Chapter 13. Memory and Learning

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Anil Ananthaswamy In the winter of 2011, Daniel Yamins, a postdoctoral researcher in computational neuroscience at the Massachusetts Institute of Technology, would at times toil past midnight on his machine vision project. He was painstakingly designing a system that could recognize objects in pictures, regardless of variations in size, position and other properties — something that humans do with ease. The system was a deep neural network, a type of computational device inspired by the neurological wiring of living brains. “I remember very distinctly the time when we found a neural network that actually solved the task,” he said. It was 2 a.m., a tad too early to wake up his adviser, James DiCarlo, or other colleagues, so an excited Yamins took a walk in the cold Cambridge air. “I was really pumped,” he said. It would have counted as a noteworthy accomplishment in artificial intelligence alone, one of many that would make neural networks the darlings of AI technology over the next few years. But that wasn’t the main goal for Yamins and his colleagues. To them and other neuroscientists, this was a pivotal moment in the development of computational models for brain functions. DiCarlo and Yamins, who now runs his own lab at Stanford University, are part of a coterie of neuroscientists using deep neural networks to make sense of the brain’s architecture. In particular, scientists have struggled to understand the reasons behind the specializations within the brain for various tasks. They have wondered not just why different parts of the brain do different things, but also why the differences can be so specific: Why, for example, does the brain have an area for recognizing objects in general but also for faces in particular? Deep neural networks are showing that such specializations may be the most efficient way to solve problems. All Rights Reserved © 2020

Keyword: Learning & Memory
Link ID: 27562 - Posted: 10.31.2020

Jon Hamilton If you fall off a bike, you'll probably end up with a cinematic memory of the experience: the wind in your hair, the pebble on the road, then the pain. That's known as an episodic memory. And now researchers have identified cells in the human brain that make this sort of memory possible, a team reports in the journal Proceedings of the National Academy of Sciences. The cells are called time cells, and they place a sort of time stamp on memories as they are being formed. That allows us to recall sequences of events or experiences in the right order. "By having time cells create this indexing across time, you can put everything together in a way that makes sense," says Dr. Bradley Lega, the study's senior author and a neurosurgeon at the University of Texas Southwestern Medical Center in Dallas. Time cells were discovered in rodents decades ago. But the new study is critical because "the final arbitrator is always the human brain," says Dr. György Buzsáki, Biggs Professor of Neuroscience at New York University. Buzsáki is not an author of the study but did edit the manuscript. Lega and his team found the time cells by studying the brains of 27 people who were awaiting surgery for severe epilepsy. As part of their pre-surgical preparation, these patients had electrodes placed in the hippocampus and another area of the brain involved in navigation, memory and time perception. In the experiment, the patients studied sequences of 12 or 15 words that appeared on a laptop screen during a period of about 30 seconds. Then, after a break, they were asked to recall the words they had seen. © 2020 npr

Keyword: Learning & Memory
Link ID: 27561 - Posted: 10.31.2020

By Laura Sanders Nearly 2,000 years ago, a cloud of scorching ash from Mount Vesuvius buried a young man as he lay on a wooden bed. That burning ash quickly cooled, turning some of his brain to glass. This confluence of events in A.D. 79 in the town of Herculaneum, which lay at the western base of the volcano, preserved the usually delicate neural tissue in a durable, glassy form. New scrutiny of this tissue has revealed signs of nerve cells with elaborate tendrils for sending and receiving messages, scientists report October 6 in PLOS ONE. That the young man once possessed these nerve cells, or neurons, is no surprise; human brains are packed with roughly 86 billion neurons (SN: 8/7/19). But samples from ancient brains are sparse. Those that do exist have become a soaplike substance or mummified, says Pier Paolo Petrone, a biologist and forensic anthropologist at the University of Naples Federico II in Italy. But while studying the Herculaneum site, Petrone noticed something dark and shiny inside this man’s skull. He realized that those glassy, black fragments “had to be the remains of the brain.” Petrone and colleagues used scanning electron microscopy to study glassy remains from both the man’s brain and spinal cord. The researchers saw tubular structures as well as cell bodies that were the right sizes and shapes to be neurons. In further analyses, the team found layers of tissue wrapped around tendrils in the brain tissue. This layering appears to be myelin, a fatty substance that speeds signals along nerve fibers. The preserved tissue was “something really astonishing and incredible,” Petrone says, because the conversion of objects to glass, a process called vitrification, is relatively rare in nature. “This is the first ever discovery of ancient human brain remains vitrified by hot ash during a volcanic eruption.” © Society for Science & the Public 2000–2020.

