Chapter 13. Memory, Learning, and Development

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By Nayef Al-Rodhan Facebook recently announced it had acquired CTRL-Labs, a U.S. start-up working on wearable tech that allows people to control digital devices with their brain. The social media company is only the latest in a long string of firms investing in what has come to be termed “neurotechnology.” Earlier this year Neuralink, a company backed by Elon Musk, announced that it hopes to begin human trials for computerized brain implants. These projects may seem like science fiction, but this drive to get more out of our brains is nothing new—from tea, caffeine and nicotine, to amphetamines and the narcolepsy drug Modafinil, drugs have long been used as rudimentary attempts at cognitive enhancement. And in our tech-driven world, the drive to cognitively enhance is stronger than ever—and is leading us to explore new and untested methods. In today’s hypercompetitive world, everyone is looking for an edge. Improving memory, focus or just the ability to work longer hours are all key to getting ahead, and a drug exists to improve each of them. In 2017, 30 percent of Americans said they had used “smart drug” supplements, known as nootropics, at least once that year, even if studies repeatedly demonstrate that they have a negligible effect on intellect. Advertisement For some, however, nootropics are not enough, and so they turn to medical-grade stimulants. The most famous of these is Adderall, which boosts focus and productivity far more than commercial nootropics. A well-established black market thrives on university campuses and in financial centers, supplying these drugs to people desperate to gain a competitive edge. © 2019 Scientific American

Keyword: Learning & Memory; Drug Abuse
Link ID: 26886 - Posted: 12.10.2019

By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Keyword: Alzheimers; Depression
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. People who took the highest amounts of the drug declined about 30 percent less, as measured by a commonly used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s Disease meeting in San Diego. With these encouraging results in hand, Biogen, based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and Drug Administration in early 2020. The results are “exhilarating, not just to the scientific community but our patients as well,” Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during a panel discussion at the meeting. Cohen participated in the clinical trials and has received funding from Biogen. The presentation marks “an important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s disease slowly kills cells in the brain, gradually erasing people’s abilities to remember, navigate and think clearly. Current Alzheimer’s medicines can hold off symptoms temporarily, but don’t fight the underlying brain destruction. A treatment that could actually slow or even stop the damage would have a “huge impact for patients and their caregivers,” she says. © Society for Science & the Public 2000–2019

Keyword: Alzheimers
Link ID: 26879 - Posted: 12.06.2019

By Kelly Servick When Samantha Budd Haeberlein, Biogen’s head of clinical development, took the stage in San Diego, California, before a room full of Alzheimer’s disease researchers and physicians this morning, she knew she had some explaining to do. In October, the pharmaceutical company, based in Cambridge, Massachusetts, unexpectedly revived an experimental Alzheimer’s drug that it had declared a failure 7 months earlier. Ever since, scientists and industry analysts have been hungry for more detail about two large clinical trials meant to prove that Biogen’s drug, an antibody called aducanumab, slows down cognitive decline in the early stages of disease. At the Clinical Trials on Alzheimer’s Disease congress today, Budd Haeberlein tried to clarify what has emboldened the company to apply to the U.S. Food and Drug Administration (FDA) for market approval for aducanumab early next year. After analyzing more patient data than were available at the time of a discouraging preliminary analysis, she explained, the company found evidence that the higher of two tested doses led to 22% less cognitive decline after 78 weeks than a placebo in one trial. However, the other trial failed to show any benefit, leaving some researchers with a grim outlook on the drug. “I surely don’t think that it should be given market approval on the basis of these data,” says Robert Howard, a psychiatrist at University College London who has run clinical trials of potential Alzheimer’s treatments. More positive results from a subset of patients that weren’t preselected at the trial’s launch are not convincing, he says. “[Biogen has] broken all the rules, really, about how you analyze data and report it.” © 2019 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 26878 - Posted: 12.06.2019

