Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Rachel Ehrenberg Patterns of neural circuitry in the brain's frontal and parietal lobes can be used to distinguish individuals on the basis of their brain scans. Our brains are wired in such distinctive ways that an individual can be identified on the basis of brain-scan images alone, neuroscientists report. In a study published in Nature Neuroscience1 on 12 October, researchers studied scans of brain activity in 126 adults who had been asked to perform various cognitive tasks, such as memory and language tests. The data were gathered by the Human Connectome Project, a US$40-million international effort that aims to map out the highways of neural brain activity in 1200 people. To study connectivity patterns, researchers divided the brain scans into 268 regions or nodes (each about two centimetres cubed and comprising hundreds of millions of neurons). They looked at areas that showed synchronized activity, rather like discerning which instruments are playing together in a 268-piece orchestra, says Emily Finn, a co-author of the study and a neuroscience PhD student at Yale University in New Haven, Connecticut. In some regions of the brain — such as those that involve networks controlling basic vision and motor skills — most people’s neural circuitry connects up in similar ways, the team found. But patterns of connectivity in other brain regions, such as the frontal lobes, seem to differ between individuals. The researchers were able to match the scan of a given individual's brain activity during one imaging session to the same person’s brain scan taken at another time — even when that person was engaged in a different task in each session. © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 21506 - Posted: 10.13.2015
By ERICA GOODE Women who suffer from anorexia are often thought of as having an extraordinary degree of self-control, even if that discipline is used self-destructively. But a new study suggests that the extreme dieting characteristic of anorexia may instead be well-entrenched habit — behavior governed by brain processes that, once set in motion, are inflexible and slow to change. The study’s findings may help explain why the eating disorder, which has the highest mortality rate of any mental illness, is so stubbornly difficult to treat. But they also add to increasing evidence that the brain circuits involved in habitual behavior play a role in disorders where people persist in making self-destructive choices no matter the consequences, like cocaine addiction or compulsive gambling. In the case of anorexia, therapists often feel helpless to interrupt the relentless dieting that anorexic patients pursue. Even when patients say they want to recover, they often continue to eat only low-fat, low-calorie foods. Neither psychiatric medications nor talk therapies that are used successfully for other eating disorders are much help in most cases. And research suggests that 50 percent or more of hospitalized anorexic patients who are discharged at a normal weight will relapse within a year. “The thing about people with anorexia nervosa is that they can’t stop,” said Dr. Joanna E. Steinglass, an associate professor in clinical psychiatry at the New York State Psychiatric Institute at Columbia University Medical Center and a co-author of the new study, which appears in the journal Nature Neuroscience. “They come into treatment saying they want to get better, and they can’t do it,” Dr. Steinglass added. Karin Foerde, a research scientist at the psychiatric institute and Columbia, was the lead author on the study. © 2015 The New York Times Company
By Nancy Szokan Sensory deprivation is Sushma Subramanian’s topic in the October issue of Women’s Health magazine, and she offers a couple of extreme examples. Julie Malloy, 33, from York, Pa., describes living without the sense of touch: “I was born with a rare sensory illness that leaves me unable to feel pain, temperature, deep pressure, or vibrations in my arms, legs, and the majority of my chest and back. I use vision to compensate as much as I can. . . . “I always wash my face with cold water; I once burned myself without realizing it. . . . When I drive, I can’t really tell how hard I’m pushing on the pedals. I watch others really enjoy it when someone kisses their arm or get tingly when someone hugs them, but I can’t even feel anything during sex.” Erin Napoleone, 31, from Havre de Grace, Md., describes losing her sense of smell: “As a teen, I was in a car accident. A few days later, I watched my father make homemade tomato sauce — but I didn’t smell a thing. Then I couldn’t detect my mom’s familiar perfume. A head CT scan confirmed my sense of smell was gone for good.” The magazine points out that some senses naturally deteriorate with age and that taking care of your skin — say, by keeping it moisturized and protecting it from damage — can help preserve the sense of touch. But olfactory nerves facing “prolonged exposure to rank odors (think freeway fumes or curbside trash)” can be permanently damaged.
