Chapter 13. Memory, Learning, and Development
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By Julia Shaw The approach to Valentine's Day is a reminder that we humans are so intrigued by the idea of love that we have made it into something to celebrate in it’s own right. Love is something amazing. Love is something special. But what are the implications of love for our memories? Remember those “your brain on drugs” awareness posters? You can essentially substitute “love” for “drugs” and the same warnings apply. Scientists have found that being in love actually makes you activate some of the same brain regions as when you take addictive drugs, like ecstasy or cocaine. Neuroscientist Kayo Takahashi and his team have described passionate love as an “all-encompassing experience” which has “disorienting effects” and is generally considered “highly pleasurable”. While you probably don’t need a bunch of scientists to tell you that, you probably do need them to explain what that actually means in the brain. In 2015 Kayo and his team were keen on exploring the role of one particular culprit of the feel-good effects of love, the neurotransmitter dopamine. Among many other effects, dopamine generally makes us feel pleasure. Kayo and his team looked into the brains of people who were in the early stages of romantic relationships, and they found that when shown pictures of their romantic partners, participants experienced a flood of dopamine to parts of their brains. As it turns out, brains need to release dopamine in order to store long-term memories. © 2016 Scientific American
By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company
By CARL ZIMMER The Zika virus has quickly gained Ebola-level notoriety as it has spread through the Western Hemisphere in recent months. Researchers in Brazil, where it was first detected in May, have linked infections in pregnant women to a condition known as microcephaly: infants born with undersize heads. Where birth defects are concerned, however, the Zika virus is far from unique. A number of other viruses, such as rubella and cytomegalovirus, pose a serious risk during pregnancy. Researchers have uncovered some important clues about how those pathogens injure fetuses — findings that are now helping to guide research into the potential link between Zika and microcephaly. “I think we’ll discover a lot of parallels,” said Dr. Mark R. Schleiss, the director of pediatric infectious diseases and immunology at the University of Minnesota Medical School. The risk that viruses pose during pregnancy came to light in the mid-1900s, when outbreaks of rubella, or German measles, led to waves of birth defects, including microcephaly, cataracts and deformed hearts and livers. The number of infants affected was staggering. In an epidemic in Philadelphia in 1965, 1 percent of all babies were born with congenital rubella syndrome, which can also cause deafness, developmental disability, low birth weight and seizures. Because of vaccinations, such devastation is now rare in the United States and a number of other countries. “I’m 52, and I’ve seen one case of congenital rubella syndrome,” said Dr. David W. Kimberlin, a professor of pediatrics at the University of Alabama at Birmingham. But the virus is still a grave threat in developing countries. Worldwide, more than 100,000 children are born each year with congenital rubella syndrome. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21883 - Posted: 02.10.2016
By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 The New York Times Company
Link ID: 21879 - Posted: 02.10.2016
It’s well known that some people report that their mood is influenced by the seasons. But can the time of year affect other cognitive functions? To find out, Gilles Vandewalle and colleagues at the University of Liege in Belgium scanned the brains of 28 volunteers while they performed attention and working memory tests at different times of the year. To ensure the results were influenced by the seasons rather than the environmental conditions on the test day, the participants were confined to a lab for 4.5 days prior to the test, exposed to a constant light level and temperature. Although their test scores didn’t change with the seasons, activity in some brain areas showed a consistent seasonal pattern among the volunteers: brain activity peaked in the summer on the attention task and in the autumn on the memory task. Many seasonally changing factors could regulate such a pattern, including day length (known as photoperiod), temperature, humidity, social interaction and physical activity. Since these weren’t all controlled for in the study, it’s impossible to say what is responsible for the seasonal changes seen. “In our data it seems that photoperiod, or the rate of change of photoperiod, was more likely to explain what we were seeing. But we can’t exclude all the others,” says Vandewalle. The results suggest that over the course of a year, the brain might work in different ways to compensate for seasonal factors that could affect its function, enabling it to maintain a stable performance. Vandewalle speculates that these mechanisms might not work as well in some people, for example, those vulnerable to the winter blues. © Copyright Reed Business Information Ltd.
Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016
Link ID: 21871 - Posted: 02.09.2016
By Jesse Singal On paper, Dr. Kenneth Zucker isn’t the sort of person who gets suddenly and unceremoniously fired. For decades, the 65-year-old psychologist had led the Child Youth and Family Gender Identity Clinic (GIC), in Toronto, one of the most well-known clinics in the world for children and adolescents with gender dysphoria — that is, the feeling that the body they were born with doesn’t fit their true gender identity. Zucker had built up quite a CV during his time leading the clinic: In addition to being one of the most frequently cited names in the research literature on gender dysphoria and gender-identity development, and the editor of the prestigious journal Archives of Sexual Behavior, he took a leading role helping devise diagnostic and treatment guidelines for gender dysphoric and transgender individuals. He headed the group which developed the DSM-5’s criteria for its “gender dysphoria” entry, for example, and also helped write the most recent “standards of care” guidelines for the World Professional Association for Transgender Health — one of the bibles for clinicians who treat transgender and gender-dysphoric patients. An impressive career, yes, but it’s doubtful any of this gave him much comfort on December 15. That was when he was called in from vacation for an 8:30 a.m. meeting with his employer, the Centre for Addiction and Mental Health (CAMH), one of the largest mental health and addiction research hospitals in Canada. Given the long-brewing investigation of his clinic by the hospital, it’s unlikely Zucker was feeling optimistic about what awaited him in downtown Toronto. The GIC, which operates out of CAMH, pronounced “Cam-H,” had been standing firm against a changing tide in the world of psychological treatment for children with gender dysphoria. The “gender-affirmative” approach, which focuses on identifying young transgender children and helping them socially transition — that is, express their gender to others through their everyday clothes, name changes, or other means — has been on the rise in recent years, and has become the favored protocol of many activists and clinicians. GIC clinicians, who saw clients between ages 3 and 18, had a much more cautious stance on social transitioning for their younger clients — they believed that in many cases, it was preferable to first “help children feel comfortable in their own bodies,” as they often put it, since in the GIC’s view gender is quite malleable at a young age and gender dysphoria will likely resolve itself with time. © 2016, New York Media LLC
By Jeneen Interlandi The human brain’s memory-storage capacity is an order of magnitude greater than previously thought, researchers at the Salk Institute for Biological Studies reported last week. The findings, recently detailed in eLife, are significant not only for what they say about storage space but more importantly because they nudge us toward a better understanding of how, exactly, information is encoded in our brains. The question of just how much information our brains can hold is a longstanding one. We know that the human brain is made up of about 100 billion neurons, and that each one makes 1,000 or more connections to other neurons, adding up to some 100 trillion in total. We also know that the strengths of these connections, or synapses, are regulated by experience. When two neurons on either side of a synapse are active simultaneously, that synapse becomes more robust; the dendritic spine (the antenna on the receiving neuron) also becomes larger to support the increased signal strength. These changes in strength and size are believed to be the molecular correlates of memory. The different antenna sizes are often compared with bits of computer code, only instead of 1s and 0s they can assume a range of values. Until last week scientists had no idea how many values, exactly. Based on crude measurements, they had identified just three: small, medium and large. But a curious observation led the Salk team to refine those measurements. In the course of reconstructing a rat hippocampus, an area of the mammalian brain involved in memory storage, they noticed some neurons would form two connections with each other: the axon (or sending cable) of one neuron would connect with two dendritic spines (or receiving antennas) on the same neighboring neuron, suggesting that duplicate messages were being passed from sender to receiver. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 21866 - Posted: 02.06.2016
By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.
