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By Elizabeth Pennisi Cave fish have long fascinated biologists because of their missing eyes and pale skin. Now, one researcher is studying them for another reason: Their behavior may provide clues to the genetic basis of some human psychiatric disorders. Last week at the 23rd International Conference on Subterranean Biology in Fayetteville, Arkansas, he demonstrated how drugs that help people with schizophrenia and autism similarly affect the fish. “I think there is a lot of potential” for these fish to teach us about mental disorders, says David Culver, an evolutionary biologist at American University in Washington, D.C., who was not involved in the study. Culver adds that—like other work on the cause of cave fish blindness—the new research may also have implications for human disease. A decade ago, the lead author on the new study, Masato Yoshizawa, wanted to understand brain evolution by investigating the effects of natural selection on behavior. The Mexican tetra (Astyanax mexicanus), a cave fish with very close surface relatives, seemed an excellent prospect for that work. Because the two populations can interbreed, it’s easier to pin down genes that might be related to the neural defects underlying behavioral differences. Such breeding studies are not possible in humans. The blind cave fish differ from their surface relatives in several notable ways. They don’t have a social structure and they don’t school. Instead, they lead solitary lives—a behavior that makes sense given their lack of natural predators. They also almost never sleep. They are hyperactive, and—unlike other fish—they are attracted to certain vibrations in the water. Finally, they tend to do the same behavior over and over again and seem to have higher anxiety than their surface relatives. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 13: Memory, Learning, and Development
Link ID: 22361 - Posted: 06.25.2016

By Ruth Williams The offspring of certain mice fed a high-fat diet have altered gut microbiomes and may be prone to autism-like behaviors including social deficits, according to a study published today (June 16) in Cell. But treating these offspring with a specific microbial species they lack can rectify the animals’ social behavior. “There’s growing evidence that the microbiome, particularly early in life, can have long-term effects on brain development and behavior,” said anatomist and neuroscientist John Cryan of University College Cork in Ireland who was not involved in the study. “What this paper does is take advantage of the fact that we get our microbiome from our mums, and looks at what happens if the mum disturbs her microbiome during pregnancy.” According to the US Centers for Disease Control and Prevention, one in 68 U.S. children have autism spectrum disorder (ASD). Recent evidence suggests that the risk of ASD is increased for the offspring of mothers with obesity. In both humans and non-human primates, the offspring of obese mothers have also been shown to have abnormal microbiomes. And some people with ASD have imbalanced gut microbes, or dysbiosis. Baylor College of Medicine’s Mauro Costa-Mattioli and colleagues sought to better understand how maternal obesity, the microbiome, and ASD are interconnected. The team turned to mice for answers. The researchers gave female animals high-fat diets before setting up matings, later finding that a “large proportion” of the offspring exhibited ASD-like behaviors, including reduced social interaction, repetitive behaviors, and anxiety. The team analyzed the microbiomes of these offspring, finding that they differed from those of control animals. © 1986-2016 The Scientist

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22336 - Posted: 06.18.2016

By Teal Burrell Sociability may be skin deep. The social impairments and high anxiety seen in people with autism or related disorders may be partly due to a disruption in the nerves of the skin that sense touch, a new study in mice suggests. Autism spectrum disorders are primarily thought of as disorders of the brain, generally characterized by repetitive behaviors and deficits in communication skills and social interaction. But a majority of people with autism spectrum disorders also have an altered tactile sense; they are often hypersensitive to light touch and can be overwhelmed by certain textures. “They tend to be very wary of social touch [like a hug or handshake], or if they go outside and feel a gust of wind, it can be very unnerving,” says neuroscientist Lauren Orefice from Harvard Medical School in Boston. An appreciation for this sensory aspect of autism has grown in recent years. The newest version of psychiatry’s bible, the Diagnostic and Statistical Manual of Mental Disorders, includes the sensory abnormalities of autism as core features of the disease. “That was a big nod and a recognition that this is a really important aspect of autism,” says Kevin Pelphrey, a cognitive neuroscientist at The George Washington University in Washington, D.C., who was not involved in the work. The sensation of touch starts in the peripheral nervous system—in receptors at the surface of the skin—and travels along nerves that connect into the central nervous system. Whereas many autism researchers focus on the end of the pathway—the brain—Orefice and colleagues wondered about the first leg of the trip. So the group introduced mutations that silenced genes associated with autism spectrum disorders in mice, adding them in a way that restricted the effects to peripheral nerve cells, they report today in Cell. The team singled out the gene Mecp2, which encodes a protein that regulates the expression of genes that help forge connections between nerve cells. © 2016 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 5: The Sensorimotor System
Link ID: 22310 - Posted: 06.11.2016