By SINDYA N. BHANOO Tiny nematode worms called Caenorhabditis elegans have a peculiar reproductive story: Most females are hermaphrodites that make sperm, self-fertilize and produce more hermaphrodites. Males are few, and are known to mate with each other. Now, a new study reports that a variation in a single gene results in male worms with excretory pores that attract the sexual attentions of other males. “Other males copulate with this excretory pore, located on the neck,” said Matthew Rockman, a biologist at New York University. He and his colleagues reported their findings in the journal Current Biology. Although male worms are rare in the wild, they are easily bred in the laboratory. Researchers report that the gene variant, known as plep-1, may somehow be altering the chemical profile of the excretions in a way that makes them more attractive to other males. Copulation often does not work out well for the male that is approached, Dr. Rockman said. Males that mate with the excretory pore of another male usually leave behind a plug that weakens the worm and reduces life expectancy. Hermaphrodites with the variation of the same gene also have a lower life expectancy and do not reproduce as well. Next, the researchers want to learn what it is about a mutation in the plep-1 gene that makes males attractive to other males. © 2015 The New York Times Company
Ed Yong This week, a team from the University of California, Los Angeles claimed to have found several epigenetic marks—chemical modifications of DNA that don’t change the underlying sequence—that are associated with homosexuality in men. Postdoc Tuck Ngun presented the results yesterday at the American Society of Human Genetics 2015 conference. Nature News were among the first to break the story based on a press release issued by the conference organisers. Others quickly followed suit. “Have They Found The Gay Gene?” said the front page of Metro, a London paper, on Friday morning. Meanwhile, the mood at the conference has been decidedly less complimentary, with several geneticists criticizing the methods presented in the talk, the validity of the results, and the coverage in the press. Ngun’s study was based on 37 pairs of identical male twins who were discordant—that is, one twin in each pair was gay, while the other was straight—and 10 pairs who were both gay. He analysed 140,000 regions in the genomes of the twins and looked for methylation marks—chemical Post-It notes that dictate when and where genes are activated. He whittled these down to around 6,000 regions of interest, and then built a computer model that would use data from these regions to classify people based on their sexual orientation. The best model used just five of the methylation marks, and correctly classified the twins 67 percent of the time. “To our knowledge, this is the first example of a biomarker-based predictive model for sexual orientation,” Ngun wrote in his abstract. The problems begin with the size of the study, which is tiny. The field of epigenetics is littered with the corpses of statistically underpowered studies like these, which simply lack the numbers to produce reliable, reproducible results.
By ANDREW SOLOMON INEXPLICABLE violence is the hardest kind to accept. The human wish to insert logic where there is none often drives bystanders to psychic violence of their own. This happened again last week, after it was reported that the shooter at Umpqua Community College in Oregon, Christopher Harper-Mercer, who killed nine people and injured several others, may have been autistic. Although there is no established connection between autism and murder, some eagerly leapt to causality and scapegoating. The killer’s “diagnosis” was based primarily on posts on Yahoo made over the last decade by his mother, Laurel Harper, in which she characterized both herself and her son as having Asperger’s syndrome — a category no longer in medical use that describes autistic people with advanced verbal skills. Mr. Harper-Mercer attended a school that caters to children with special needs, including autism. While Ms. Harper is not a doctor, her descriptions of her son across his childhood are consistent with the syndrome. A Facebook page called “Families Against Autistic Shooters” ranted about “the soulless, dead eyes of autistic children,” and characterized them as “cold, calculating killing machines with no regard for human life!” Its author announced: “What do all shooters over the last few years have in common? A lack of empathy and compassion due to Autism!” If Mr. Harper-Mercer were rumored to have been diabetic or afflicted with male-pattern baldness, no such “explanations” of his behavior would have surfaced. But despite a huge increase in awareness of autism among the public, those with the condition are often subject to this type of disparagement. This was evident in both the Facebook page and the response to it by Facebook’s management, who, despite the site’s anti-bullying policy, initially refused to remove it on grounds that it did not target named individuals. “Families Against Autistic Shooters” remained accessible until last Monday, by which time escalating media attention and a petition on Change.org with nearly 5,000 signatures embarrassed administrators into action. For the time it was viewable, the page stigmatized a population far more likely to be attacked than to attack, far less likely to receive justice when injured, and far more likely to be misunderstood. © 2015 The New York Times Company