By Anisha Kalidindi The room is pitch black. Every light, from the power button on the computer to the box controlling the microscope, is covered with electrical tape. I feel a gush of air as the high-powered AC kicks on, offsetting the heat emitted from the microscope’s lasers. I take my mouse out of its cage and get ready to image its brain. I’m wearing a red headlamp so I can see, but it is still quite dim. I peer closely at my lab notebook and note the two positions: –1, +2. I recite them repeatedly in a hushed tone, so I don’t forget; it is 1 A.M., after all. I hook the mouse up to the stage of the microscope and then use my handy toothpick to make sure its head position is correct. While there are many unsung heroes of science—veterinarians, lab technicians, graduate students (I might be a bit biased with this one!)—these aren’t the ones I’m talking about. I’m talking about a toothpick that played a significant role in my research project. Advertisement I am lucky enough to have access to a cutting-edge microscope and several other pieces of expensive equipment in my lab. But can also find things you might never guess were used in science: red-light headlamps, black electrical tape, and toothpicks. Using the microscope, I can take a picture of a mouse’s living, working brain through a literal window: a piece of glass that replaces a small piece of the animal’s skull. To image the mouse, we affix a plastic bar on the front of its head and then secure the bar to a head-mounting device on the stage under the microscope lens. Using this mount, we can precisely position the head up and down and right to left. This is where our problem starts. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26877 - Posted: 12.06.2019

Richard Harris Scientists know that if they transfuse blood from a young mouse to an old one, then they can stave off or even reverse some signs of aging. But they don't know what in the blood is responsible for this remarkable effect. Researchers now report that they've identified hundreds of proteins in human blood that wax and wane in surprising ways as we age. The findings could provide important clues about which substances in the blood can slow aging. The scientists studied nearly 3,000 proteins in blood plasma that was drawn from more than 4,000 people with a span of ages from 18 to 95. The project focused on proteins that change in both men and women. "When we went into this, we assumed you aged gradually, so we would see these changes taking place relatively steadily as individuals get older," said Tony Wyss-Coray, a professor of neurology at Stanford University. Instead, Wyss-Coray and his colleagues report in Nature Medicine on Thursday that these proteins change in three distinct waves, the first of which happens "very surprisingly" during our 30s, peaking around age 34. "Then we found a second wave around 60, and then we found a third one, the most prominent one, really around 80 years of age," Wyss-Coray said. (An earlier version of their paper is freely available on the bioRxiv preprint server.) This observation raises a host of questions about the biology of aging. What age-related transition is occurring in our 30s? And what do the changes in the blood actually mean? "Most of the proteins in the blood are actually from other tissue sources," he said. "So we can start to ask where ... these proteins come from and if they change with age," he said. For example, in proteins traced back to the liver, "that would tell us that the liver is aging." © 2019 npr

Keyword: Alzheimers
Link ID: 26876 - Posted: 12.06.2019

By Aimee Cunningham Socially isolated and faced with a persistently white polar landscape, a long-term crew of an Antarctic research station saw a portion of their brains shrink during their stay, a small study finds. “It’s very exciting to see the white desert at the beginning,” says physiologist Alexander Stahn, who began the research while at Charité-Universitätsmedizin Berlin. “But then it’s always the same.” The crew of eight scientists and researchers and a cook lived and worked at the German research station Neumayer III for 14 months. Although joined by other scientists during the summer, the crew alone endured the long darkness of the polar winter, when temperatures can plummet as low as –50° Celsius and evacuation is impossible. That social isolation and monotonous environment is the closest thing on Earth to what a space explorer on a long mission may experience, says Stahn, who is interested in researching what effect such travel would have on the brain. Animal studies have revealed that similar conditions can harm the hippocampus, a brain area crucial for memory and navigation (SN: 11/6/18). For example, rats are better at learning when the animals are housed with companions or in an enriched environment than when alone or in a bare cage, Stahn says. But whether this is true for a person’s brain is unknown. Stahn, now at the Perelman School of Medicine at the University of Pennsylvania, and his colleagues used magnetic resonance imaging to capture views of the team members’ brains before their polar stay and after their return. On average, an area of the hippocampus in the crew’s brains shrank by 7 percent over the course of the expedition, compared with healthy people matched for age and gender who didn’t stay at the station, the researchers report online December 4 in the New England Journal of Medicine. © Society for Science & the Public 2000–2019