By Sarah DeWeerdt, Spectrum Brains from people with autism show patterns of gene expression similar to those from people with schizophrenia, according to a new analysis. The findings, published May 24 in Translational Psychiatry, deepen the connections between the two conditions, says study leader Dan Arking, associate professor of genetic medicine at Johns Hopkins University in Baltimore, Maryland. People who have either autism or schizophrenia share features such as language problems and difficulty understanding other people’s thoughts and feelings. They also have genetic risk factors in common. “And now I think we can show that they share overlap in gene expression,” Arking says. The study builds on previous work, in which Arking’s team characterized gene expression in postmortem brain tissue from 32 individuals with autism and 40 controls. In the new analysis, the researchers made use of that dataset as well as one from the Stanley Medical Research Institute that looked at 31 people with schizophrenia, 25 with bipolar disorder and 26 controls3. They found 106 genes expressed at lower levels in autism and schizophrenia brains than in controls. These genes are involved in the development of neurons, especially the formation of the long projections that carry nerve signals and the development of the junctions, or synapses, between one cell and the next. The results are consistent with those from previous studies indicating a role for genes involved in brain development in both conditions. “On the one hand, it’s exciting because it tells us that there’s a lot of overlap,” says Jeremy Willsey, assistant professor of psychiatry at the University of California, San Francisco, who was not involved in the work. “On the other hand, these are fairly general things that are overlapping.” © 2016 Scientific American

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22294 - Posted: 06.07.2016

By Ann Griswold, Women who develop infections during pregnancy run an increased risk of having a child with autism. Most data indicate that an overactive maternal immune response underlies the risk. But a new analysis runs contrary to this view: It ties high levels of an inflammatory protein in pregnant women to a low risk of autism in their children, suggesting that a strong immune response is protective. Researchers looked at 1,315 mother-child pairs, including 500 children with autism and 235 with developmental delay. They found that healthy pregnant women with high levels of C-reactive protein (CRP), a marker of inflammation, are less likely to have a child with autism than are women with typical levels of the protein. The findings contradict a 2013 report from a large Finnish cohort that tied high CRP levels during pregnancy to an increased risk of having a child with autism. “It was the opposite of what we expected to find,” says senior researcher Lisa Croen, director of the Autism Research Program at Kaiser Permanente in Oakland, California. The work appeared in April in Translational Psychiatry. The results suggest that the strength of a woman’s immune system, rather than its response to infection, is the important factor in determining autism risk. Moderate or low baseline levels of CRP might indicate a relatively weak ability to fight off infection. And a less vigorous immune response might boost the risk in some women, the researchers say. © 2016 Scientific American,

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22275 - Posted: 06.02.2016

By Geraldine Dawson There’s a popular saying in the autism community: “If you’ve met one person with autism, you’ve met one person with autism.” Although this phrase is meant to convey the remarkable variation in abilities and disabilities among people with autism spectrum disorder (ASD), we’re learning that it also applies to the extraordinary variability in how ASD develops. When I first began doing research on autism decades ago, we thought of it as one condition and aimed to discover its “cause.” Now we know ASD is actually a group of lifelong conditions that can arise from a complex combination of multiple genetic and environmental factors. In the same way that each person with ASD has a unique personality and profile of talents and disabilities, each also has a distinct developmental history shaped by a specific combination of genetic and environmental factors. More evidence of this extraordinary variety will be presented this week in Baltimore, where nearly 2,000 of the world’s leading autism researchers will gather for the International Meeting for Autism Research (IMFAR). As president of the International Society for Autism Research, which sponsors the conference, I am more impressed than ever with the progress we are making. New findings being presented at the conference will highlight the importance of the prenatal period in understanding how various environmental factors such as exposure to alcohol, smoking and certain chemical compounds can increase risk for ASD. The impact of many environmental factors depends, however, on an individual’s genetic background and the timing of the exposure. Other research links inflammation—detected in blood spot tests taken at birth—with a higher likelihood of an ASD diagnosis later on. Researchers suggest that certain factors such as maternal infection and other factors during pregnancy may influence an infant’s immune system and contribute to risk. As our knowledge of these risk factors grows, so do the opportunities for promoting healthy pregnancies and better outcomes. © 2016 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22199 - Posted: 05.10.2016

