t have osteocalcin have increased circulating glucose, and they tend to look a bit stupid,” says Ferron. “It may sound silly to say this, but they don’t learn very well, they appear kind of depressed. But it took Karsenty and his team some time to understand how a protein in bone could be affecting these functions. They were initially a bit surprised and terrified as it didn’t really make any sense to them.” © 2020 Read It Later, Inc.

Keyword: Hormones & Behavior; Obesity
Link ID: 27473 - Posted: 09.16.2020

by Angie Voyles Askham . Many problems associated with fragile X syndrome stem from a leak in mitochondria, organelles that act as the power stations of the cell, a new study suggests1. Stopping this leak eases some of the autism-like traits of mice that model the syndrome. “The paper is very solid,” says John Jay Gargus, director of the Center for Autism Research and Translation at the University of California, Irvine, who was not involved in the study. And because mitochondrial energy deficiency is seen in other forms of autism, the findings may be relevant beyond fragile X syndrome, Gargus says. Fragile X syndrome results from mutations in the FMR1 gene, which lead to a loss of the protein FMRP. Without FMRP, cells have immature dendritic spines — the bumps along a neuron’s arms that receive input from other neurons — and produce other proteins in excess. These differences are thought to contribute to the syndrome’s characteristic traits, such as developmental delay, intellectual disability and, often, autism. The new study shows that a leak in the mitochondrial membrane, possibly caused by the lack of FMRP, may drive the affected cells’ immaturity and excess protein production. The leak affects a cell’s metabolism, causing it to produce energy quickly but not efficiently, says lead researcher Elizabeth Jonas, professor of internal medicine and neuroscience at Yale University. All cells start out with mitochondrial leaks; the rapid energy production these leaks allow may be useful in early development. As typical cells mature and efficiency becomes more important than speed, however, they seem to close the leaks, Jonas says. Because cells with a fragile X mutation cannot close their leaks, they remain in an immature state. © 2020 Simons Foundation

Keyword: Development of the Brain
Link ID: 27466 - Posted: 09.12.2020

Ian Sample Science editor Brain scans of cosmonauts have revealed the first clear evidence of how the organ adapts to the weird and often sickness-inducing challenge of moving around in space. Analysis of scans taken from 11 cosmonauts, who spent about six months each in orbit, found increases in white and grey matter in three brain regions that are intimately involved in physical movement. The changes reflect the “neuroplasticity” of the brain whereby neural tissue, in this case the cells that govern movement or motor activity, reconfigures itself to cope with the fresh demands of life in orbit. “With the techniques we used, we can clearly see there are microstructural changes in three major areas of the brain that are involved in motor processing,” said Steven Jillings, a neuroscientist at the University of Antwerp in Belgium. Visitors to the International Space Station face a dramatic shock to the system for a whole host of reasons, but one of the most striking is weightlessness. While the space station and its occupants are firmly in the grip of gravity – they are constantly falling around the planet – the body must recalibrate its senses to cope with the extreme environment. Images of the cosmonauts’ brains, taken before and after missions lasting on average 171 days, and again seven months later, confirmed that the cerebrospinal fluid that bathes the brain redistributes itself in orbit, pushing the brain up towards the top of the skull. This also expands fluid-filled cavities called ventricles, which may be linked to a loss of sharpness in the cosmonauts’ vision, a condition called spaceflight-associated neuro-ocular syndrome or Sans. © 2020 Guardian News & Media Limited