Keyword: Development of the Brain
Link ID: 27558 - Posted: 10.31.2020

By Abby Goodnough PHILADELPHIA — Steven Kelty had been addicted to crack cocaine for 32 years when he tried a different kind of treatment last year, one so basic in concept that he was skeptical. He would come to a clinic twice a week to provide a urine sample, and if it was free of drugs, he would get to draw a slip of paper out of a fishbowl. Half contained encouraging messages — typically, “Good job!” — but the other half were vouchers for prizes worth between $1 and $100. “I’ve been to a lot of rehabs, and there were no incentives except for the idea of being clean after you finished,” said Mr. Kelty, 61, of Winfield, Pa. “Some of us need something to motivate us — even if it’s a small thing — to live a better life.” The treatment is called contingency management, because the rewards are contingent on staying abstinent. A number of clinical trials have found it highly effective in getting people addicted to stimulants like cocaine and methamphetamine to stay in treatment and to stop using the drugs. But outside the research arena and the Department of Veterans Affairs, where Mr. Kelty is a patient, it is nearly impossible to find programs that offer such treatment — even as overdose deaths involving meth, in particular, have soared. There were more than 16,500 such deaths last year, according to preliminary data, more than twice as many as in 2016. Early data suggests that overdoses have increased even more during the coronavirus pandemic, which has forced most treatment programs to move online. Researchers say that one of the biggest obstacles to contingency management is a moral objection to the idea of rewarding someone for staying off drugs. That is one reason publicly funded programs like Medicaid, which provides health coverage for the poor, do not cover the treatment. Some treatment providers are also wary of giving prizes that they say patients could sell or trade for drugs. Greg Delaney, a pastor and the outreach coordinator at Woodhaven, a residential treatment center in Ohio, said, “Until you’re at the point where you can say, ‘I can make a good decision with this $50,’ it’s counterproductive.” © 2020 The New York Times Company

Keyword: Drug Abuse; Learning & Memory
Link ID: 27556 - Posted: 10.28.2020

R. Douglas Fields As I opened my copy of Science at home one night, an unfamiliar word in the title of a new study caught my eye: dopaminylation. The term refers to the brain chemical dopamine’s ability, in addition to transmitting signals across synapses, to enter a cell’s nucleus and control specific genes. As I read the paper, I realized that it completely upends our understanding of genetics and drug addiction. The intense craving for addictive drugs like alcohol and cocaine may be caused by dopamine controlling genes that alter the brain circuitry underlying addiction. Intriguingly, the results also suggest an answer to why drugs that treat major depression must typically be taken for weeks before they’re effective. I was shocked by the dramatic discovery, but to really understand it, I first had to unlearn some things. “Half of what you learned in college is wrong,” my biology professor, David Lange, once said. “Problem is, we don’t know which half.” How right he was. I was taught to scoff at Jean-Baptiste Lamarck and his theory that traits acquired through life experience could be passed on to the next generation. The silly traditional example is the mama giraffe stretching her neck to reach food high in trees, resulting in baby giraffes with extra-long necks. Then biologists discovered we really can inherit traits our parents acquired in life, without any change to the DNA sequence of our genes. It’s all thanks to a process called epigenetics — a form of gene expression that can be inherited but isn’t actually part of the genetic code. This is where it turns out that brain chemicals like dopamine play a role. All genetic information is encoded in the DNA sequence of our genes, and traits are passed on in the random swapping of genes between egg and sperm that sparks a new life. Genetic information and instructions are coded in a sequence of four different molecules (nucleotides abbreviated A, T, G and C) on the long double-helix strand of DNA. The linear code is quite lengthy (about 6 feet long per human cell), so it’s stored neatly wound around protein bobbins, similar to how magnetic tape is wound around spools in cassette tapes. All Rights Reserved © 2020

