Chapter 13. Memory and Learning

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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

Keyword: Alzheimers
Link ID: 29193 - Posted: 03.16.2024

By Meghan Rosen Leakiness in the brain could explain the memory and concentration problems linked to long COVID. In patients with brain fog, MRI scans revealed signs of damaged blood vessels in their brains, researchers reported February 22 in Nature Neuroscience. In these people, dye injected into the bloodstream leaked into their brains and pooled in regions that play roles in language, memory, mood and vision. It’s the first time anyone’s shown that long COVID patients can have leaky blood brain barriers, says study coauthor Matthew Campbell, a geneticist at Trinity College Dublin in Ireland. That barrier, tightly knit cells lining blood vessels, typically keeps riffraff out of the brain, like bouncers guarding a nightclub. If the barrier breaks down, bloodborne viruses, cells and other interlopers can sneak into the brain’s tissues and wreak havoc, says Avindra Nath, a neurologist at the National Institutes of Health in Bethesda, Md. It’s too early to say definitively whether that’s happening in people with long COVID, but the new study provides evidence that “brain fog has a biological basis,” says Nath, who wasn’t involved with the work. That alone is important for patients, he says, because their symptoms may be otherwise discounted by physicians. For some people, brain fog can feel like a slowdown in thinking or difficulty recalling short-term memories, Campbell says. For example, “patients will go for a drive, and forget where they’re driving to.” That might sound trivial, he says, but it actually pushes people into panic mode. © Society for Science & the Public 2000–2024.

Keyword: Attention; Learning & Memory
Link ID: 29192 - Posted: 03.16.2024

By Ellen Barry Twins are a bonanza for research psychologists. In a field perpetually seeking to tease out the effects of genetics, environment and life experience, they provide a natural controlled experiment as their paths diverge, subtly or dramatically, through adulthood. Take Dennis and Douglas. In high school, they were so alike that friends told them apart by the cars they drove, they told researchers in a study of twins in Virginia. Most of their childhood experiences were shared — except that Dennis endured an attempted molestation when he was 13. At 18, Douglas married his high school girlfriend. He raised three children and became deeply religious. Dennis cycled through short-term relationships and was twice divorced, plunging into bouts of despair after each split. By their 50s, Dennis had a history of major depression, and his brother did not. Why do twins, who share so many genetic and environmental inputs, diverge as adults in their experience of mental illness? On Wednesday, a team of researchers from the University of Iceland and Karolinska Institutet in Sweden reported new findings on the role played by childhood trauma. Their study of 25,252 adult twins in Sweden, published in JAMA Psychiatry, found that those who reported one or more trauma in childhood — physical or emotional neglect or abuse, rape, sexual abuse, hate crimes or witnessing domestic violence — were 2.4 times as likely to be diagnosed with a psychiatric illness as those who did not. If a person reported one or more of these experiences, the odds of being diagnosed with a mental illness climbed sharply, by 52 percent for each additional adverse experience. Among participants who reported three or more adverse experiences, nearly a quarter had a psychiatric diagnosis of depressive disorder, anxiety disorder, substance abuse disorder or stress disorder. © 2024 The New York Times Company

Keyword: Depression; Genes & Behavior
Link ID: 29184 - Posted: 03.07.2024

By Laura Dattaro Steven McCarroll just wanted to compare how different cell types express genes in people with and without schizophrenia. But when he sequenced the transcriptomes of more than 1 million cortical cells from 191 postmortem brains, what leapt out from the data went far beyond his simple case-control comparison: Astrocytes and neurons from all of the brains coordinate their expression of certain genes needed for healthy synapses, a relationship the team dubbed the Synaptic Neuron-and-Astrocyte Program (SNAP) and described in a paper published in Nature today. “The data led us to something much more exciting and surprising than what we set out to do,” says McCarroll, professor of biomedical science and genetics at Harvard Medical School. SNAP is an intricate dance, McCarroll and his colleagues found: The more a person’s neurons express synaptic genes, so too do their astrocytes, but this coordination wanes in older people and those with schizophrenia. Because astrocytes — a type of glial cell — and neurons are in constant communication and the findings are correlational, it’s unclear which cell type choreographs this dance. But other evidence suggests that astrocytes take the lead, says Stephen Quake, professor of bioengineering at Stanford University, who was not involved in McCarroll’s work. In mice trained to fear a foot shock, for example, neurons involved in memory formation express neurotensin, whereas astrocytes express a receptor for it, Quake and his colleagues reported last month in Nature. But when they inhibited the animals’ astrocytes during fear training, the mice performed worse on memory tests, suggesting those cells play an active role in long-term memory formation, Quake says — and govern the relationship McCarroll found. © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29183 - Posted: 03.07.2024