By Kat Long In the delivery room, the (slight) odds are that a newborn is a baby boy, not a girl. Males make up 51.3 percent of live births in the U.S., a rate that has remained about constant for the past seven decades. Experts assumed that this male-skewed sex ratio began at conception, but a new analysis of fetal records shows that the chances overall of finding a boy or a girl start out at 50–50 and change over the course of pregnancy—leaning female, then male, then female again as nine months pass. In the most comprehensive study of its kind to date, biologist Steven Hecht Orzack of the Fresh Pond Research Institute in Massachusetts and his collaborators analyzed roughly 36 million fertility treatment records, prenatal tests, induced abortions and U.S. Census data points. They discovered several nodes at which the sex ratio wavered from 50–50. Those vacillations most likely arise because of genetic and chromosomal abnormalities that cause natural abortions at various stages of gestation, write the study's authors in the Proceedings of the National Academy of Sciences USA. “This is basic knowledge about human pregnancy that we didn't have before,” Orzack says. “Demographers, developmental biologists, and many more can all get something out of this study.” © 2015 Scientific American
Keyword: Sexual Behavior
Link ID: 21500 - Posted: 10.12.2015
By KENNETH D. MILLER SOME hominid along the evolutionary path to humans was probably the first animal with the cognitive ability to understand that it would someday die. To be human is to cope with this knowledge. Many have been consoled by the religious promise of life beyond this world, but some have been seduced by the hope that they can escape death in this world. Such hopes, from Ponce de León’s quest to find a fountain of youth to the present vogue for cryogenic preservation, inevitably prove false. In recent times it has become appealing to believe that your dead brain might be preserved sufficiently by freezing so that some future civilization could bring your mind back to life. Assuming that no future scientists will reverse death, the hope is that they could analyze your brain’s structure and use this to recreate a functioning mind, whether in engineered living tissue or in a computer with a robotic body. By functioning, I mean thinking, feeling, talking, seeing, hearing, learning, remembering, acting. Your mind would wake up, much as it wakes up after a night’s sleep, with your own memories, feelings and patterns of thought, and continue on into the world. I am a theoretical neuroscientist. I study models of brain circuits, precisely the sort of models that would be needed to try to reconstruct or emulate a functioning brain from a detailed knowledge of its structure. I don’t in principle see any reason that what I’ve described could not someday, in the very far future, be achieved (though it’s an active field of philosophical debate). But to accomplish this, these future scientists would need to know details of staggering complexity about the brain’s structure, details quite likely far beyond what any method today could preserve in a dead brain. © 2015 The New York Times Company
The month of your birth influences your risk of developing dementia. Although the effect is small compared to risk factors such as obesity, it may show how the first few months of life can affect cognitive health for decades to come. Demographers Gabriele Doblhammer and Thomas Fritze from the University of Rostock, Germany, studied data from the Allgemeine Ortskrankenkasse – Germany’s largest public health insurer – for nearly 150,000 people aged 65 and over. After adjusting for age, they found that those born in the three months from December to February had a 7 per cent lower risk of developing dementia than those born in June to August, with the risk for other months falling in between. There’s nothing astrological about the effect, however. Instead, birth month is a marker for environmental conditions such as weather and nutrition, says Gerard van den Berg, an economist at the University of Bristol, UK, who studies the effects of economic circumstances on health. Summer-born babies are younger when they face the respiratory infections of their first winter, for example. And in the past, babies born in spring and summer would have been in late gestation when the supply of fresh fruit and vegetables from the autumn harvest would have largely run out. Pollution from wood fires or coal heating might also have played a role. There’s evidence from other studies that such factors can have lifelong effects on metabolism and the immune system, increasing the risk of conditions such as diabetes, obesity and high blood pressure. Doblhammer and Fritze’s results show this is true for dementia too. © Copyright Reed Business Information Ltd.