Keyword: Learning & Memory
Link ID: 27453 - Posted: 09.05.2020

— Joe Louis Martinez Jr., founder and former director of UTSA’s Neurosciences Institute, passed away on August 29 after a long battle with liver cancer. He was 76. Martinez was born in Albuquerque, New Mexico, on August 1, 1944. He received his B.A. from the University of California, San Diego; graduated with his M.S. in experimental psychology from New Mexico Highlands University in 1968; and earned his Ph.D. in physiological psychology in 1971 from the University of Delaware. He completed his postdoctoral training at the University of California, Irvine, and the Salk Institute in San Diego. Martinez served as a professor in the Department of Psychology at the University of California, Berkeley, from 1982 to 1995. During this time he led an internationally recognized research laboratory and departed as professor emeritus. In 1995 he joined UTSA as the Ewing Halsell Distinguished Chair in psychology. From 1995 to 2012 he was a beloved professor who founded and directed the Cajal Neuroscience Research Center, now known as the UTSA Neurosciences Institute. He oversaw the design and construction of the Biosciences Building, UTSA’s first research building. Each floor in the BSB contains tiles representing the neuroanatomical drawings of Santiago Ramon y Cajal. During his tenure at UTSA, Martinez brought over $15 million in grant funding to the university. In 2013 he moved to the University of Illinois at Chicago to become the chair of the department of psychology. He retired in 2016. © 2020 The University of Texas at San Antonio

Keyword: Learning & Memory
Link ID: 27450 - Posted: 09.05.2020

By Nicholas Bakalar Being overweight may be linked to an increased risk for dementia. British researchers used data on 6,582 men and women, age 50 and older, who were cognitively healthy at the start of the study. The analysis, in the International Journal of Epidemiology, tracked the population for an average of 11 years, recording incidents of physician-diagnosed dementia. Almost 7 percent of the group developed dementia. Compared with people of normal weight (body mass index between 18.5 and 24.9), overweight people with a B.M.I. of 25 to 29.9 were 27 percent more likely to develop dementia, and the obese, with a B.M.I. of 30 or higher, were 31 percent more likely to become demented. The researchers also found that women with central obesity — a waist size larger than 34.6 inches — were 39 percent more likely to develop dementia than those with normal waist size. Fat around the middle was not associated with a higher dementia risk in men. The study controlled for age, sex, APOE4 (a gene known to increase the risk of Alzheimer’s disease, the most common form of dementia), education, marital status, smoking and other known dementia risks. The lead author, Yixuan Ma, a student at University College London, said that this observational study does not prove cause and effect. “Being overweight is just a risk,” she said. “It doesn’t mean that an overweight person will necessarily get dementia. But for many reasons, it’s good to maintain a normal weight and engage in vigorous physical activity over a lifetime.” © 2020 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27449 - Posted: 09.05.2020

By Esther Landhuis A researcher slips stickers under some colored cups on a lazy Susan, then gives the tray a whirl. When the spinning stops, a preschooler must find the hidden stickers. Most children remember where the stickers are, but a few have to check every single cup. The game tests working memory, which is among the set of mental skills known as executive function that can be impaired in children who faced trauma early in life. Adversity wreaks havoc, and from there, “you have a system that responds differently,” says Megan Gunnar, a developmental psychobiologist at the University of Minnesota in Minneapolis who has spent two decades studying the impact of early-life adversity in adopted children. The focus of this work is extreme adversity, such as being orphaned, rather than everyday challenges, which might teach beneficial resilience. A childhood characterized by hardship, negligence or abuse can also alter the neuroendocrine system that regulates how the body responds to stress. Problems in the stress response can set kids on a path toward behavior struggles along with increased risk for depression, diabetes and a host of other health problems. But recent studies offer hints that such a difficult future may not be inevitable. As Gunnar and others have shown, impaired stress responses can return to normal during puberty, raising the possibility that imbalances created by early trauma can be erased. The research is prompting a new view of puberty as an opportunity — a chance for people who had a shaky start to reset their physiological responses to stress. © Society for Science & the Public 2000–2020.