By Veronique Greenwood It can be hard to tell, at first, when a cell is on the verge of self-destruction. It appears to be going about its usual business, transcribing genes and making proteins. The powerhouse organelles called mitochondria are dutifully churning out energy. But then a mitochondrion receives a signal, and its typically placid proteins join forces to form a death machine. They slice through the cell with breathtaking thoroughness. In a matter of hours, all that the cell had built lies in ruins. A few bubbles of membrane are all that remains. “It’s really amazing how fast, how organized it is,” said Aurora Nedelcu, an evolutionary biologist at the University of New Brunswick who has studied the process in algae. Apoptosis, as this process is known, seems as unlikely as it is violent. And yet some cells undergo this devastating but predictable series of steps to kill themselves on purpose. When biologists first observed it, they were shocked to find self-induced death among living, striving organisms. And although it turned out that apoptosis is a vital creative force for many multicellular creatures, to a given cell it is utterly ruinous. How could a behavior that results in a cell’s sudden death evolve, let alone persist? The tools for apoptosis, molecular biologists have found, are curiously widespread. And as they have sought to understand its molecular process and origins, they’ve found something even more surprising: Apoptosis can be traced back to ancient forms of programmed cell death undertaken by single-celled organisms — even bacteria — that seem to have evolved it as a social behavior. © 2024 the Simons Foundation.

Keyword: Apoptosis; Development of the Brain
Link ID: 29181 - Posted: 03.07.2024

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.

Keyword: Alzheimers; Learning & Memory
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

Keyword: Alzheimers
Link ID: 29177 - Posted: 03.05.2024

By Erica Goode Authors don’t get to choose what’s going on in the world when their books are published. More than a few luckless writers ended up with a publication date of Sept. 11, 2001, or perhaps Nov. 8, 2016, the day Donald Trump was elected. But Charan Ranganath, the author of “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,”was more fortunate. His book went on sale last month, not long after the Department of Justice released a report describing President Joe Biden as an “elderly man with a poor memory” who, in interviews, was “struggling to remember events,” including the year that his son Beau died. BOOK REVIEW — “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,” by Charan Ranganath (Doubleday, 304 pages). The special counsel’s report immediately became a topic of intense discussion — disputed by the White House, seized on by many Republicans, analyzed by media commentators, and satirized by late-night television hosts. But for Ranganath, a psychologist and neuroscientist at the University of California, Davis, who for decades has been studying the workings of memory, the report’s release was a stroke of luck. His book, which dispels many widespread but wrongheaded assumptions about memory — including some to which that special counsel Robert K. Hur appears to subscribe — could easily have been written as a corrective response. If Ranganath has a central message, it is that we are far too concerned about forgetting. Memory does not work like a recording device, preserving everything we have heard, seen, said, and done. Not remembering names or exact dates; having no recollection of the details of a conversation; being unable to recall where you left your glasses or your keys; or watching movies you saw in the past as if you are seeing them for the first time — these are not the symptoms of a failing brain.

Keyword: Learning & Memory
Link ID: 29172 - Posted: 03.02.2024

By Pam Belluck Long Covid may lead to measurable cognitive decline, especially in the ability to remember, reason and plan, a large new study suggests. Cognitive testing of nearly 113,000 people in England found that those with persistent post-Covid symptoms scored the equivalent of 6 I.Q. points lower than people who had never been infected with the coronavirus, according to the study, published Wednesday in The New England Journal of Medicine. People who had been infected and no longer had symptoms also scored slightly lower than people who had never been infected, by the equivalent of 3 I.Q. points, even if they were ill for only a short time. The differences in cognitive scores were relatively small, and neurological experts cautioned that the results did not imply that being infected with the coronavirus or developing long Covid caused profound deficits in thinking and function. But the experts said the findings are important because they provide numerical evidence for the brain fog, focus and memory problems that afflict many people with long Covid. “These emerging and coalescing findings are generally highlighting that yes, there is cognitive impairment in long Covid survivors — it’s a real phenomenon,” said James C. Jackson, a neuropsychologist at Vanderbilt Medical Center, who was not involved in the study. He and other experts noted that the results were consistent with smaller studies that have found signals of cognitive impairment. The new study also found reasons for optimism, suggesting that if people’s long Covid symptoms ease, the related cognitive impairment might, too: People who had experienced long Covid symptoms for months and eventually recovered had cognitive scores similar to those who had experienced a quick recovery, the study found. © 2024 The New York Times Company