By John Elder Robison Manipulating your brain with magnetic fields sounds like science fiction. But the technique is real, and it’s here. Called transcranial magnetic stimulation (TMS), it is approved as a therapy for depression in the US and UK. More controversially, it is being studied as a way to treat classic symptoms of autism, such as emotional disconnection. With interest and hopes rising, it’s under the spotlight at the International Meeting for Autism Research in Baltimore, Maryland, next week. I can bear witness to the power of TMS, which induces small electrical currents in neurons. As someone with Asperger’s, I tried it for medical research, and described its impact in my book Switched On. After TMS, I could see emotional cues in other people – signals I had always been blind to, but that many non-autistic people pick up with ease. That sounds great, so why the need for debate? Relieving depression isn’t controversial, because there is no question people suffer as a result of it. I too felt that I suffered – from emotional disconnection. But changing “emotional intelligence” to relieve that comes closer to changing the essence of how we think. Yes, emerging brain therapies like TMS have great potential. Several of the volunteers who went into the TMS lab at Harvard Medical School emerged with new self-awareness, and lasting changes. While I can’t speak with certainty for the others, I believe some of us have a degree of emotional insight that we didn’t have before. I certainly feel better able to fit in. As fellow participant Michael Wilcox put it, we have more emotional reactions to things we see or read. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 22187 - Posted: 05.07.2016

By Karen Weintraub The four members of Asperger’s Are Us decided a long time ago that their main goal would be to amuse themselves. But after nearly a decade of laughing and writing punch lines together, Asperger’s Are Us, which is probably the only comedy troupe made up of people on the autism spectrum, is on the cusp of comedic success. A documentary about the group premiered at the SXSW conference in Austin in March and was recently sold to Netflix. The troupe is also preparing for its first national tour this summer. Comedy might be a surprising choice for someone with Asperger’s syndrome, since stereotypically, people with autism are generally regarded as socially awkward loners. But the four men in the group bonded at summer camp 11 years ago, when one was a counselor and the other three were campers, and are clearly great friends. An “Aspergers Are Us” performance from 2011. Talking recently via Skype, Noah Britton, the former counselor, settles giant black rabbit ears onto his head. Jack Hanke, another member of the troupe, dons his favorite sombrero – the black one he took with him to Oxford University during his recent junior year abroad – accessorized with a red sombrero on top. They slip into their usual banter when asked what they thought of the film, named for the group, which will be shown publicly for the first time on Friday at the Somerville Theater outside of Boston. “I liked the four weird guys in it,” Mr. Britton said. “It was better than ‘Jaws 2,’ but not as good as ‘Jaws 3,’” Mr. Hanke insisted. “I found it kind of annoying myself,” added Ethan Finlan, another member of the group. The fourth member, who changed his first name to New Michael to distinguish himself from his father, Michael Ingemi, didn’t want to join the call. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22169 - Posted: 05.03.2016

New York's Tribeca Film Festival will not show Vaxxed, a controversial film about the MMR vaccine, its founder Robert De Niro says. As recently as Friday, Mr De Niro stood by his decision to include the film by anti-vaccination activist Andrew Wakefield in next month's festival. The link the film makes between the measles, mumps and rubella vaccine and autism has been widely discredited. "We have concerns with certain things in this film," said Mr De Niro. Mr De Niro, who has a child with autism, said he had hoped the film would provide the opportunity for discussion of the issue. But after reviewing the film with festival organisers and scientists, he said: "We do not believe it contributes to or furthers the discussion I had hoped for." Image caption Wakefield published his controversial study in 1998 Vaxxed was directed and co-written by Mr Wakefield, who described it as a "whistle-blower documentary". In a statement issued following the Tribeca Film Festival's decision, he and the film's producer Del Bigtree said that "we have just witnessed yet another example of the power of corporate interests censoring free speech, art and truth". The British doctor was the lead author of a controversial study published in 1998, which argued there might be a link between MMR and autism and bowel disease. Mr Wakefield suggested that parents should opt for single jabs against mumps, measles and rubella instead of the three-in-one vaccine. His comments and the subsequent media furore led to a sharp drop in the number of children being vaccinated against these diseases. But the study, first published in The Lancet, was later retracted by the medical journal. Mr Wakefield's research methods were subsequently investigated by the General Medical Council and he was struck off the medical register.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22037 - Posted: 03.28.2016