Keyword: Stress; Development of the Brain
Link ID: 27441 - Posted: 08.29.2020

by Jonathan Moens Conversations between an autistic and a typical person involve less smiling and more mismatched facial expressions than do interactions between two typical people, a new study suggests1. People engaged in conversation tend to unconsciously mimic each other’s behavior, which may help create and reinforce social bonds. But this synchrony can break down between autistic people and their neurotypical peers, research shows. And throughout an autistic person’s life, these disconnects can lead to fewer opportunities to meet people and maintain relationships. Previous studies have looked at autistic people’s facial expressions as they react to images of social scenes on a computer screen2. The new work, by contrast, is one of a growing number of experiments to capture how facial expressions unfold during ordinary conversation. Changes in facial expressions are easy to observe but notoriously hard to measure, says lead investigator John Herrington, assistant professor of psychiatry at the Children’s Hospital of Philadelphia in Pennsylvania. He and his colleagues devised a new method to quantify these changes over time in an automated and granular way using machine-learning techniques. Atypical facial expressions are in part a manifestation of difficulties with social coordination, Herrington says. So tracking alterations in facial expression may be a useful way to monitor whether interventions targeting these traits are effective. The new study included 20 autistic people and 16 typical controls, aged 9 to 16 years and matched for their scores on intelligence and verbal fluency. Each participant engaged in two 10-minute conversations — first with their mother and then with a research assistant — to plan a hypothetical two-week trip. © 2020 Simons Foundation

Keyword: Autism; Emotions
Link ID: 27440 - Posted: 08.29.2020

by Nicholette Zeliadt An experimental drug prevents seizures and death in a mouse model of Dravet syndrome, a severe form of epilepsy that is related to autism, researchers reported 18 October 2019. The drug works by silencing a DNA segment called a ‘poison exon’ and is expected to enter clinical trials next year. If it works, it offers hope for treating not just Dravet, but other forms of autism as well: Another team has identified a poison exon in SYNGAP1, an autism gene that also causes epilepsy. Poison exons seem to impede the production of certain crucial proteins; blocking these segments would restore normal levels of the proteins. “The beauty of the technology,” says Gemma Carvill, assistant professor of neurology and pharmacology at Northwestern University in Chicago, Illinois, “is that “any gene that has a poison exon is potentially a target.” Several teams presented unpublished work on poison exons in a standing-room-only session at the 2019 American Society of Human Genetics meeting in Houston, Texas. People with Dravet often have autism, and most die in childhood2. The syndrome typically stems from mutations in a gene called SCN1A, which encodes an essential sodium channel in neurons. Only about 25 percent of mice with mutations in SCN1A live beyond 30 days of age. The new drug consists of short strands of ‘antisense’ RNA that restore normal levels of the channel, said Lori Isom of the University of Michigan, who presented the work. And all but 1 of 33 mice that received a single injection of the drug at 2 days of age remained alive 88 days later. © 2020 Simons Foundation

Keyword: Epilepsy; Autism
Link ID: 27437 - Posted: 08.29.2020

Although the number of people with dementia continues to increase, the rate of growth has declined by 13 percent in each of the past three decades. The brain disorder currently affects nearly 50 million people worldwide and nearly 6 million in the United States. The new finding, reported by Harvard researchers in the journal Neurology, suggests that the number of people developing dementia in coming years may be less than expected. Nonetheless, that number — known as the prevalence of dementia — is expected to triple in the next 30 years, growing to more than 150 million people worldwide, due in large part to increases in life expectancy and population size. Dementia, which involves deterioration in memory, thinking and behavior beyond what is considered a normal part of aging, includes but is not limited to Alzheimer’s disease, which accounts for 60 to 70 percent of dementia cases. The researchers cited a “somewhat stronger” decline in the rate of growth — referred to as the incidence rate — among men than women (24 percent vs. 8 percent). They projected that, if the trend continues, it is possible that up to 60 million fewer people than expected would develop dementia worldwide by 2040. The researchers did not determine underlying causes of the decline in incidence, but they did note that improvements in lifestyle overall — as well as better control of blood pressure and cardiovascular issues — may have contributed to the decline. Their research was based on data from seven long-term studies, involving 49,202 people 65 and older from six countries in Europe and North America, including the United States. But the database included only people of European ancestry, and other research has found stable or increasing rates of dementia diagnoses in other ethnic and geographic regions. — Linda Searing