By Ariana Eunjung Cha When it comes to studies on birth order, first-borns tend to make out pretty well. Research says they tend to be smarter, more outgoing, and exhibit more leadership qualities. Unfortunately, it's not all good news. A new paper published in JAMA Ophthalmology shows that first-borns also tend to be 10 percent more likely to be near-sighted and 20 percent more likely to have severe myopia than their siblings. In fact, the risk for myopia appeared to be progressively lower the later you were born in terms of your birth order. The researchers from Cardiff University suggested that the cause was “parental investment in education” because parents may have a tendency to put more pressure on first-borns. They theorized that parents may be more demanding that first-borns do more "near" activities, such as reading, which may impact their eyesight. Previous studies have shown a strong link between time spent outdoors and a diminished risk of myopia, and it may stand to reason that children who spend more time on studies may be spending less time outdoors. Jeremy Guggenheim, a doctoral student, and colleagues wrote that while there's no way to make a definitive causal link, their study found that when they adjusted for a proxy for educational exposure — the highest educational degree or age at completion of full-time education — they saw a less dramatic association between near-sightedness and birth order.
Link ID: 21497 - Posted: 10.10.2015
By Bill Berkrot (Reuters) - U.S. researchers on Thursday said they had found a way to predict male sexual orientation based on molecular markers that control DNA function, but genetics experts warned that the research has important limitations and will not provide definitive answers to a potential biological basis for sexual preference. Findings from the study, which has yet to be published or reviewed in detail by other scientists, were presented at a meeting of the American Society of Human Genetics in Baltimore. It followed 37 pairs of identical male twins in which one was homosexual and one heterosexual, and 10 sets of twins in which both males were homosexual. The study found that the presence of specific epigenetic marks in nine areas of the human genome could predict homosexual preference with up to 70% accuracy. The epigenome is sometimes described as molecular "switches" that can turn on or silence individual genes in DNA. Scientists believe epigenetic differences can be influenced by environmental and lifestyle factors, from exposure to chemicals to parental nurturing. "To our knowledge, this is the first example of a predictive model for sexual orientation based on molecular markers," Tuck Ngun, lead researcher on the study from the David Geffen School of Medicine of the University of California, Los Angeles, said in a statement. Genetics experts who critiqued the findings said it was premature to draw any conclusions on the predictive powers of epigenetic markers. © 2015 Scientific American
By Hanae Armitage Schools of fish clump together for a very simple reason: safety in numbers. But for some, banding together offers more than just protection. It’s a way of getting to the head of the class. Schooling fish learn from each other, and new research shows that when they’re taken out of their normal social group, individuals struggle to learn on their own. Scientists have long known that schooling fish observe and learn from each other’s failures and successes, behaviors that stimulate neural development, especially in the part of the brain responsible for memory and learning. But this is the first time they have found evidence of that link in spatial learning. To test their theory, scientists divided a school of social cichlid fish into two categories: 14 social fish and 15 loners. Researchers kept the social fish grouped together while they partitioned the loners into single-fish isolation tanks. They ran both groups through a simple T-shaped maze, color coding the side that harbored food—a yellow mark for food, a green mark for no food. Seven of the 14 socialized fish learned to associate yellow with food (high marks for the cichlids, which are not the brightest fish in the animal kingdom), whereas only three of the 15 isolated fish successfully made the same association. Writing in this month’s issue of Applied Animal Behaviour Science, the researchers say this suggests fish in group settings are able to learn better and faster than their singled out counterparts. The moral? Simple: Fish should stay in school. © 2015 American Association for the Advancement of Science