John Consentino After multiple doctors had conflicted about ADHD, I decided to move away from psychiatry and seek a neuropsychologist. I thought that autism made sense, but what ultimately led me to seek help was my focus problem. When I was 8 years old, it would take me HOURS to do homework. On Wednesdays, we got out of school at noon, and I wouldn't finish homework until about 8 p.m. No one understood why this was happening, and with all of the screaming and punishments I withstood, nothing improved. I still had GPAs near the high 90s, so all was OK, supposedly. I struggled with eye contact during that time, and this is very much apparent now. I struggled speaking to waiters/waitresses, to teachers, to family members. Speaking to members of the opposite sex was a near-impossible task. I never understood social groups. I went through all of high school in the same fashion. However, my family felt that everything was OK. I still had a mid-90 GPA, and I had made numerous friends. Unfortunately, my GPA had dropped by about 15-plus points by my senior year. I struggled badly during my first two years of college. I was constantly unhappy, and I made little to no friends. My GPA was horrid, and my time at the university was dwindling. I dropped out of school twice, and my future felt bleak. After transferring schools, I did great. So, everything was OK yet again. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22036 - Posted: 03.28.2016

Nicola Davis The same genes involved in predisposing people to autism appear to influence social skills in the wider population, suggesting that the autism spectrum has no clear cut-off point, scientists have discovered. Researchers have previously shown that autism is linked not just to one or two powerful genes, but to the combined effect of many small genetic changes. The latest findings, published in Nature Genetics, suggest that social charm, empathy and the ability to make friends is about more than just practice and upbringing, but is also affected by how many of these autism risk gene variants we possess. Dr Elise Robinson, from Harvard University and a lead author on the paper, said: “This is the first study that specifically shows that ... factors that we have unambiguously associated with autism are also very clearly associated with social communication differences in the general population.” Rather than viewing a person as either having or not having such a disorder, Robinson believes our social skills are better viewed as sitting on a sliding scale across the whole population. “The primary implication is that the line at which we say people are affected or unaffected is arbitrary,” said Robinson. “There is no clear objective point either in terms of genetic risk or in terms of behavioural traits, where you can say quite simply or categorically that you’re affected or unaffected. It’s like trying to pick a point where you say someone is tall or not.” © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22014 - Posted: 03.22.2016

By Emily Underwood People with autism spectrum disorder (ASD) die on average 18 years before the general population, according to a report released today by Autistica, a philanthropic group based in the United Kingdom. People with both ASD and an intellectual disability die even younger, on average 30 years earlier than those without the conditions. Fatal accidents—often by drowning, when a child or adult with ASD wanders away from caregivers—are one of the classic causes of premature death in people who have both ASD and an intellectual disability, says Sven Bölte, a clinical psychologist at the Karolinksa Institute in Stockholm, whose research is cited in the Autistica report. Epilepsy, along with several other neurological disorders, is another common cause of death among people with both ASD and learning difficulties, suggesting that early disruption of neurodevelopment is to blame. These “classic” causes of premature death in autism, however, do not fully account for a decades-long life span gap between autistic and nonautistic people, or the difference in mortality between autistic people with and without an intellectual disability, Bölte says. To explore these gaps, in 2015 Bölte’s group published a large epidemiological study of more than 27,000 Swedish people with ASD, 6500 of whom had an intellectual disability. They found that risk of premature death was about 2.5 times higher for the entire group, a gap largely due to increased prevalence of common health problems such as diabetes and respiratory disease. Patients may be being diagnosed too late because they do not know how to express health concerns to their doctors, Bölte says, making it “extremely important” for general practitioners to thoroughly explore autistic patients’ symptoms and histories. © 2016 American Association for the Advancement of Scienc