Keyword: Alzheimers
Link ID: 27432 - Posted: 08.26.2020

by Angie Voyles Askham A new study pinpoints genes and cell types that may account for the atypical brain structure in people with genetic conditions related to autism1. The work offers insight into how the brain develops differently in people with these conditions and identifies new potential therapeutic targets, says Mallar Chakravarty, associate professor of psychiatry at McGill University in Montreal. Chakravarty has collaborated with the researchers previously but was not involved in the new work. The analysis considered people with six genetic conditions associated with atypical brain development, including syndromes associated with deletions in the chromosomal regions 11p13 and 22q11.2, both of which increase the likelihood of autism2. “We used known genetic conditions as a kind of foothold into the complex biology of neurodevelopmental disorders,” says lead researcher Armin Raznahan, chief of the Developmental Neurogenomics section at the U.S. National Institute of Mental Health intramural research program. Previous studies of mice with autism-linked genetic conditions have shown that brain structure changes tend to crop up in regions where the relevant genes are ordinarily expressed3. The same holds true for people, Raznahan and his colleagues found after comparing measurements from brain scans with existing data from postmortem brains. “It’s wildly creative,” Chakravarty says of the method. Raznahan and his colleagues used magnetic resonance imaging to scan the brains of 231 adolescents and adults with one of the six genetic conditions and 287 controls. Each of the six conditions results from a deletion or duplication of a chromosome or set of genes within a chromosome. © 2020 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27430 - Posted: 08.22.2020

When it comes to brain cells, one size does not fit all. Neurons come in a wide variety of shapes, sizes, and contain different types of brain chemicals. But how did they get that way? A new study in Nature suggests that the identities of all the neurons in a worm are linked to unique members of a single gene family that control the process of converting DNA instructions into proteins, known as gene expression. The results of this study could provide a foundation for understanding how nervous systems have evolved in many other animals, including humans. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The central nervous systems of all animals, from worms to humans, are incredibly intricate and highly ordered. The generation and diversity of a plethora of neuronal cell types is driven by gene expression,” said Robert Riddle, Ph.D., program director at NINDS. “So, it is surprising and exciting to consider that the cell diversity we see in the entire nervous system could come from a just a single group of genes.” Researchers led by Oliver Hobert, Ph.D., professor of biochemistry and molecular biophysics at Columbia University in New York City and graduate student Molly B. Reilly, wanted to know how brain cells in the C. elegans worm got their various shapes and functions. For these experiments, the researchers used a genetically engineered worm in which individual neurons were color coded. In addition, coding sequences for green fluorescence protein were inserted into homeobox genes, a highly conserved set of genes known to play fundamental roles in development. Homeobox gene expression patterns were determined by examining the patterns of the glowing fluorescent marker.

Keyword: Development of the Brain; Brain imaging
Link ID: 27428 - Posted: 08.20.2020

Alison Abbott Two years ago, Jennifer Li and Drew Robson were trawling through terabytes of data from a zebrafish-brain experiment when they came across a handful of cells that seemed to be psychic. The two neuroscientists had planned to map brain activity while zebrafish larvae were hunting for food, and to see how the neural chatter changed. It was their first major test of a technological platform they had built at Harvard University in Cambridge, Massachusetts. The platform allowed them to view every cell in the larvae’s brains while the creatures — barely the size of an eyelash — swam freely in a 35-millimetre-diameter dish of water, snacking on their microscopic prey. Out of the scientists’ mountain of data emerged a handful of neurons that predicted when a larva was next going to catch and swallow a morsel. Some of these neurons even became activated many seconds before the larva fixed its eyes on the prey1. Something else was strange. Looking in more detail at the data, the researchers realized that the ‘psychic’ cells were active for an unusually long time — not seconds, as is typical for most neurons, but many minutes. In fact, more or less the duration of the larvae’s hunting bouts. “It was spooky,” says Li. “None of it made sense.” Li and Robson turned to the literature and slowly realized that the cells must be setting an overall ‘brain state’ — a pattern of prolonged brain activity that primed the larvae to engage with the food in front of them. The pair learnt that, in the past few years, other scientists using various approaches and different species had also found internal brain states that alter how an animal behaves, even when nothing has changed in its external environment. © 2020 Springer Nature Limited