By Susana Martinez-Conde Take a look at the red chips on the two Rubik cubes below. They are actually orange on the left and purple on the right, if you look at them in isolation. They only appear more or less equally red across the images because your brain is interpreting them as red chips lit by either yellow or blue light. This kind of misperception is an example of perceptual constancy, the mechanism that allows you to recognize an object as being the same in different environments, and under very diverse lighting conditions. Constancy illusions are adaptive: consider what would have happened if your ancestors thought a friend became a foe whenever a cloud hid the sun, or if they lost track of their belongings–and even their own children—every time they stepped out of the cave and into the sunlight. Why, they might have even eaten their own kids! You are here because the perceptual systems of your predecessors were resistant to annoying changes in the physical reality–as is your own (adult) perception. There are many indications that constancy effects must have helped us survive (and continue to do so). One such clue is that we are not born with perceptual constancy, but develop it many months after birth. So at first we see all differences, and then we learn to ignore certain types of differences so that we can recognize the same object as unchanging in many varied scenarios. When perceptual constancy arises, we lose the ability to detect multiple contradictions that are nevertheless highly noticeable to young babies. © 2016 Scientific American
Mo Costandi The human brain is immediately recognizable by its cortex (meaning bark in Latin), the prominent outer layer of tissue, with its characteristic pattern of ridges and furrows, which sits atop the deep structures. The cortex is just several millimetres thick, but has a surface area of about two-and-a-half square feet, and is therefore heavily convoluted so it can be packed into the skull. This fleshy landscape begins to form during the second trimester of pregnancy, and continues into the first year of life. It is often assumed to be the result of genetics, like most other aspects of brain development. Forty years ago, however, Harvard researchers put forward the controversial idea that the brain folds up because of physical forces, and a new study now provides the first evidence this. According to this old model, the brain’s folds form as a result of differential growth which causes the cortex to grow in size far more quickly than other brain structures, leading it to buckle and fold as its surface area increases, due to the constraints of the skull. To test this, Tuomos Tallinen of the University of Jyväskylä in Finland and his colleagues used magnetic resonance images to create a 3D-printed cast of an unfolded 22-week-old human brain. This was made with a technique called layer-by-layer drop casting, and consisted of a soft polymer core coated with a thin sheet of an absorbent elastomer gel representing the cortex. © 2016 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21857 - Posted: 02.04.2016
Heidi Ledford Difficulty with concentration, memory and other cognitive tasks is often associated with depression. In the past quarter of a century, a wave of drugs has transformed the treatment of depression. But the advances have struggled to come to grips with symptoms that often linger long after people start to feel better: cognitive problems such as memory loss and trouble concentrating. On 3 February, the US Food and Drug Administration (FDA) will convene a meeting of its scientific advisers to discuss whether such cognitive impairments are components of the disorder that drugs might be able to target — or just a result of depressed mood. The discussion will help the agency to decide whether two companies that sell the antidepressant vortioxetine should be allowed to label it as a treatment for the cognitive effects. A ‘yes’ could spur drug developers to invest in ways to test cognitive function during their antidepressant trials. Psychiatrists have long noted that some people with depression also struggle to concentrate and to make decisions. The question has been whether such difficulties are merely an offshoot of altered mood and would thus clear up without specific treatment, says Diego Pizzagalli, a neuroscientist at McLean Hospital, an affiliate of Harvard Medical School in Belmont, Massachusetts. But some patients who report improved mood after treatment still struggle with cognitive deficits — so psychiatrists sometimes prescribe concentration-enhancing drugs that are approved to treat attention deficit hyperactivity disorder to people with depression. © 2016 Nature Publishing Group
Fears over surveillance seem to figure large in the bird world, too. Ravens hide their food more quickly if they think they are being watched, even when no other bird is in sight. It’s the strongest evidence yet that ravens have a “theory of mind” – that they can attribute mental states such as knowledge to others. Many studies have shown that certain primates and birds behave differently in the presence of peers who might want to steal their food. While some researchers think this shows a theory of mind, others say they might just be reacting to visual cues, rather than having a mental representation of what others can see and know. Through the peephole Thomas Bugnyar and colleagues at the University of Vienna, Austria, devised an experiment to rule out the possibility that birds are responding to another’s cues. The setup involved two rooms separated by a wooden wall, with windows and peepholes that could be covered. First, a raven was given food with another raven in the next room, with the window open or covered, to see how quickly it caches its prize. With the window open, the birds hid their food more quickly and avoided going back to conceal it further. Then individual ravens were then trained to use the peephole to see where humans were putting food in the other room. The idea here was to allow the bird to realise it could be seen through the peephole. © Copyright Reed Business Information Ltd.