Keyword: Drug Abuse; Epigenetics
Link ID: 27555 - Posted: 10.28.2020

Sara Reardon In Alysson Muotri’s laboratory, hundreds of miniature human brains, the size of sesame seeds, float in Petri dishes, sparking with electrical activity. These tiny structures, known as brain organoids, are grown from human stem cells and have become a familiar fixture in many labs that study the properties of the brain. Muotri, a neuroscientist at the University of California, San Diego (UCSD), has found some unusual ways to deploy his. He has connected organoids to walking robots, modified their genomes with Neanderthal genes, launched them into orbit aboard the International Space Station, and used them as models to develop more human-like artificial-intelligence systems. Like many scientists, Muotri has temporarily pivoted to studying COVID-19, using brain organoids to test how drugs perform against the SARS-CoV-2 coronavirus. But one experiment has drawn more scrutiny than the others. In August 2019, Muotri’s group published a paper in Cell Stem Cell reporting the creation of human brain organoids that produced coordinated waves of activity, resembling those seen in premature babies1. The waves continued for months before the team shut the experiment down. This type of brain-wide, coordinated electrical activity is one of the properties of a conscious brain. The team’s finding led ethicists and scientists to raise a host of moral and philosophical questions about whether organoids should be allowed to reach this level of advanced development, whether ‘conscious’ organoids might be entitled to special treatment and rights not afforded to other clumps of cells and the possibility that consciousness could be created from scratch. The idea of bodiless, self-aware brains was already on the minds of many neuroscientists and bioethicists. Just a few months earlier, a team at Yale University in New Haven, Connecticut, announced that it had at least partially restored life to the brains of pigs that had been killed hours earlier. By removing the brains from the pigs’ skulls and infusing them with a chemical cocktail, the researchers revived the neurons’ cellular functions and their ability to transmit electrical signals2.

Keyword: Consciousness; Development of the Brain
Link ID: 27552 - Posted: 10.28.2020

By Nicholas Bakalar Long-term exposure to noise may be linked to an increased risk for Alzheimer’s disease and other forms of dementia. Researchers did periodic interviews with 5,227 people 65 and older participating in a study on aging. They assessed them with standard tests of orientation, memory and language, and tracked average daytime noise levels in their neighborhoods for the five years preceding the cognitive assessments. About 11 percent had Alzheimer’s disease, and 30 percent had mild cognitive impairment, which often progresses to full-blown dementia. Residential noise levels varied widely, from 51 to 78 decibels, or from the level of a relatively quiet suburban neighborhood to that of an urban setting near a busy highway. The study is in Alzheimer’s & Dementia. After controlling for education, race, smoking, alcohol consumption, neighborhood air pollution levels and other factors, they found that each 10 decibel increase in community noise level was associated with a 36 percent higher likelihood of mild cognitive impairment, and a 29 percent increased risk for Alzheimer’s disease. The associations were strongest in poorer neighborhoods, which also had higher noise levels. The reasons for the connection are unknown, but the lead author, Jennifer Weuve, an associate professor of epidemiology at Boston University, suggested that excessive noise can cause sleep deprivation, hearing loss, increased heart rate, constriction of the blood vessels and elevated blood pressure, all of which are associated with an increased risk for dementia. © 2020 The New York Times Company