Keyword: Attention; Learning & Memory
Link ID: 27417 - Posted: 08.12.2020

By Chimamanda Ngozi Adichie My daughter and I were playing tag, or a kind of tag. Before that, we traced the letter P and we danced to James Brown’s “I feel good,” a song she selected from the iPod. We laughed as we danced, she with a natural rhythm striking for a 4-year-old, and I with my irretrievable gracelessness. Next on our plan was “Sesame Street.” It was about 2 p.m. on May 28. A day complacent with the promise of no surprises, like all the other days of the lockdown, shrunken days with shriveled routines. “When coronavirus is over,” my daughter often said, words filled with yearning for her preschool, her friends, her swimming lessons. And I, amid snatches of joy and discovery, often felt bored, and then guilty for feeling boredom, in this expanded boundless role of parent-playmate. My daughter picked up a green balloon pump, squirted the air at me, and ran off, around the kitchen counter. When I caught her, squealing, it was her turn to chase me. I was wearing white slippers, from some hotel somewhere, back when international travel was normal. They felt soft and thin-soled. I recall all these clearly, because of all the things I will be unable to recall later. I turned away from the kitchen to make the chase longer and something happened. I slipped or I tripped or my destiny thinned and I fell and hit my head on the hardwood floor. At the beginning of the stay-at-home order, plagued by amorphous anxieties, I taught my daughter how to call my doctor husband at work. Just in case. My daughter says that after I fell I told her, “Call Papa.” My husband says I spoke coherently. I told him that I fell and that the pain in my head was “excruciating,” and when I said “excruciating,” I seemed to wince. He says he asked my daughter to get me the ice pack in the freezer and that I said, “Thank you, baby,” when she gave it to me. I do not remember any of this.

Keyword: Learning & Memory; Brain Injury/Concussion
Link ID: 27412 - Posted: 08.11.2020

By Simon Makin New research could let scientists co-opt biology's basic building block—the cell—to construct materials and structures within organisms. A study, published in March in Science and led by Stanford University psychiatrist and bioengineer Karl Deisseroth, shows how to make specific cells produce electricity-carrying (or blocking) polymers on their surfaces. The work could someday allow researchers to build large-scale structures within the body or improve brain interfaces for prosthetic limbs. In the medium term, the technique may be useful in bioelectric medicine, which involves delivering therapeutic electrical pulses. Researchers in this area have long been interested in incorporating polymers that conduct or inhibit electricity without damaging surrounding tissues. Stimulating specific cells—to intervene in a seizure, for instance—is much more precise than flooding the whole organism with drugs, which can cause broad side effects. But current bioelectric methods, such as those using electrodes, still affect large numbers of cells indiscriminately. The new technique uses a virus to deliver genes to desired cell types, instructing them to produce an enzyme (Apex2) on their surface. The enzyme sparks a chemical reaction between precursor molecules and hydrogen peroxide, infused in the space between cells; this reaction causes the precursors to fuse into a polymer on the targeted cells. “What's new here is the intertwining of various emerging fields in one application,” says University of Florida biomedical engineer Kevin Otto, who was not involved in the research but co-authored an accompanying commentary in Science. “The use of conductive polymers assembled [inside living tissue] through synthetic biology, to enable cell-specific interfacing, is very novel.” © 2020 Scientific American

Keyword: Development of the Brain; Epigenetics
Link ID: 27411 - Posted: 08.11.2020

by Laura Dattaro Extra repeating bits of DNA may account for nearly 3 percent of the genetic architecture of autism, according to a new study1. The work is the first to examine such genetic variants in autism on a large scale. About half of the identified repeating sections occur in genes that have not been previously linked to autism, suggesting new lines of inquiry for geneticists. “These genes are involved in autism, absolutely,” says study investigator Steve Scherer, professor of medicine at the University of Toronto in Canada. “Those [genes] will become diagnostic tests for the autism screening panel.” The researchers looked at areas of the genome with tandem repeats — stretches of 2 to 20 nucleotides, which are the ‘building blocks’ of DNA, that are repeated two or more times in one spot. These repeats can expand when they are passed down from parents to children: If a nucleotide, or combination of them, is repeated 10 times in a parents’ DNA, it may be repeated hundreds of times in their child, for example. The more a repeat expands, the more likely it is that it will disrupt the gene’s function. Some specific repeats are already associated with autism: About 5 percent of autistic people have fragile X syndrome, which is nearly always caused by the expansion of a particular repeat in the FMR1 gene. But less than a quarter of people with autism have a known genetic cause, even though twin studies suggest that autism is highly heritable2. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27410 - Posted: 08.11.2020