By Jonathan Webb Science reporter, BBC News Scientists have reproduced the wrinkled shape of a human brain using a simple gel model with two layers. They made a solid replica of a foetal brain, still smooth and unfolded, and coated it with a second layer which expanded when dunked into a solvent. That expansion produced a network of furrows that was remarkably similar to the pattern seen in a real human brain. This suggests that brain folds are caused by physics: the outer part grows faster than the rest, and crumples. Such straightforward, mechanical buckling is one of several proposed explanations for the distinctive twists and turns of the brain's outermost blanket of cells, called the "cortex". Alternatively, researchers have suggested that biochemical signals might trigger expansion and contraction in particular parts of the sheet, or that the folds arise because of stronger connections between specific areas. "There have been several hypotheses, but the challenge has been that they are difficult to test experimentally," said Tuomas Tallinen, a soft matter physicist at the University of Jyväskylä in Finland and a co-author of the study, which appears in Nature Physics. "I think it's very significant... that we can actually recreate the folding process using this quite simple, physical model." Humans are one of just a few animals - among them whales, pigs and some other primates - that possess these iconic undulations. In other creatures, and early in development, the cortex is smooth. The replica in the study was based on an MRI brain scan from a 22-week-old foetus - the stage just before folds usually appear. © 2016 BBC.
Keyword: Development of the Brain
Link ID: 21848 - Posted: 02.02.2016
By CATHERINE SAINT LOUIS The images pouring out of Brazil are haunting: struggling newborns with misshapen heads, cradled by mothers who desperately want to know whether their babies will ever walk or talk. There are thousands of these children in Brazil, and scientists fear thousands more might come as the Zika virus leaps across Latin America and the Caribbean. But the striking deformity at the center of the epidemic, microcephaly, is not new: It has pained families across the globe and mystified experts for decades. For parents, having a child with microcephaly can mean a life of uncertainty. The diagnosis usually comes halfway through pregnancy, if at all; the cause may never be determined — Zika virus is only suspected in the Brazilian cases, while many other factors are well documented. And no one can say what the future might hold for a particular child with microcephaly. For doctors, the diagnosis means an ailment with no treatment, no cure and no clear prognosis. If the condition surges, it will significantly burden a generation of new parents for decades. Dr. Hannah M. Tully, a neurologist at Seattle Children’s Hospital, sees the pain regularly, particularly among expectant parents who have just been told that an ultrasound showed their child to be microcephalic: “a terrible situation with which to be confronted in a pregnancy,” she said. An estimated 25,000 babies receive a microcephaly diagnosis each year in the United States. Microcephaly simply means that the baby’s head is abnormally small — sometimes just because the parents themselves have unusually small heads. “By itself, it doesn’t necessarily mean you have a neurological problem,” said Dr. Marc C. Patterson, a pediatric neurologist at the Mayo Clinic Children’s Center in Rochester, Minn. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21844 - Posted: 02.01.2016
By Lisa Rapaport Mothers who are obese during pregnancy have almost twice the odds of having a child with autism as women who weigh less, a U.S. study suggests. When women are both obese and have diabetes, the autism risk for their child is at least quadrupled, researchers reported online January 29 in Pediatrics. "In terms of absolute risk, compared to common pediatric diseases such as obesity and asthma, the rate of autism spectrum disorder (ASD) in the U.S. population is relatively low, however, the personal, family and societal impact of ASD is enormous," said senior study author Dr. Xiaobin Wang, a public health and pediatrics researcher at Johns Hopkins University in Baltimore. About one in 68 children have ASD, according to the U.S. Centers for Disease Control and Prevention, or about 1.5 percent of U.S. children. The study findings suggest the risk rises closer to about 3 percent of babies born to women who are obese or have diabetes, and approaches 5 percent to 6 percent when mothers have the combination of obesity and diabetes. Wang and colleagues analyzed data on 2,734 mother-child pairs followed at Boston Medical Center between 1998 and 2014. Most of the children, 64 percent, weren't diagnosed with any other development disorders, but there were 102 kids who did receive an ASD diagnosis. © 2016 Scientific American