Keyword: Alzheimers; Hearing
Link ID: 27551 - Posted: 10.28.2020

By Stephani Sutherland Many of the symptoms experienced by people infected with SARS-CoV-2 involve the nervous system. Patients complain of headaches, muscle and joint pain, fatigue and “brain fog,” or loss of taste and smell—all of which can last from weeks to months after infection. In severe cases, COVID-19 can also lead to encephalitis or stroke. The virus has undeniable neurological effects. But the way it actually affects nerve cells still remains a bit of a mystery. Can immune system activation alone produce symptoms? Or does the novel coronavirus directly attack the nervous system? Some studies—including a recent preprint paper examining mouse and human brain tissue—show evidence that SARS-CoV-2 can get into nerve cells and the brain. The question remains as to whether it does so routinely or only in the most severe cases. Once the immune system kicks into overdrive, the effects can be far-ranging, even leading immune cells to invade the brain, where they can wreak havoc. Some neurological symptoms are far less serious yet seem, if anything, more perplexing. One symptom—or set of symptoms—that illustrates this puzzle and has gained increasing attention is an imprecise diagnosis called “brain fog.” Even after their main symptoms have abated, it is not uncommon for COVID-19 patients to experience memory loss, confusion and other mental fuzziness. What underlies these experiences is still unclear, although they may also stem from the body-wide inflammation that can go along with COVID-19. Many people, however, develop fatigue and brain fog that lasts for months even after a mild case that does not spur the immune system to rage out of control. Another widespread symptom called anosmia, or loss of smell, might also originate from changes that happen without nerves themselves getting infected. Olfactory neurons, the cells that transmit odors to the brain, lack the primary docking site, or receptor, for SARS-CoV-2, and they do not seem to get infected. Researchers are still investigating how loss of smell might result from an interaction between the virus and another receptor on the olfactory neurons or from its contact with nonnerve cells that line the nose. © 2020 Scientific American,

Keyword: Learning & Memory; Chemical Senses (Smell & Taste)
Link ID: 27547 - Posted: 10.24.2020

The plant compound apigenin improved the cognitive and memory deficits usually seen in a mouse model of Down syndrome, according to a study by researchers at the National Institutes of Health and other institutions. Apigenin is found in chamomile flowers, parsley, celery, peppermint and citrus fruits. The researchers fed the compound to pregnant mice carrying fetuses with Down syndrome characteristics and then to the animals after they were born and as they matured. The findings raise the possibility that a treatment to lessen the cognitive deficits seen in Down syndrome could one day be offered to pregnant women whose fetuses have been diagnosed with Down syndrome through prenatal testing. The study appears in the American Journal of Human Genetics. Down syndrome is a set of symptoms resulting from an extra copy or piece of chromosome 21. The intellectual and developmental disabilities accompanying the condition are believed to result from decreased brain growth caused by increased inflammation in the fetal brain. Apigenin is not known to have any toxic effects, and previous studies have indicated that it is an antioxidant that reduces inflammation. Unlike many compounds, it is absorbed through the placenta and the blood brain barrier, the cellular layer that prevents potentially harmful substances from entering the brain. Compared to mice with Down symptoms whose mothers were not fed apigenin, those exposed to the compound showed improvements in tests of developmental milestones and had improvements in spatial and olfactory memory. Tests of gene activity and protein levels showed the apigenin-treated mice had less inflammation and increased blood vessel and nervous system growth. Guedj, F. et al. Apigenin as a candidate prenatal treatment for Trisomy 21: effects in human amniocytes and the Ts1Cje mouse model. American Journal of Human Genetics. 2020.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27546 - Posted: 10.24.2020

