Links for Keyword: Autism

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By William Kenower My youngest son, Sawyer, used to spend far more time relating to his imagination than he did to the world around him. He would run back and forth humming, flapping his hands and thumping on his chest. By the time he was in first grade, attempts to draw him out of his pretend world to join his classmates or do some class work led to explosions and timeouts. At 7 he was given a diagnosis of being on the autism spectrum. That was when my wife, Jen, learned about the practice called joining. The idea behind it, which she discovered in Barry Neil Kaufman’s book “Son-Rise,” is brilliant in its simplicity. We wanted Sawyer to be with us. We did not want him to live in this bubble of his own creation. And so, instead of telling him to stop pretending and join us, we started pretending and joined him. The first time Jen joined him, the first time she ran beside him humming and thumping her chest, he stopped running, stopped thumping, stopped humming and, without a single word from us, turned to her and said, “What are you doing?” We took turns joining him every day, and a week later we got an email from his special education teacher telling us to keep doing whatever we were doing. He’d gone from five timeouts a day to one in a week. The classroom was the same, the work was the same – all that was different was that we had found a way to say to him in a language he could understand, “You’re not wrong.” Emboldened by our success, we set about becoming more fluent in this language. For the next couple of years we taught ourselves to join him constantly. This meant that whatever we were doing had to stop whenever we heard him running back and forth and humming. But we could not join him simply to get him to stop running and thumping and humming. We had to join him without any judgment or impatience. That was the trickiest part. The desire to fix him was great. I had come to believe that there were broken people in need of fixing. Sometimes, I looked like one of those people. I was a 40-year-old unpublished writer working as a waiter. My life reeked of failure. Many days I looked in the mirror and asked, “What is wrong with me?” © 2016 The New York Times Company

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: 22451 - Posted: 07.16.2016

By Rebecca Brewer, Jennifer Murphy, There is a persistent stereotype that people with autism are individuals who lack empathy and cannot understand emotion. It’s true that many people with autism don’t show emotion in ways that people without the condition would recognize. But the notion that people with autism generally lack empathy and cannot recognize feelings is wrong. Holding such a view can distort our perception of these individuals and possibly delay effective treatments. We became skeptical of this notion several years ago. In the course of our studies of social and emotional skills, some of our research volunteers with autism and their families mentioned to us that people with autism do display empathy. Many of these individuals said they experience typical, or even excessive, empathy at times. One of our volunteers, for example, described in detail his intense empathic reaction to his sister’s distress at a family funeral. Yet some of our volunteers with autism agreed that emotions and empathy are difficult for them. We were not willing to brush off this discrepancy with the ever-ready explanation that people with autism differ from one another. We wanted to explain the difference, rather than just recognize it. So we looked into the overlap between autism and alexithymia, a condition defined by a difficulty understanding and identifying one’s own emotions. People with high levels of alexithymia (which we assess with questionnaires) might suspect they are experiencing an emotion, but are unsure which emotion it is. They could be sad, angry, anxious or maybe just overheated. About 10 percent of the population at large — and about 50 percent of people with autism — has alexithymia. © 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: 22433 - Posted: 07.13.2016

By Tara Parker-Pope Hoping to alert parents to “red flags” that might signal autism, two advocacy groups yesterday launched a Web site, the ASD Video Glossary, that provides online glimpses of kids with autism to worried parents. But some experts fear the site, though well intentioned, also may cause anxiety among parents whose children are perfectly fine. The site contains videos that show subtle differences in how kids with autism speak, react, play and express themselves. The organizations behind it, Autism Speaks and First Signs, hope that parents who see resemblances in their own kids will be emboldened to seek early diagnosis and treatment, which many experts believe can improve outcomes for kids with autism. Visitors to the new site must register in order to watch the videos, and in the first two hours of its release, more than 10,000 people did so. Yet some researchers fear the video glossary is certain to be troubling for the parents of children without autism, too, because the behavior of kids without the condition can resemble that depicted in the videos. “Just as there’s a spectrum in autism…there’s a spectrum in normal development,” Dr. Michael Wasserman, a pediatrician at Ochsner Medical Center in New Orleans told the Associated Press. “Children don’t necessarily develop in a straight line.” But Amy Wetherby, a professor of communications disorders at Florida State University who helped create the site, said the videos would embolden parents to persist when doctors don’t listen to legitimate concerns about a child’s behavior. As she told the Associated Press, sometimes “parents are the first to be concerned, and the doctors aren’t necessarily worried,” she said. “This will help give them terms to take to the doctor and say, ‘I’m worried about it.”’ © 2016 The New York Times Company

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: 22432 - Posted: 07.13.2016

By David Dobbs It’s difficult to tell what Gina Pace wants unless you already know what she wants. But sometimes that’s easy, and this is one of those times: Gina wants pizza. “I-buh!” she says repeatedly—her version of “I want.” We all do. We are sitting at Abate’s in New Haven, Connecticut, a town famous for—among other things—pizza and science. Gina and her father, Bernardo, who live on Staten Island in New York City, have made the two-hour drive here for both. The pizza is in the oven. The science is already at the table, represented by Abha Gupta, a developmental pediatrician at Yale’s renowned Child Study Center. Gupta is one of the few scientific experts on a condition that Bernardo and Gina know through hard experience. Gina, now 24, was diagnosed 20 years ago with childhood disintegrative disorder, or CDD. CDD is the strangest and most unsettling developmental condition you have probably never heard of. Also known as Heller’s syndrome, for the Austrian special educator who first described it in 1908, it is a late-blooming, viciously regressive form of autism. It’s rare, striking about 1 or 2 in every 100,000 children. After developing typically for two to 10 years (the average is three or four), a child with CDD will suffer deep, sharp reversals along multiple lines of development, which may include language, social skills, play skills, motor skills, cognition, and bladder or bowel control. The speed and character of this reversal varies, but it often occurs in a horrifyingly short period—as short as a couple of months, says Gupta. In about 75 percent of cases, this loss of skills is preceded by days or weeks in which the child experiences intense anxiety and even terror: nightmares and waking nightmares and bouts of confused, jumpy disturbance that resemble psychosis.

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: 22423 - Posted: 07.11.2016

By David Shultz Making eye contact for an appropriate length of time is a delicate social balancing act: too short, and we look shifty and untrustworthy; too long, and we seem awkward and overly intimate. To make this Goldilocks-like dilemma even trickier, it turns out that different people prefer to lock eyes for different amounts of time. So what’s too long or too short for one person might be just right for another. In a new study, published today in Royal Society Open Science, researchers asked a group of 498 volunteers to watch a video of an actor staring out from a screen and press a button if their gazes met for an uncomfortably long or short amount of time (above). During the test, the movement of their eyes and the size of their pupils were recorded with eye-tracking technology. On average, participants had a “preferred gaze duration” of 3.3 seconds, give or take 0.7 seconds. That’s a pretty narrow band for someone on their first date! Making things even harder, individual preferences can also be measured: Researchers found that how quickly people’s pupils dilated—an automatic reflex whenever someone looks into the eyes of another—was a good indicator of how long they wanted to gaze. The longer their preferred gaze, the faster their pupils expanded. The differences are so subtle, though, that they can only be seen with the eye-tracking software—making any attempts to game the system is likely to end up awkward rather than informative. © 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: 22398 - Posted: 07.06.2016

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