Keyword: Learning & Memory; Biological Rhythms
Link ID: 26874 - Posted: 12.05.2019

Ian Sample Science editor Scientists have created artificial neurons that could potentially be implanted into patients to overcome paralysis, restore failing brain circuits, and even connect their minds to machines. The bionic neurons can receive electrical signals from healthy nerve cells, and process them in a natural way, before sending fresh signals on to other neurons, or to muscles and organs elsewhere in the body. One of the first applications may be a treatment for a form of heart failure that develops when a particular neural circuit at the base of the brain deteriorates through age or disease and fails to send the right signals to make the heart pump properly. Rather than implanting directly into the brain, the artificial neurons are built into ultra-low power microchips a few millimetres wide. The chips form the basis for devices that would plug straight into the nervous system, for example by intercepting signals that pass between the brain and leg muscles. “Any area where you have some degenerative disease, such as Alzheimer’s, or where the neurons stop firing properly because of age, disease, or injury, then in theory you could replace the faulty biocircuit with a synthetic circuit,” said Alain Nogaret, a physicist who led the project at the University of Bath. The breakthrough came when researchers found they could model live neurons in a computer program and then recreate their firing patterns in silicon chips with more than 94% accuracy. The program allows the scientists to mimic the full variety of neurons found in the nervous system. © 2019 Guardian News & Media Limited

Keyword: Robotics; Learning & Memory
Link ID: 26872 - Posted: 12.04.2019

By Gaby Maimon What is the biological basis of thought? How do brains store memories? Questions like these have intrigued humanity for millennia, but the answers still remain largely elusive. You might think that the humble fruit fly, Drosophila melanogaster, has little to add here, but since the 1970s, scientists have actually been studying the neural basis of higher brain functions, like memory, in these insects. Classic work––performed by several labs, including those of Martin Heisenberg and Seymour Benzer––focused on studying the behavior of wild-type and genetically mutated Drosophila in simple learning and memory tasks, ultimately leading to the discovery of several key molecules and other underlying mechanisms. However, because one could not peer into the brain of behaving flies to eavesdrop on neurons in action, this field, in its original form, could only go so far in helping to explain the mechanisms of cognition. In 2010, when I was a postdoctoral researcher in the lab of Michael Dickinson, we developed the first method for measuring electrical activity of neurons in behaving Drosophila. A similar method was developed in parallel by Johannes Seelig and Vivek Jayaraman. In these approaches, one glues a fly to a custom plate that allows one to carefully remove the cuticle over the brain and measure neural activity via electrodes or fluorescence microscopy. Even though the fly is glued in place, the animal can still flap her wings in tethered flight or walk on an air-cushioned ball, which acts like a spherical treadmill beneath her legs. These technical achievements attracted the attention of the Drosophila neurobiology community, but should anyone really care about seeing a fly brain in action beyond this small, venerable, group of arthropod-loving nerds (of which I'm honored to be a member)? In other words, will these methods help to reveal anything of general relevance beyond flies? Increasingly, the answer looks to be yes. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26871 - Posted: 12.04.2019