Jon Hamilton Medical research was an early casualty of the COVID-19 pandemic. After cases began emerging worldwide, thousands of clinical trials unrelated to COVID-19 were paused or canceled amid fears that participants would be infected. But now some researchers are finding ways to carry on in spite of the coronavirus. "It's been a struggle of course," says Joshua Grill, who directs the Institute for Memory Impairments and Neurological Disorders at the University of California, Irvine. "But I think there's an imperative for us to find ways to move forward." Grill got a close-up view of the challenge in July when COVID-19 cases were spiking nationwide as he was trying to launch a study. UC Irvine and dozens of other research centers had just begun enrolling participants in the AHEAD study, a global effort that will test whether an investigational drug can slow down the earliest brain changes associated with Alzheimer's disease. Finding individuals willing and able to sign up for this sort of research is difficult even without a pandemic, says Grill, who also co-directs recruitment for the Alzheimer's Clinicals Trial Consortium, funded by the National Institute on Aging. "We're asking people do a lot, including enroll in long studies that require numerous visits," he says, "and in the AHEAD study, taking an investigational drug or placebo that's injected into a vein." Participants will receive either a placebo or a drug called BAN2401, made by Eisai, which is meant to reduce levels of amyloid, a toxic protein associated with Alzheimer's. People in the study will also have positron emission tomography, or PET, scans of their brains to measure changes in amyloid and another toxic protein called tau. © 2020 npr

Keyword: Alzheimers
Link ID: 27545 - Posted: 10.24.2020

By Jeremy Hsu Artificial intelligence could soon help screen for Alzheimer’s disease by analyzing writing. A team from IBM and Pfizer says it has trained AI models to spot early signs of the notoriously stealthy illness by looking at linguistic patterns in word usage. Other researchers have already trained various models to look for signs of cognitive impairments, including Alzheimer’s, by using different types of data, such as brain scans and clinical test results. But the latest work stands out because it used historical information from the multigenerational Framingham Heart Study, which has been tracking the health of more than 14,000 people from three generations since 1948. If the new models’ ability to pick up trends in such data holds up in forward-looking studies of bigger and more diverse populations, researchers say they could predict the development of Alzheimer’s a number of years before symptoms become severe enough for typical diagnostic methods to pick up. And such a screening tool would not require invasive tests or scans. The results of the Pfizer-funded and IBM-run study were published on Thursday in EClinicalMedicine. The new AI models provide “an augmentation to expert practitioners in how you would see some subtle changes earlier in time, before the clinical diagnosis has been achieved,” says Ajay Royyuru, vice president of health care and life sciences research at IBM. “It might actually alert you to some changes that [indicate] you ought to then go do a more complete exam.” To train these models, the researchers used digital transcriptions of handwritten responses from Framingham Heart Study participants who were asked to describe a picture of a woman who is apparently preoccupied with washing dishes while two kids raid a cookie jar behind her back. These descriptions did not preserve the handwriting from the original responses, says Rhoda Au, director of neuropsychology at the Framingham study and a professor at Boston University. © 2020 Scientific American,

Keyword: Alzheimers; Language
Link ID: 27544 - Posted: 10.24.2020

By Bruce Bower A type of bone tool generally thought to have been invented by Stone Age humans got its start among hominids that lived hundreds of thousands of years before Homo sapiens evolved, a new study concludes. A set of 52 previously excavated but little-studied animal bones from East Africa’s Olduvai Gorge includes the world’s oldest known barbed bone point, an implement probably crafted by now-extinct Homo erectus at least 800,000 years ago, researchers say. Made from a piece of a large animal’s rib, the artifact features three curved barbs and a carved tip, the team reports in the November Journal of Human Evolution. Among the Olduvai bones, biological anthropologist Michael Pante of Colorado State University in Fort Collins and colleagues identified five other tools from more than 800,000 years ago as probable choppers, hammering tools or hammering platforms. The previous oldest barbed bone points were from a central African site and dated to around 90,000 years ago (SN: 4/29/95), and were assumed to reflect a toolmaking ingenuity exclusive to Homo sapiens. Those implements include carved rings around the base of the tools where wooden shafts were presumably attached. Barbed bone points found at H. sapiens sites were likely used to catch fish and perhaps to hunt large land prey. The Olduvai Gorge barbed bone point, which had not been completed, shows no signs of having been attached to a handle or shaft. Ways in which H. erectus used the implement are unclear, Pante and his colleagues say. © Society for Science & the Public 2000–2020.