Fragment of rat brain simulated in supercomputer Moheb Costandi A controversial European neuroscience project that aims to simulate the human brain in a supercomputer has published its first major result: a digital imitation of circuitry in a sandgrain-sized chunk of rat brain. The work models some 31,000 virtual brain cells connected by roughly 37 million synapses. The goal of the Blue Brain Project, which launched in 2005 and is led by neurobiologist Henry Markram of the Swiss Federal Institute of Technology in Lausanne (EPFL), is to build a biologically-detailed computer simulation of the brain based on experimental data about neurons' 3D shapes, their electrical properties, and the ion channels and other proteins that different cell types typically produce (see ‘Brain in a box’). Such a simulation would provide deep insights into the way the brain works, says Markram. But other neuroscientists have argued that it will reveal no more about the brain’s workings than do simpler, more abstract simulations of neural circuitry — while sucking up a great deal of computing power and resources. The initiative has links with the Human Brain Project, a €1-billion (US$1.1-billion), decade-long initiative which Markram helped persuade the European Commission to fund, and which also aims to advance supercomputer brain simulation. It launched in 2013, with Markram as co-leader, although this March its leadership was switched and its scientific programme altered, after criticism of the way it was being managed. © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 21494 - Posted: 10.09.2015
Gay or straight? A saliva test can predict the answer, and get it right 67 per cent of the time – for male identical twins at least. The test, which uses clues from tiny modifications to a person’s genome, is the first that claims to detect sexual orientation. Many scientists have expressed caution over the results, while concerns over potential misuse of the test have led the study’s lead researcher to quit the project entirely. “The scientific benefit to understanding [why people vary in sexual orientation] is obvious to anyone with an iota of curiosity,” says Michael Bailey at Northwestern University in Evanston, Illinois. “The predictive test needs replication on larger samples in order to know how good it is, but in theory it’s quite interesting.” Over the last two decades, several studies have suggested that sexual orientation is, in part, down to our genes. Perhaps the biggest splash was made in 1993 by Dean Hamer’s team at the National Cancer Institute in Bethesda, Maryland, when they found that gay brothers tended to share a sequence of five genetic markers in a region of the X chromosome. The same region has been implicated in other studies of sexual orientation since, although researchers haven’t been able to single out “gay genes”. Other observations also suggest a genetic basis for sexual orientation, such as the mysterious fraternal birth order effect. For every male pregnancy a woman has, a subsequent son has a 33 per cent higher chance of being homosexual, although no one knows why. The overall chance is still low, however, rising from around 2 per cent to just 6 per cent for a third son. © Copyright Reed Business Information Ltd.
Elaine Korry Efforts to protect children in foster care from being inappropriately medicated with powerful antipsychotic drugs got a big boost forward on Tuesday, when California Gov. Jerry Brown signed three bills into law designed to reform prescribing. Overprescribing of psychiatric meds for foster youth is a persistent problem nationwide, with children given the drugs at double or triple the rate of those not in foster care. In 2011, the federal Government Accounting Office found nearly 1 in 4 children in foster care was taking psychotropic medications, which include antipsychotics, antidepressants, mood stabilizers and stimulants. Hundreds of children were found to be taking five or more psychotropic medications at a time, and thousands were prescribed doses that exceeded FDA-approved guidelines. According to the report, monitoring programs fell short of guidelines established by the American Academy of Child and Adolescent Psychiatry. Many of the medications have side effects that include lethargy, weight gain, diabetes and tremors. The California legislation, which covers 63,000 children and teens in foster care, will allow public health nurses access to medical records to monitor the foster children who are prescribed psychotropic drugs; identify the group homes that rely most on these medications and potentially require them to take corrective action; and provide child welfare workers with better training and oversight tools to spot dangerous prescribing practices. © 2015 NPR