By Gina Kolata Despite the lack of effective treatments or preventive strategies, the dementia epidemic is on the wane in the United States and Europe, scientists reported on Monday. The risk for a person to develop dementia over a lifetime is now 13 percent lower than it was in 2010. Incidence rates at every age have steadily declined over the past quarter-century. If the trend continues, the paper’s authors note, there will be 15 million fewer people in Europe and the United States with dementia than there are now. The study is the most definitive yet to document a decline in dementia rates. Its findings counter warnings from advocacy groups of a coming tsunami of Alzheimer’s disease, the most common form of dementia, said Dr. John Morris, director of the Center for Aging at Washington University in St. Louis. It is correct that there are now more people than ever with dementia, but that is because there are more and more older people in the population. The new incidence data are “hopeful,” Dr. Morris said. “It is such a strong study and such a powerful message. It suggests that the risk is modifiable.” Researchers at Harvard University in Cambridge, Mass., reviewed data from seven large studies with a total of 49,202 individuals. The studies followed men and women aged 65 and older for at least 15 years, and included in-person exams and, in many cases, genetic data, brain scans and information on participants’ risk factors for cardiovascular disease. The data also include a separate assessment of Alzheimer’s disease. Its incidence, too, has steadily fallen, at a rate of 16 percent per decade, the researchers found. Their study was published in the journal Neurology. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27404 - Posted: 08.06.2020

by Chloe Williams A new atlas lays bare how neuronal connections, or synapses, change from birth to old age in mice1. The ‘synaptome’ may help researchers investigate how mutations linked to autism affect these connections at different stages of life. Synapses are the junctions where information is transferred between cells, and they are integral to functions such as learning, behavior and movement. Autism is linked to several mutations that alter synaptic proteins. In 2018, researchers created the first synaptome of the mouse brain, mapping billions of synapses and sorting them into types based on their size, shape and composition2. The map revealed that synapse subtypes have distinct distributions in the brain, suggesting they have specific functions. This synaptome mapped the mouse brain only at one point in time, however. In the new work, the team charted five billion synapses in mice at 10 different ages, revealing how synapses change in number, structure and molecular makeup throughout life. “It’s the first time anybody’s ever done that in any species,” says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland, who led the research. To create the atlas, the team engineered mice to express fluorescent markers of different colors on two proteins — PSD95 and SAP102 — that frequently line the signal-receiving end of excitatory synapses, which make up the preponderance of synapses in the brain. Mutations in these proteins have been linked to autism, schizophrenia and intellectual disability. © 2020 Simons Foundation

Keyword: Development of the Brain
Link ID: 27402 - Posted: 08.06.2020

Nicola Davis Excessive drinking, exposure to air pollution and head injuries all increase dementia risk, experts say in a report revealing that up to 40% of dementia cases worldwide could be delayed or prevented by addressing 12 such lifestyle factors. Around 50 million people around the world live with dementia, including about 850,000 people in the UK. By 2040, it has been estimated there will be more than 1.2 million people living with dementia in England and Wales. There is currently no cure. However, while some risk factors for dementia cannot be changed, for example particular genes or ethnicity, many are down to lifestyle. “Dementia is potentially preventable – you can do things to reduce your risk of dementia, whatever stage of life you are at,” said Gill Livingston, professor of psychiatry of older people at University College London and a co-author of the report. She added such lifestyle changes could reduce the chances of developing dementia in both those with and without a high genetic risk for such conditions. The report from the Lancet Commission on dementia prevention, intervention and care builds on previous work revealing that about a third of dementia cases could be prevented by addressing nine lifestyle factors, including midlife hearing loss, depression, less childhood education and smoking. The research weighs up the latest evidence, largely from high-income countries, supporting the addition of a further three risk factors to the list. It suggests that 1% of dementia cases worldwide are attributable to excessive mid-life alcohol intake, 3% to mid-life head injuries and 2% a result of exposure to air pollution in older age – although they caution that the latter could be an underestimate. © 2020 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 27394 - Posted: 07.31.2020