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22010 - Posted: 03.19.2016

By John Elder Robison What happens to your relationships when your emotional perception changes overnight? Because I’m autistic, I have always been oblivious to unspoken cues from other people. My wife, my son and my friends liked my unflappable demeanor and my predictable behavior. They told me I was great the way I was, but I never really agreed. For 50 years I made the best of how I was, because there was nothing else I could do. Then I was offered a chance to participate in a study at Beth Israel Deaconess Medical Center, a teaching hospital of Harvard Medical School. Investigators at the Berenson-Allen Center there were studying transcranial magnetic stimulation, or T.M.S., a noninvasive procedure that applies magnetic pulses to stimulate the brain. It offers promise for many brain disorders. Several T.M.S. devices have been approved by the Food and Drug Administration for the treatment of severe depression, and others are under study for different conditions. (It’s still in the experimental phase for autism.) The doctors wondered if changing activity in a particular part of the autistic brain could change the way we sense emotions. That sounded exciting. I hoped it would help me read people a little better. They say, be careful what you wish for. The intervention succeeded beyond my wildest dreams — and it turned my life upside down. After one of my first T.M.S. sessions, in 2008, I thought nothing had happened. But when I got home and closed my eyes, I felt as if I were on a ship at sea. And there were dreams — so real they felt like hallucinations. It sounds like a fairy tale, but the next morning when I went to work, everything was different. Emotions came at me from all directions, so fast that I didn’t have a moment to process them. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22009 - Posted: 03.19.2016

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

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21843 - Posted: 02.01.2016

Ian Sample Science editor Genetically modified (GM) monkeys that develop symptoms of autism have been created to help scientists discover treatments for the condition. The macaques carry a genetic fault that causes a rare disorder in humans called MeCP2 duplication syndrome. This produces a wide range of medical conditions, some of which mirror those seen in autism, such as difficulties with social interactions. Researchers say groups of the GM monkeys could be used to identify brain circuits involved in common autistic behaviours and to test new treatments designed to alleviate the symptoms. Because the monkeys pass the genetic defects on to their offspring, scientists can breed large populations of the animals for medical research. A group of 200 monkeys has been established at the scientists’ lab in China. The research, described in the journal Nature, paves the way for more varieties of GM monkeys that develop different mental and psychiatric problems which are almost impossible to study in other animals. “The first cohort of transgenic monkeys shows very similar behaviour to human autism, including increased anxiety, but most importantly, defects in social interactions,” said Zilong Qiu who led the research at the Institute of Neuroscience in Shanghai. © 2016 Guardian News and Media Limited or it

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21824 - Posted: 01.26.2016

By Melinda Wenner Moyer There's a reason your mother told you to look people in the eye when you talk to them: eye contact conveys important social cues. Yet when someone holds your gaze for more than a few seconds, the experience can take on a different tenor. New work elucidates the factors that affect whether we like or loathe locking eyes for a lengthy period. Researchers have long known that eye contact is an important social signal. Our recognition of its import may even be hardwired. One study found that five-day-old babies prefer looking at faces that make direct eye contact compared with faces that have an averted gaze. “Eye contact provides some of the strongest information during a social interaction,” explains James Wirth, a social psychologist now at Ohio State University at Newark, because it conveys details about emotions and intentions. (Lack of eye contact is one of the early signs of autism in infants and toddlers.) The power of eye contact is so great that, according to a 2010 study co-authored by Wirth, if someone avoids your gaze for even a short period, you may feel ostracized. But what determines how we feel about prolonged eye contact? One recent study explored this question. In research presented in May 2015 at the Vision Sciences Society conference, psychologist Alan Johnston and his colleagues at University College London collected information from more than 400 volunteers about their personalities. Then the subjects indicated their comfort level while watching video clips of actors who appeared to be looking directly at them for varying lengths of time. © 2016 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21746 - Posted: 01.04.2016

By Andrea Anderson Mom's ovaries could hold clues to some autism cases, new research suggests—and this time it's not because of genetic vulnerabilities carried in her eggs. A new, large-scale study out of Sweden suggests that women with polycystic ovarian syndrome (PCOS)—an endocrine disorder that affects 5 to 10 percent of women of childbearing age—have an increased risk of giving birth to children with autism spectrum disorder (ASD). The Karolinska Institute's Renee Gardner, along with colleagues from Sweden and the U.S., tapped into a Swedish national population health database to look at potential ties between PCOS and ASD. As they reported online December 8 in Molecular Psychiatry, the team looked at 23,748 individuals with ASD and nearly 209,000 unaffected individuals, all born in Sweden between 1984 and 2007. Although identifying information about the individuals was removed, the researchers had access to information about their relationships to others in the database as well as documented diagnoses and use of health care services. The group found that ASD was 59 percent more prevalent in children born to women with PCOS—a relationship that was independent of PCOS complications such as increased neonatal distress or C-section delivery. This risk level is roughly comparable with that of having a father over age 50 (estimated to be 66 percent) but lower than it is in those with certain rare genetic syndromes or mutations. The authors of the analysis believe PCOS increases ASD risk in offspring to a greater extent than maternal infection, one of many factors previously implicated in autism. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21694 - Posted: 12.12.2015