By Mitch Leslie Identical twins may be alike in everything from their eye color to their favorite foods, but they can diverge in one important characteristic: their weight. A new study uncovers a molecular mechanism for obesity that might explain why one twin can be extremely overweight even while the other is thin. Heredity influences whether we become obese, but the genes researchers have linked to the condition don’t explain many of the differences in weight among people. Identical twins with nonidentical weights are a prime example. So what accounts for the variation? Changes in the intestinal microbiome—the collection of bacteria living in the gut—are one possibility. Another is epigenetic changes, or alterations in gene activity. These changes occur when molecules latch on to DNA or the proteins it wraps around, turning sets of genes “on” or “off.” Triggered by factors in the environment, epigenetic modifications can be passed down from one generation to the next. This type of transmission happened during the Hunger Winter, a famine that occurred when the Germans cut off food supplies to parts of the Netherlands in the final months of World War II. Mothers who were pregnant during the famine gave birth to children who were prone to obesity decades later, suggesting that the mothers’ diets had a lasting impact on their kids’ metabolism. However, which epigenetic changes in people promote obesity remains unclear. © 2016 American Association for the Advancement of Science
By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company
By Ellen Hendriksen This topic comes by request on the Savvy Psychologist Facebook page from listener Anita M. of Detroit. Anita works with foster kids and, too often, sees disadvantaged kids who have been on a cocktail of psychiatric medications from as early as age 6. She asks, does such early use alter a child’s brain or body? And have the effects of lifelong psychiatric medication been studied? Childhood mental illness (and resulting medication) is equally overblown and under-recognized. Approximately 21% of American kids - that’s 1 in 5 - will battle a diagnosable mental illness before they reach the age of 17, whether or not they actually get treatment. The problem is anything but simple. Some childhood illnesses - ADHD and autism, for example - often get misused as “grab-bag” diagnoses when something’s wrong but no one knows what. This leads to overdiagnosis and sometimes, overmedicating. Other illnesses, like substance abuse, get overlooked or written off as rebellion or experimentation, leading to underdiagnosis and kids slipping through the cracks. But the most common problem is inconsistent diagnosis. For example, a 2008 study found that fewer than half of individuals diagnosed with bipolar disorder actually had the illness, while 5% of those diagnosed with something completely different actually had bipolar disorder. But let’s get back to Anita’s questions: Does early psychotropic medication alter a child’s brain? The short answer is yes, but the long answer might be different than you think. © 2016 Scientific American
Nell Greenfieldboyce The state of New Jersey has been trying to help jurors better assess the reliability of eyewitness testimony, but a recent study suggests that the effort may be having unintended consequences. That's because a new set of instructions read to jurors by a judge seems to make them skeptical of all eyewitness testimony — even testimony that should be considered reasonably reliable. Back in 2012, New Jersey's Supreme Court did something groundbreaking. It said that in cases that involve eyewitness testimony, judges must give jurors a special set of instructions. The instructions are basically a tutorial on what scientific research has learned about eyewitness testimony and the factors that can make it more dependable or less so. "The hope with this was that jurors would then be able to tell what eyewitness testimony was trustworthy, what sort wasn't, and at the end of the day it would lead to better decisions, better court outcomes, better justice," says psychologist David Yokum. Yokum was a graduate student at the University of Arizona, doing research on decision-making, when he and two colleagues, Athan Papailiou and Christopher Robertson, decided to test the effect of these new jury instructions, using videos of a mock trial that they showed to volunteers. © 2016 npr
Keyword: Learning & Memory
Link ID: 21828 - Posted: 01.27.2016