Shawna Williams In September of this year, pharmaceutical companies Biogen and Eisai announced that they were halting Phase 3 clinical trials of a drug, elenbecestat, aimed at thwarting amyloid-β buildup in Alzheimer’s disease. Although the drug had seemed so promising that the companies elected to test it in two Phase 3 trials simultaneously, preliminary analyses determined that elenbecestat’s risks outweighed its benefits, and the drug shouldn’t be moved to market. The cancellation “amounts to a further step in the unwinding of Biogen’s expensive, painful, and ultimately fruitless investment in Alzheimer’s disease (AD) drug development,” analyst Geoffrey Porges told Reuters at the time. Biogen’s misfortune is just the latest in a slew of late-stage Alzheimer’s drug failures. Six months earlier, the company had halted another set of parallel Phase 3 trials due to lack of efficacy of a different drug candidate, aducanumab (though after further data analysis, Biogen announced that it will seek approval for aducanumab after all). And between 2013 and 2018, Pfizer, Eli Lilly, Merck, and Johnson & Johnson all terminated Phase 3 or Phase 2/3 trials due to poor early results. Yet some Alzheimer’s researchers say they think they’ve spotted a silver lining in this cloud of bad news—a hint in the data from these studies about how future work might meet with more success. In some of these trials, Alzheimer’s patients who were at earlier stages of the disease did better than those with more advanced cognitive decline, says Colin Masters, a neuroscientist at Florey Institute of Neuroscience and Mental Health in Australia who was not involved in the trials. This indicates that the key to finding an effective treatment might be to catch subjects before their condition advances too far, he adds. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26868 - Posted: 12.04.2019

By Claudia Wallis For more than 25 years one idea has dominated scientific thinking about Alzheimer's disease: the amyloid cascade hypothesis. It holds that the disorder, which afflicts about one in 10 Americans age 65 or older, is caused by a buildup in the brain of abnormal amyloid-beta protein, which eventually destroys neurons and synapses, producing the tragic symptoms of dementia. There's plenty of evidence for this. First, the presence of sticky clumps or “plaques” containing amyloid is a classic hallmark of the disease (along with tangles of a protein called tau). It was what Alois Alzheimer saw in the autopsied brain of patient zero in 1906. Second, families with inherited defects in amyloid precursor protein (APP) or in genes encoding proteins that process APP are plagued by early-onset Alzheimer's. Third, mice genetically engineered to churn out excess amyloid tend to develop memory problems and do better when the amyloid pileup is stopped. This evidence and more has led grant makers and drug companies to pour billions of dollars into amyloid-targeting therapies. More than a dozen have been tested, and one by one they have flopped. One of the biggest heartbreaks came last March, when a promising antibody to amyloid, called aducanumab, performed no better than placebo in patients with very early Alzheimer's. Meanwhile researchers pursuing nonamyloid approaches were often left out in the cold, struggling to get grants and to have their work published. Science journalist Sharon Begley spent more than a year reporting on the lost opportunities in an article for the Web site Stat entitled “The Maddening Saga of How an Alzheimer's ‘Cabal’ Thwarted Progress toward a Cure for Decades.” Begley notes that the amyloid crowd was “neither organized nor nefarious,” but its outsized influence stifled other avenues of investigation. © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26867 - Posted: 12.04.2019

By Donald McCarthy I lived only half a childhood. Friendships were difficult, because I often did not know what to say. I had little patience for small talk and a dislike of new situations. Thrust into unfamiliar surroundings, my whole body would warm, my hands would shake, and I would feel a tightening in my chest and a deep, almost primal urge to scream. Even as an adult, I felt like I viewed reality through a foggy window. I thought it was simply me — that my personality was just odd — and I would need to learn to cope with the fact that I did not fit in well with most people. Then, at age 28, I was diagnosed with autism spectrum disorder (ASD). My diagnosis was a relief. Suddenly, I knew why I felt the way I did, and why I had a hard time living the way others did. But I can only imagine how much better my life would have been if I had been diagnosed as a child and had the chance to understand myself at a younger age. Might I have made emotional connections with my peers, instead of just with Bruce Springsteen songs and characters in Stephen King novels? It turns out I’m not alone. Many people go more than half of their lives before learning that they are autistic; the exact number remains a mystery, as research on adults with autism has been scarce. Although public awareness of ASD and its symptoms has improved in recent decades, many children still slip through the cracks, especially girls and children of color. We as a society have the power and resources to change that; all we need is the will. Consider the science: There is little question among psychologists specializing in autism that an early diagnosis can change a person’s life for the better. Therapy aimed at reworking the way a young person with ASD thinks and comprehends has shown success. Children who undergo therapy see results that allow them to curb undesirable behavior, improve social interactions, and better their own quality of life.