By CATHERINE SAINT LOUIS Ever since the Food and Drug Administration approved the use of the narcotic painkiller OxyContin for certain children in August, it has faced unabated criticism from lawmakers and public officials who are wrestling with devastating rates of prescription opioid abuse in their communities. Last week, Hillary Rodham Clinton brought the issue to the presidential race, calling the agency’s action “absolutely incomprehensible.” The crux of the issue is whether the agency’s approval will lead to more prescriptions for OxyContin in young patients. For years, the powerful long-acting drug has been prescribed off-label to very sick children in severe pain from cancer or spinal-fusion surgery. (Doctors can prescribe an approved drug to anyone and for any use they see fit regardless of specifications on the label.) The agency’s approval means those doctors will finally have “information about how to do it appropriately,” like dosage recommendations, said Dr. Stephen Ostroff, the agency’s acting commissioner, in an interview. “We recognize this is a very nuanced issue,” said Dr. Ostroff, when asked about Mrs. Clinton’s recent comments. “It needs to be understood in the context of why this was done.” Dr. Kathleen A. Neville, a pediatric oncologist at Arkansas Children’s Hospital, routinely treats children with unremitting pain caused by cancer or sickle cell anemia. Her patients are the kind the F.D.A. envisioned would benefit from OxyContin, despite its “risks of addictions, abuse and misuse” as a warning on the new label says. Dr. Neville, who said she had no financial ties to makers of painkillers, applauded the agency’s approval. “Just because OxyContin has been abused or prescribed inappropriately doesn’t mean we should deprive the children who need the drug,” she said, adding it is “our obligation to have the best level of evidence for its use in children.” © 2015 The New York Times Company
A new drug for multiple sclerosis can cut relapses by almost 50% more than the current standard treatment, its manufacturer claims, raising the hopes of sufferers of the disease. The Swiss pharmaceutical giant Roche announced the headline results for its drug, ocrelizumab, but has not published the detailed outcome of its trials. The announcement was warmly welcomed by patients, not least because Roche claims the drug also has an impact on a form of the disease, called primary-progressive, which affects 10-15% of people with MS in the UK and for which there are no treatments. Roche claimed it cut disability in those patients by nearly a quarter. “These phase three trial results will provide a great deal of hope for people with primary-progressive MS, who currently don’t have any treatments available that can slow down the worsening of their condition,” said Nick Rijke, the MS Society’s executive director for policy and research. “Finding effective treatments for multiple sclerosis is our number one priority at the MS Society and this is a big moment. The drug was compared in the trials with Rebif, an established drug made by Merck that reduces relapses by about a third. Ocrelizumab – which does not yet have a brand name – was said to cut annual relapses by 46% and 47% compared with Rebif in the two trials. The biggest advantage, however, may be that it is claimed to cause fewer side effects than the established drug. © 2015 Guardian News and Media Limited
It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21488 - Posted: 10.08.2015
By Somer Bishop Subtle, significant. In a nutshell, these two words capture the symptoms of many girls with autism. Like many in my field, I’ve seen this subtlety firsthand. One 6-year-old girl I met several years ago seemed, at first, to have good social skills. She responded appropriately when I introduced myself, complimented my outfit, and politely answered all of my questions. It was only when I saw her again a few days later that I understood her family’s concerns: She made nearly identical overtures, as if our interaction were part of a play she had rehearsed. I also met a teenage girl with autism who was highly intelligent. Because she could not relate to the other girls at her high school, she began interacting exclusively with boys, whose social behaviors she found easier to imitate. She even went through a period of wanting to become a boy, reasoning that she might have more success navigating the social world as a male. The past several years have seen an explosion of studies aimed at backing up these one-off observations about how autism presents differently in girls than in boys. This is a welcome development, as understanding the unique presentation of autism in girls will help us to better identify and treat the disorder. Consistently recognizing autism in girls can be challenging, however. This is not only because girls with autism are as diverse as any other group of individuals with the disorder but also because most autism screening and diagnostic tools were developed based primarily on observations of behaviors in boys. © 2015 The Slate Group LLC.