Keyword: Attention; Learning & Memory
Link ID: 29171 - Posted: 02.29.2024

Terry Gross When cognitive neuroscientist Charan Ranganath meets someone for the first time, he's often asked, "Why am I so forgetful?" But Ranganath says he's more interested in what we remember, rather than the things we forget. "We're not designed to carry tons and tons of junk with us. I don't know that anyone would want to remember every temporary password that they've ever had," he says. "I think what [the human brain is] designed for is to carry what we need and to deploy it rapidly when we need it." Ranganath directs the Dynamic Memory Lab at the University of California, Davis, where he's a professor of psychology and neuroscience. In the new book, Why We Remember, he writes about the fundamental mechanisms of memory — and why memories often change over time. Sponsor Message Ranganath recently wrote an op-ed for The New York Times in which he reflected on President Biden's memory gaffes — and the role that memory plays in the current election cycle. "I'm just not in the position to say anything about the specifics of [either Biden or Trump's] memory problems," he says. "This is really more of an issue of people understanding what happens with aging. And, one of the nice things about writing this editorial is I got a lot of feedback from people who felt personally relieved by this because they're worried about their own memories." I think it would be a good idea to have a comprehensive physical and mental health evaluation that's fairly transparent. We certainly have transparency or seek transparency about other things like a candidate's finances, for instance. And obviously health is a very important factor. And I think at the end of the day, we'll still be in a position of saying, "OK, what's enough? What's the line between healthy and unhealthy?" But I think it's important to do because yes, as we get older we do have memory problems. ... © 2024 npr

Keyword: Learning & Memory; Development of the Brain
Link ID: 29166 - Posted: 02.27.2024

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.

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
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

Keyword: Alzheimers; Neuroimmunology
Link ID: 29160 - Posted: 02.25.2024

By Tina Hesman Saey One particular retrovirus — embedded in the DNA of jawed vertebrates — helps turn on production of a protein needed to insulate nerve fibers, researchers report February 15 in Cell. Such insulation, called myelin, may have helped make speedy thoughts and complex brains possible. The retrovirus trick was so handy, in fact, that it showed up many times in the evolution of vertebrates with jaws, the team found. Retroviruses — also known as jumping genes or retrotransposons — are RNA viruses that make DNA copies of themselves to embed in a host’s DNA. Scientists once thought of remnants of ancient viruses as genetic garbage, but that impression is changing, says neuroscientist Jason Shepherd, who was not involved in the study. “We’re finding more and more that these retrotransposons and retroviruses have influenced the evolution of life on the planet,” says Shepherd, of the University of Utah Spencer Fox Eccles School of Medicine in Salt Lake City. Remains of retroviruses were already known to have aided the evolution of the placenta, the immune system and other important milestones in human evolution (SN: 5/16/17). Now, they’re implicated in helping to produce myelin. Myelin is a coating of fat and protein that encases long nerve fibers known as axons. The coating works a bit like the insulation around an electrical wire: Nerves sheathed in myelin can send electrical signals faster than uninsulated nerves can. © Society for Science & the Public 2000–2024.

Keyword: Glia; Evolution
Link ID: 29154 - Posted: 02.20.2024

By Matt Richtel Growing numbers of children and adolescents are being prescribed multiple psychiatric drugs to take simultaneously, according to a new study by researchers at the University of Maryland. The phenomenon is increasing despite warnings that psychotropic drug combinations in young people have not been tested for safety or studied for their impact on the developing brain. The study, published Friday in JAMA Open Network, looked at the prescribing patterns among patients 17 or younger enrolled in Medicaid from 2015 to 2020 in a single U.S. state that the researchers declined to name. In this group, there was a 9.5 percent increase in the prevalence of “polypharmacy,” which the study defined as taking three or more different classes of psychiatric medications, including antidepressants, mood-stabilizing anticonvulsants, sedatives and drugs for A.D.H.D. and anxiety drugs. The study looked at only one state, but state data have been used in the past to explore this issue, in part because of the relative ease of gathering data from Medicaid, the health insurance program administered by states. At the same time, some research using nationally weighted samples have revealed the increasing prevalence of polypharmacy among young people. One recent paper drew data from the National Ambulatory Medical Care Survey and found that in 2015, 40.7 percent of people aged 2 to 24 in the United States who took a medication for A.D.H.D. also took a second psychiatric drug. That figure had risen from 26 percent in 2006. The latest data from the University of Maryland researchers show that, at least in one state, the practice continues to grow and “was significantly more likely among youths who were disabled or in foster care,” the new study noted. Mental health experts said that psychotropic medications can prove very helpful and that doctors have discretion to prescribe what they see fit. A concern among some experts is that many drugs used in frequently prescribed cocktails have not been approved for use in young people. And it is unclear how the simultaneous use of multiple psychotropic medications affects brain development long-term. © 2024 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 29152 - Posted: 02.20.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024