Keyword: Autism
Link ID: 26856 - Posted: 11.29.2019

By Lisa Sanders, M.D “Where am I?” the 68-year-old man asked. His daughter explained again: He was at Yale-New Haven Hospital in Connecticut. He had been found on the ground in the parking lot of the grocery store near his apartment. The man nodded, as if taking it all in, but minutes later asked again: Where am I? He had never had any memory issues before, but now he couldn’t remember that it was Saturday. Didn’t remember that he spent the morning moving the last of the boxes he had stored at his daughter’s house to his new apartment. He didn’t even remember that he had spent the past few months hashing out a pretty messy divorce. His soon-to-be ex-wife was also in the E.R., and again and again he asked her: Are we really getting divorced? Why? What happened? Earlier that day, his daughter received a call from the hospital saying that her father had fallen outside the supermarket and was brought in by an ambulance called by a good Samaritan. No one could tell her any more than that, and her father clearly didn’t remember. He had a scrape on his right cheek and over his eye, but otherwise he seemed fine. Except he couldn’t remember the events of the recent past. When asked his name and address, he responded promptly, but the address he gave was the house he shared for many years with his future ex-wife. He seemed stunned to find out he no longer lived there. The doctor in the E.R. was also surprised by the extent of the man’s memory loss. He seemed to have lost both his retrograde memory, recall of the events of the recent past, and his anterograde memory, the ability to form new memories from the present. But on examination, everything else seemed basically normal — except that his blood pressure was high, and he had the scrapes on his face. There was no sign of infection. His kidneys and liver seemed to be working just fine. A head CT scan showed no injuries to the bones of the face, the spinal cord in the neck or the brain. There was no trace of alcohol or drugs in his system. After a few hours, the man’s memory was still not functioning properly, and he was admitted to the hospital. © 2019 The New York Times Company

Keyword: Learning & Memory
Link ID: 26854 - Posted: 11.26.2019

By Meredith Wadman Tony Magana, chief of neurosurgery at Mekelle University School of Medicine in Ethiopia’s Tigray province, confronts his country’s high prevalence of neural tube defects nearly every day. His team operates on more than 400 babies annually to repair these severe, often lethal birth malformations, in which babies can be born without brains or with their spinal cords protruding from their backs. “Probably every other day we see a child that is so bad we can’t help them,” Magana says. The holes where the spinal cord protrudes “are so big that you can’t close them.” This month, a team of nutrition experts converged in Addis Ababa to lay groundwork for an unproven but possibly highly effective intervention: fortifying Ethiopia’s salt supply with folic acid, a synthetic form of the B vitamin folate. In the first 4 weeks of pregnancy, folate is essential to proper closure of the neural tube, which gives rise to the brain and spinal cord, and since the mid-1990s, more than 80 countries have mandated flour fortification with folic acid. Ethiopia, where fewer than one-third of people eat flour, is not among them. Last year, a pair of studies that surveyed births at 11 public hospitals there shook the global health community. The studies—one co-authored by Magana—found that among every 10,000 births, between 126 and 131 babies suffered from neural tube defects (NTDs). That’s seven times their global prevalence and 26 times the prevalence in high-income, flour-fortifying countries such as the United States. According to Ethiopian government data, 84% of Ethiopian women of reproductive age have folate levels in their red blood cells that put them at risk of giving birth to a child with an NTD. © 2019 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 26851 - Posted: 11.26.2019