Keyword: Evolution; Learning & Memory
Link ID: 27543 - Posted: 10.24.2020

By Meagan Cantwell Although bird brains are tiny, they’re packed with neurons, especially in areas responsible for higher level thinking. Two studies published last month in Science explore the structure and function of avian brains—revealing they are organized similarly to mammals’ and are capable of conscious thought. © 2020 American Association for the Advancement of Science.

Keyword: Evolution; Learning & Memory
Link ID: 27541 - Posted: 10.24.2020

Catherine Offord Overactivation of the brain’s immune cells, called microglia, may play a role in cognitive impairments associated with Down syndrome, according to research published today (October 6) in Neuron. Researchers in Italy identified elevated numbers of the cells in an inflammation-promoting state in the brains of mice with a murine version of the syndrome as well as in postmortem brain tissue from people with the condition. The team additionally showed that drugs that reduce the number of activated microglia in juvenile mice could boost the animals’ performance on cognitive tests. “This is a fabulous study that gives a lot of proof of principle to pursuing some clinical trials in people,” says Elizabeth Head, a neuroscientist at the University of California, Irvine, who was not involved in the work. “The focus on microglial activation, I thought, was very novel and exciting,” she adds, noting that more research will be needed to see how the effects of drugs used in the study might translate from mice to humans. Down syndrome is caused by an extra copy of part or all of human chromosome 21, and is the most commonly occurring chromosomal condition in the US. Children with Down syndrome often experience cognitive delays compared to typically developing children, although there’s substantial variation and the effects are usually mild or moderate. People with the syndrome also have a higher risk of certain medical conditions, including Alzheimer’s disease. © 1986–2020 The Scientist.

Keyword: Development of the Brain; Glia
Link ID: 27537 - Posted: 10.21.2020

By Nicholas Bakalar A mother’s psychological distress during pregnancy may increase the risk for asthma in her child, a new study suggests. Researchers had the parents of 4,231 children fill out well-validated questionnaires on psychological stress in the second trimester of pregnancy, and again three years later. The mothers also completed questionnaires at two and six months after giving birth. The study, in the journal Thorax, found that 362 of the mothers and 167 of the fathers had clinically significant psychological distress during the mothers’ pregnancies. When the children were 10 years old, parents reported whether their child had ever been diagnosed with asthma. As an extra measure, the researchers tested the children using forced expiratory volume, or FEV, a standard clinical test of lung function. After controlling for age, smoking during pregnancy, body mass index, a history of asthma and other factors, they found that maternal depression and anxiety during pregnancy was significantly associated with both diagnoses of asthma and poorer lung function in their children. There was no association between childhood asthma and parents’ psychological distress in the years after pregnancy, and no association with paternal psychological stress at any time. “Of course, this could be only one of many causes of asthma,” said the lead author, Dr. Evelien R. van Meel of Erasmus University in Rotterdam, “but we corrected for many confounders, and we saw the effect only in mothers. This seems to suggest that there’s something going on in the uterus. But this is an observational study, and we can’t say that it’s a causal effect.” © 2020 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 27534 - Posted: 10.21.2020