By Darold A. Treffert The headlines read “New study suggests autism can be outgrown”, or “outgrowing autism: a doctor’s surprise and wonder.” The stories are based on studies reporting that 7-9% of children with a documented early autistic syndrome disorder (ASD) have no symptoms of the disorder on follow-up later in childhood or adolescence. That is good news. The question is how to account for it. Is it possible to simply “outgrow” autism? Was the initial diagnosis wrong? Did some interventions work? Or might there be other explanations for this welcome news? "In an earlier column titled “Oops. When “autism” isn’t autistic disorder,” I outlined three types of hyperlexia, or precocious reading ability, which is sometimes an element of a diagnosis of ASD. Type 1 are neurotypical children who simply read way ahead of their chronological age. Listening to a 4 year old reading books to his or her nursery school classmates is a startling experience. Type 2 are children in which intense fascination with letters and numbers, along with early reading and remarkable memory represent ‘splinter skills’ as a part of autistic syndrome disorder (ASD) Type 3 are children who likewise show intense fascination and preoccupation with numbers and letters very early, along with precocious reading skills and remarkable memory. They do have “autistic-like” symptoms or behaviors but those disappear over time as the child gets older. The outcome in these children is much more positive than those with ASD to their benefit and the great relief of their parents. Following the “Oops” article I received numerous reports from parents who identified with hyperlexia 3. “You just described my child,” the puzzled, and relieved parents would write as they read the case examples in my Wisconsin Medical Journal article in December, 2011. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21689 - Posted: 12.10.2015

By Jennie Baird Last week’s news that Sesame Street was introducing the first autistic Muppet was met in my house with a resounding, “Huh?” “But there already is an autistic Muppet,” my high-functioning 14-year-old said. “Fozzie Bear.” I had never thought of Fozzie that way, but my son had a point. Fozzie is not good at taking social cues; he doesn’t read a room well and he tends to monologue and perseverate (to repeat himself long after the need has passed). He interprets figurative language as literal — remember that fork in the road in “The Muppet Movie?” He has a verbal tic he falls back on, “wokka-wokka.” And he hates to be separated from his hat for no obvious reason. I’ve tested this theory on friends and have seen the light bulb of recognition go off every time. Of course Fozzie has autism! One friend, a mother whose son is also on the spectrum even told me her family had the exact same conversation. Sesame Street hopes children will identify with their new character Julia, described as a “friend who has autism,” and appearing, for now, only in the book “We’re Amazing 1-2-3!” There is no question, the mere presence of Julia is a positive development. But she also introduces a rarely discussed complication of autism. Let’s call it the Fozzie Conundrum. I’m particularly sensitive to the Fozzie Conundrum now that my son attends regular honors classes in a regular public high school. Naturally sociable and charismatic — and with eight years of support and interventions from a team of terrific teachers and therapists at specialized schools — he can easily “pass” as a regular, funny, quirky teenager. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21590 - Posted: 11.02.2015

Elizabeth Blair The muppet Julia has not yet made her TV debut, but the wide-eyed little girl with a big smile is the star of her own "digital storybook" called "We're Amazing, 1,2,3." For over a year now, Sesame Street has been working with organizations such as Autism Speaks and Autism Self Advocacy to help reduce the stigma associated with autism spectrum disorder. As part of the campaign "See Amazing in All Children," the adorable muppet Abby Cadabby explains in one YouTube video, "Lots of kids have autism and that just means their brains work a little differently." Julia is not the first fictional media character with autism. But Michael Robb, Director of Research for Common Sense Media, an organization that rates and reviews media aimed at children, says Sesame Street's move is "pretty groundbreaking." "It can be difficult to start a conversation about children with disabilities. It's even harder when that difference isn't visible," he says. After looking through "We're Amazing, 1,2,3," Robb says the story could help children be more understanding of how Julia is different. "It's very real in terms of talking in simple language. It spells out these things in concrete ways that kids can understand. It shows ways she's just like other kids. It shows how making simple accommodations can help Julia." According to Dr. Jeanette Betancourt, Senior Vice President of U.S. Social Impact at Sesame Workshop, says Sesame Street producers are waiting to hear back from the autism community before introducing Julia to the show on TV. © 2015 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21557 - Posted: 10.24.2015