A disturbing aspect of Canada's opioid crisis is that more babies are being born to mothers who use fentanyl and other opioid drugs. The Canadian Institute for Health Information says more than 1,800 infants per year are born with symptoms of opioid withdrawal. A study presented Monday at the 105th Scientific Assembly and Annual Meeting of the Radiological Society of North America suggests that prenatal exposure to opioids may have a significant impact on the brain development of unborn children. A team of obstetricians, neonatologists, psychologists and radiologists led by Dr. Rupa Radhakrishnan, a radiologist at Indiana University School of Medicine, did functional MRI brain scans on 16 full-term infants. Eight of the infants had mothers who used opioids during pregnancy and eight had mothers who did not use opioids. The brain imaging technique used by the researchers is called resting state functional MRI (fMRI). The technique enabled researchers to measure brain activity by detecting changes in blood flow. The technique permits researchers to measure how well different regions of the brain talk to one another. The researchers found abnormal connections to and from a part of the brain called the amygdala. It's a region that is responsible for the perception and regulation of emotions such as anger, fear, sadness and aggression. This is one of the first studies to suggest that the brain function of infants may be affected by prenatal exposure to opioids. Abnormal function in the amygdala could make it difficult for children exposed to opioids to regulate their emotions. That could have serious implications on their social development and on their behaviour. The researchers say the study is small. They say they aren't certain as to the clinical implications of this study. A long-term outcome study is underway to understand better the functional brain changes caused by prenatal opioid exposure and their associated long-term developmental outcomes. How newborns face opioid withdrawal This research may become even more important should current trends continue, and we see an increase in the number of infants exposed to opioids prenatally. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Drug Abuse
Link ID: 26850 - Posted: 11.26.2019

By Nicholas Bakalar Long-term exposure to air pollution is associated with lower scores on tests of mental acuity, researchers have found. And one reason may be that air pollution causes changes in brain structure that resemble those of Alzheimer’s disease. The scientists studied 998 women ages 73 to 87 and free of dementia, periodically giving them tests of learning and memory. They used magnetic resonance imaging to detect brain atrophy, or wasting, and then scored the deterioration on its degree of similarity to the brain atrophy characteristic of Alzheimer’s disease. They matched Environmental Protection Agency data on air pollution to the women’s residential addresses. Over 11 years of follow-up, they found that the greater the women’s exposure to PM 2.5, the tiny particulate matter that easily penetrates the lungs and bloodstream, the lower their scores on the cognitive tests. After excluding cases of dementia and stroke, they also found a possible reason for the declining scores: The M.R.I. results showed that increased exposure to PM 2.5 was associated with increased brain atrophy, even before clinical symptoms of dementia had appeared. The study is in the journal Brain. “PM 2.5 alters brain structure, which then accelerates memory decline,” said the lead author, Diana Younan, a postdoctoral researcher at the University of California. “I just want people to be aware that air pollution can affect their health, and possibly their brains.” © 2019 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 26849 - Posted: 11.26.2019

By Tina Hesman Saey Picking embryos based on genetics might not give prospective parents the “designer baby” they’re after. DNA predictions of height or IQ might help would-be parents select an embryo that would grow into a child who is, at most, only about three centimeters taller or about three IQ points smarter than an average embryo from the couple, researchers report November 21 in Cell. But offspring predicted by their DNA to be the tallest among siblings were actually the tallest in only seven of 28 real families, the study found. And in five of those families, the child predicted to be tallest was actually shorter than the average for the family. Even if it were ethical to select embryos based on genetic propensity for height or intelligence, “the impact of doing so is likely to be modest — so modest that it’s not likely to be practically worth it,” says Amit Khera, a physician and geneticist at the Center for Genomics Medicine at Massachusetts General Hospital in Boston who was not involved in the new study. For years, couples have been able to use genetic diagnosis to screen out embryos carrying a disease-causing DNA variant. The procedure, called preimplantation genetic diagnosis, or PGD, involves creating embryos through in vitro fertilization. Clinic staff remove a single cell from the embryo and test its DNA for genetic variants that cause cystic fibrosis, Tay-Sachs or other life-threatening diseases caused by defects in single genes. © Society for Science & the Public 2000–2019