By Laurie Archbald-Pannone The number of cases of dementia in the United States is rising as baby boomers age, raising questions for boomers themselves and also for their families, caregivers and society. Dementia, which is not technically a disease but a term for impaired ability to think, remember or make decisions, is one of the most feared impairments of old age. Incidence increases dramatically as people move into their 90s. About 5 percent of those 71 to 79 have dementia, and about 37 percent of those about 90 live with it. Older people may worry about their own loss of function as well as the cost and toll of caregiving for someone with dementia. A 2018 study estimated that the lifetime cost of care for a person with Alzheimer’s, the most common form of dementia, to be $329,360. That figure, too, will no doubt rise, putting even more burdens on family, Medicare and Medicaid. There’s also been a good deal of talk and reporting about dementia in recent months because of the presidential election. Some voters have asked whether one or both candidates might have dementia. But is this even a fair question to ask? When these types of questions are posed — adding further stigma to people with dementia — it can unfairly further isolate them and those caring for them. We need to understand dementia and the impact it has on more than 5 million people in the United States who now live with dementia and their caregivers. That number is expected to triple by 2060. First, it is important to know that dementia cannot be diagnosed from afar or by someone who is not a doctor. A person needs a detailed doctor’s exam for a diagnosis. Sometimes, brain imaging is required. And, forgetting an occasional word — or even where you put your keys — does not mean a person has dementia. There are different types of memory loss and they can have different causes, such as other medical conditions, falls or even medication, including herbals, supplements and anything over-the-counter. © 1996-2020 The Washington Post

Keyword: Alzheimers
Link ID: 27532 - Posted: 10.19.2020

By Benedict Carey Scott Lilienfeld, an expert in personality disorders who repeatedly disturbed the order in his own field, questioning the science behind many of psychology’s conceits, popular therapies and prized tools, died on Sept. 30 at his home in Atlanta. He was 59. The cause was pancreatic cancer, his wife, Candice Basterfield, said. Dr. Lilienfeld’s career, most of it spent at Emory University in Atlanta, proceeded on two tracks: one that sought to deepen the understanding of so-called psychopathic behavior, the other to expose the many faces of pseudoscience in psychology. Psychopathy is characterized by superficial charm, grandiosity, pathological lying and a lack of empathy. Descriptions of the syndrome were rooted in research in the criminal justice system, where psychopaths often end up. In the early 1990s, Dr. Lilienfeld worked to deepen and clarify the definition. In a series of papers, he anchored a team of psychologists who identified three underlying personality features that psychopaths share, whether they commit illegal acts or not: fearless dominance, meanness and impulsivity. The psychopath does what he or she wants, without anxiety, regret or regard for the suffering of others. “When you have these three systems interacting, it’s a bad brew, and it creates the substrate for what can become psychopathy,” said Mark F. Lenzenweger, a professor of psychology at the State University of New York at Binghamton. “This was Scott’s great contribution: He helped change the thinking about psychopathy, in a profound way, by focusing on aspects of personality, rather than on a list of bad behaviors.” Dr. Lilienfeld’s parallel career encompassed clinical psychology and aimed to shake it free of empty theorizing, softheadedness and bad practice. In the late 1990s and early 2000s, he led a loose group of researchers who began to question the validity of some of the field’s favored constructs, like repressed memories of abuse and multiple personality disorder. The Rorschach inkblot test took a direct hit as largely unreliable. The group also attacked treatments including psychological debriefing and eye movement desensitization and reprocessing, or E.M.D.R., both of which are used for trauma victims. © 2020 The New York Times Company