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

Keyword: Alzheimers
Link ID: 29146 - Posted: 02.13.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024

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

Keyword: Alzheimers
Link ID: 29138 - Posted: 02.08.2024

By David Marchese Our memories form the bedrock of who we are. Those recollections, in turn, are built on one very simple assumption: This happened. But things are not quite so simple. “We update our memories through the act of remembering,” says Charan Ranganath, a professor of psychology and neuroscience at the University of California, Davis, and the author of the illuminating new book “Why We Remember.” “So it creates all these weird biases and infiltrates our decision making. It affects our sense of who we are.” Rather than being photo-accurate repositories of past experience, Ranganath argues, our memories function more like active interpreters, working to help us navigate the present and future. The implication is that who we are, and the memories we draw on to determine that, are far less fixed than you might think. “Our identities,” Ranganath says, “are built on shifting sand.” What is the most common misconception about memory? People believe that memory should be effortless, but their expectations for how much they should remember are totally out of whack with how much they’re capable of remembering.1 Another misconception is that memory is supposed to be an archive of the past. We expect that we should be able to replay the past like a movie in our heads. The problem with that assumption is that we don’t replay the past as it happened; we do it through a lens of interpretation and imagination. Semantic memory is the term for the memory of facts and knowledge about the world. standpoint? It’s exceptionally hard to answer the question of how much we can remember. What I’ll say is that we can remember an extraordinary amount of detail that would make you feel at times as if you have a photographic memory. We’re capable of these extraordinary feats. I would argue that we’re all everyday-memory experts, because we have this exceptional semantic memory, which is the scaffold for episodic memory. I know it sounds squirmy to say, “Well, I can’t answer the question of how much we remember,” but I don’t want readers to walk away thinking memory is all made up. © 2024 The New York Times Company

Keyword: Learning & Memory
Link ID: 29134 - Posted: 02.06.2024

By Sabrina Malhi Researchers have found a possible link between the common hormone disorder PCOS and cognitive decline later in life. PCOS, which stands for polycystic ovary syndrome, is the most common endocrine disorder among women ages 15 to 44. However, it is often underdiagnosed because many of its symptoms, including abnormal menstrual cycles and excess hair, can be attributed to other causes. The syndrome was first described in 1935 by American gynecologists Irving F. Stein and Michael L. Leventhal. They published a paper documenting a group of women with lack of periods, excess body hair and enlarged ovaries with multiple cysts. Their work helped identify and characterize PCOS as it is known today. Health experts hypothesize that genetic factors could contribute to the development of the condition, but the exact causes are still unknown. Here’s what to know about PCOS and its potential link to cognitive health. PCOS is a chronic hormonal disorder characterized by overproduction of androgens, which are typically considered male hormones. High androgen levels can lead to irregular menstrual cycles and fertility issues when excessively produced in women. In the United States, 6 to 12 percent of people assigned female at birth who are of reproductive age are affected by PCOS, according to data from the Centers for Disease Control and Prevention. The condition is associated with an increased risk of obesity, high blood pressure, high cholesterol and endometrial cancer. PCOS is also often linked to insulin resistance, which can result in elevated blood sugar levels and an escalated risk of Type 2 diabetes. The condition can contribute to various metabolic issues, including high blood pressure, excess abdominal fat, and abnormal cholesterol or triglyceride levels. People with PCOS face an elevated risk of developing cardiovascular problems, such as high blood pressure, high cholesterol levels and an increased risk of heart disease. A recent study in the journal Neurology found that people with PCOS performed lower than normal on a suite of cognitive tests.

Keyword: Hormones & Behavior; Learning & Memory
Link ID: 29132 - Posted: 02.06.2024