Keyword: Genes & Behavior; Intelligence
Link ID: 26847 - Posted: 11.23.2019

By Veronique Greenwood A few years back, Ryan Herbison, then a graduate student in parasitology at the University of Otago, painstakingly collected about 1,300 earwigs and more than 2,500 sandhoppers from gardens and a beach in New Zealand. Then, he dissected and examined the insides of their heads. This macabre scavenger hunt was in search of worms that lay coiled within some of the insects. The worms are parasites that force earwigs and sandhoppers to march into bodies of water, drowning themselves so the worms’ aquatic offspring can thrive. “Like a back-seat driver, but a bit more sinister,” said Mr. Herbison, describing these mind-controlling parasites. “And sometimes they may just grab the steering wheel.” Just how they do that, though, has remained a bit of a mystery. But in a paper published Wednesday in Proceedings of the Royal Society B, Mr. Herbison and fellow researchers reported that the parasites seemed to be manipulating the production of host proteins involved in generating energy and movement in their unfortunate hosts. The analysis is limited, but the researchers speculated that the parasites may be affecting neuronal connections in the bugs’ brains and perhaps even interfering with memory in a way that puts the hosts at risk. Parasites use a variety of similar strategies. Some make cat urine suicidally attractive to mice, which are promptly eaten so that the parasites can go through the next phase of their life cycle in the cat. Others prompt ants to expose themselves on high tree branches, the better to be eaten by birds. And still others cause snails to hang out in open spaces, with swollen eyestalks pulsing like neon signs, for apparently the same reason. © 2019 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 26845 - Posted: 11.22.2019

Ruth Williams After copulation, Drosophila melanogaster females are able to create long-term memories of unpleasant events—electric shocks—that virgin females cannot, according to a study published today in Science Advances (November 20). The authors suspect the memory boost may improve the chance of survival of the female during the subsequent egg-laying period as well as guide her choice of laying sites. Whatever the reason, the enhanced memory joins a list of physiological and behavioral effects on female flies that result from sex. “It’s quite impressive and convincing [data],” says entomologist Elwyn Isaac of the University of Leeds who was not involved in the research. “They propose that the sex peptide gets into the [female’s] circulation and somehow gets across the blood brain barrier [to activate memory].” It’s “very interesting,” Isaac continues, because until now, sex peptide—a protein produced in the male reproductive system and found in ejaculate—was thought to act on sensory neurons in the female’s uterus. These neurons produce a receptor protein to which sex peptide binds and are thought to be necessary for the peptide’s many effects on females, which include ramping up ovulation, increasing egg-laying behavior, changing food preference to a high-protein diet, and causing the female to reject other males. But, the authors of the new study, “show definitely that those neurons are not required for this [long-term memory] effect,” Isaac says. Indeed, deletion of the receptor in these neurons made no difference to the flies’ long-term memory formation after sex. © 1986–2019 The Scientist

Keyword: Learning & Memory; Sexual Behavior
Link ID: 26843 - Posted: 11.22.2019

By Nicholas Bakalar People who never learned to read and write may be at increased risk for dementia. Researchers studied 983 adults 65 and older with four or fewer years of schooling. Ninety percent were immigrants from the Dominican Republic, where there were limited opportunities for schooling. Many had learned to read outside of school, but 237 could not read or write. Over an average of three and a half years, the participants periodically took tests of memory, language and reasoning. Illiterate men and women were 2.65 times as likely as the literate to have dementia at the start of the study, and twice as likely to have developed it by the end. Illiterate people, however, did not show a faster rate of decline in skills than those who could read and write. The analysis, in Neurology, controlled for sex, hypertension, diabetes, heart disease and other dementia risk factors. “Early life exposures and early life social opportunities have an impact on later life,” said the senior author, Jennifer J. Manly, a professor of neuropsychology at Columbia. “That’s the underlying theme here. There’s a life course of exposures and engagements and opportunities that lead to a healthy brain later in life.” “We would like to expand this research to other populations,” she added. “Our hypothesis is that this is relevant and consistent across populations of illiterate adults.” © 2019 The New York Times Company

Keyword: Language; Alzheimers
Link ID: 26838 - Posted: 11.21.2019