Keyword: Aggression; Learning & Memory
Link ID: 27529 - Posted: 10.19.2020

By Lydia Denworth, Spectrum, Brendan Borrell, Allyson Berent is a specialty veterinarian in New York City. She treats animals that other doctors cannot help. When no good therapies are available, she invents one. Cats and dogs consumed almost all of her time—until 6 years ago, when her second daughter was born. As a baby, Quincy appeared healthy and happy, smiling at an early age and giggling frequently. But during her first few months of life, she missed many developmental milestones: At 10 weeks, she was not making eye contact. When her parents waved toys in front of her, she stared blankly. She had trouble feeding. And when she was lying on her stomach, she could not lift her head. Doctors kept telling Berent and her husband to give it time, but the couple insisted on genetic testing: At 7 months old, their daughter was diagnosed with Angelman syndrome, a neurodevelopmental condition that affects as many as one in 12,000 people. Most people with Angelman syndrome have severe intellectual disability. They never talk or live an independent life. They experience seizures, gut issues, and sleeping and feeding difficulties. Due to balance and motor problems, they are usually unable or barely able to walk. Many also meet the diagnostic criteria for autism. Within days of learning her daughter’s diagnosis, Berent set herself a new goal: curing Quincy. With her medical background, she had no trouble parsing the scientific research on Angelman syndrome. She learned that it stems from a missing or mutated copy of a gene called UBE3A, which generates a protein essential for healthy brain activity. People inherit two copies of UBE3A, one from each parent, but the paternal copy is typically silent. In about 70% of people with Angelman, the maternal copy is absent, and they produce none of the protein. Many others with the syndrome have a small mutation in the mother’s copy, rendering it ineffective. © 2020 American Association for the Advancement of Science.

Keyword: Autism; Development of the Brain
Link ID: 27528 - Posted: 10.16.2020

by Angie Voyles Askham Autism is a neurodevelopmental condition. Although it is diagnosed based on the presence of two core behaviors — restricted interests and repetitive behaviors, as well as difficulties with social interactions and communication — those traits are thought to arise because of alterations in how different parts of the brain form and connect to one another. No research has uncovered a ‘characteristic’ brain structure for autism, meaning that no single pattern of changes appears in every autistic person. Studies of brain structure often turn up dissimilar results — there is great variety across individuals in general. But some trends have begun to emerge for subsets of autistic people. These differences might one day provide some insight into how some autistic people’s brains function. They may also point to bespoke treatments for particular subtypes of autism. Here is what we know about how brain structure differs between people with and without autism. Which brain regions are known to be structurally different between autistic and non-autistic people? Children and adolescents with autism often have an enlarged hippocampus, the area of the brain responsible for forming and storing memories, several studies suggest, but it is unclear if that difference persists into adolescence and adulthood1,2. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27526 - Posted: 10.16.2020

Frank R. Lin, M.D., Ph.D. When I was going through my otolaryngology residency at Johns Hopkins in the early 2000s, I was struck by the disparity between how hearing loss was managed in children and in older adults. In the case of the child, it was a medical priority to ensure access to a hearing aid so he or she could communicate optimally at home and in school, and such devices were covered by insurance. This approach was justified based on extensive research demonstrating that hearing loss could have a substantial impact on a child’s cognitive and brain development, with lifetime consequences for educational and vocational achievement. For the older adult, the approach was radically different, even if the degree of hearing impairment was the same as in the child. The adult would be reassured that the deficit was to be expected, based on his or her age, and told that a hearing aid, if desired, would represent an out-of-pocket expense averaging about $4,000. Medicare provided no coverage for hearing aids. There was no robust research demonstrating meaningful consequences of hearing loss for older adults, as there was for children, and the clinical approach was typically guided by the notion that it was a very common, and hence inconsequential, aspect of aging. But this approach didn’t make sense, given what I had observed clinically. Older adults with hearing loss recounted to me their sense of isolation and loneliness, and the mental fatigue of constantly concentrating in trying to follow conversations. Family members would often describe a decline in patients’ general well-being and mental acuity as they struggled to hear. For those who obtained effective treatment for their hearing loss with hearing aids or a cochlear implant, the effects were often equally dramatic. Patients spoke of reengaging with family, no longer getting fatigued from straining to listen, and becoming their “old selves” again. If hearing was fundamentally important for children and represented a critical sensory input that could affect brain function, wouldn’t loss of hearing have corresponding implications for the aging brain and its function? © 2020 The Dana Foundation.

Keyword: Hearing; Alzheimers
Link ID: 27525 - Posted: 10.16.2020