Premature infants are more likely to develop autism, according to a study published in Cerebral Cortex, which shows that babies born more than 13 weeks before their due date are more likely to grow up with “severe brain damage, autism spectrum disorder (ASD), ADHD and learning difficulties. Researchers believe that this may be due to the fact that premature babies experience high levels of stress early in the critical brain development period. Researchers at Karolinska Medical School and Karolinska University Hospital in Sweden studied 100 newborns born before 27 weeks of gestation. With parental permission, the researchers used MRI to probe the children’s brain development in infancy and then assessed them at age 6 for clinical manifestations of autism. The results found that close to 30% of the ultra-preterm infants developed symptoms of autism later in life, compared with a 1% chance of developing autism symptoms at full term. Antidepressants during pregnancy linked to autism In a study of Canadian newborns published in the Journal of the American Medical Association, it was shown that antidepressants taken by women during pregnancy can increase the risk of fetal autism. Professor Anick Bérard of the University of Montreal and St. Justin’s Children’s Hospital followed the group for 10 years by studying 145,456 cases of pregnant women who successfully delivered babies in Quebec, Canada. The study documented the number and dosage of antidepressants taken by pregnant women in their first trimester. If a woman took antidepressants in the middle and second trimesters of pregnancy, the risk of fetal autism increased by 87 percent, the researchers said. Selective 5-hydroxytryptamine reuptake inhibitors (SSRIs) are common antidepressants that increase the risk of fetal autism when women take them in the middle and second trimesters of pregnancy. These drugs have a negative impact on fetal brain development. The study provides additional information for clinicians deciding whether to continue antidepressant treatment in pregnant women. Pregnant women with polycystic ovary syndrome (PCOS) are at increased risk for fetal autism. Androgens are the sex hormones responsible for the development of male characteristics and play a role in the development of the central nervous system of the brain. Research suggests that early exposure of fetuses to androgenic hormones may predispose them to autism. Polycystic ovary syndrome is a disease in which hormonal imbalances may alter a woman’s menstrual cycle, cause ovarian cysts, make it difficult to become pregnant and cause other health problems. Kyriaki Kosidou, lead researcher at the Karolinska School of Medicine School of Public Health in Sweden, and colleagues published their findings in the Journal of Molecular Psychiatry and found that a mother’s diagnosis of polycystic ovary syndrome can increase a child’s risk of developing an autism spectrum disorder by 59 percent. The researchers identified about 24,000 children with autism spectrum disorder born in Sweden between 1984 and 2007 and compared them to 200,000 children without the disorder. The risk of autism in children was further increased in mothers with both PCOS and obesity, which is common in PCOS patients and is associated with an excessive increase in androgens, the researchers said. Women with PCOS have higher androgen levels, even during pregnancy. However, this study only showed an association between PCOS and autism in the offspring and could not identify a causal relationship between the two. It is too early to make specific recommendations for the care of pregnant women with PCOS, but increased awareness of the association could help children born to these mothers obtain a diagnosis early. Brain changes caused by gene linked to autism explored for the first time University of Utah School of Medicine study shows that minor cellular changes caused by the Kirrel3 gene are potentially associated with multiple intellectual developmental disorders and autism. Harvard Medical School published in the journal eLife about how three proteins regulate chemical messengers in cells that are importantly linked to autism, Down syndrome and Rett syndrome. All human cognitive activity requires neurons in the brain to cooperate with each other via brain synapses. Considering that variations in the Kirrel3 gene are strongly associated with intellectual disability, autism and Yabu’s syndrome, experts at the University of Utah studied how variations in Kirrel3 affect brain circuits associated with memory learning functions in the brain. The study showed that the brain can help form mossy fiber synapses in the hippocampus through the Kirrel3 gene. In mice studies, mice without the Kirrel3 protein in their genes had malformed mossy fiber synapses, resulting in overactive hippocampus. The results of the experiment showed that subtle changes in brain synapses affect brain activity and can lead to mental retardation. In addition, the defects that appear in other parts of the brains of mice without Kirrel3 protein might be related to the neurodevelopmental disorder caused by Kirrel3. Also, the experimental results showed that in autism, the inhibitory synapses are not active enough; while in psychosis the inhibitory synapses are overactive. Researchers at Harvard Medical School proposed that mutations in the proteins Neurixin synaptic protein, Neuroligin neural connectivity protein and CASK protein cause chemical messengers to reduce neuronal activity. The experimental results explain the biochemical relationship between autism and neuronal inhibition. Chinese Professor Gong Chen PNAS: New Target for Autism Treatment Recently, scientists at Penn State University, have identified a new drug target that successfully repairs functional defects in neuronal cells from patients with Rett syndrome, a severe form of autism spectrum disorder. The research, led by Penn State biology professor Gong Chen, may lead to a new treatment for Rett syndrome and other forms of autism spectrum disorders. Related findings were published in the Jan. 4, 2016, issue of PNAS. The researchers took stem cells derived from skin cells of patients with Rett syndrome and differentiated them into neuronal cells that could be studied in the laboratory. These nerve cells carry a mutation in the MECP2 gene, a gene mutation thought to be responsible for most cases of Rett syndrome. The researchers found that these nerve cells lacked an important molecule, KCC2, which is extremely important for the normal function of nerve cells and brain development. KCC2 controls the function of the neurotransmitter GABA at a critical point in early brain development,” said Professor Chen. Interestingly, when we put KCC2 back into neurons of Rett syndrome patient origin, GABA function returned to normal. So we think that increasing KCC2 function in patients with Rett syndrome could lead to a potential new therapy.” The researchers also showed that treating diseased nerve cells with insulin-like growth factor 1 (IGF1) increased KCC2 levels and modified GABA neurotransmitter function.IGF1, a molecule that has been shown to reduce symptoms in mouse models of Rett syndrome, is the subject of an ongoing phase II clinical trial of the disease in humans. New directions in genetic testing! Advanced technology for autism spectrum disorder (ASD) diagnosis A team of researchers at Toronto Children’s Hospital in Canada published a study on Sept. 1, 2015, saying that the use of two new technologies-chromosomal microarray analysis and whole-genome exome sequencing-can screen for genes associated with ASD and help parents and doctors better understand their child’s chances of developing ASD. The results of the study were published in the Journal of the American Medical Association. Chromosome microarray analysis, which detects chromosomal abnormalities, has been recommended as the primary genetic test for patients with ASD. Whole-genome exome sequencing tests the genes that encode proteins for the presence of potential causative factors. This test is commonly used for scientific research. Stephen Scherer, MD, of Toronto Children’s Hospital in Canada, and colleagues used 258 unrelated children with ASD to explore their chances of having a certain genetic variant associated with ASD. Results: Molecular microarray analysis identified a genetic variant in 24 of 258 children (9.3%); whole-genome exome sequencing identified a genetic variant in 8 of 95 children. The odds ratio was found to increase to 15.8 percent by both methods. Subtypes were found to exist in ASD. When a child has a physical defect, such as oddly shaped ears or abnormally wrinkled hands, the chance of the child having a mutation causing ASD is as high as 37.5 percent. Although genetic test results are not currently the primary basis for diagnosis, 80 percent of parents in one poll said they would choose to send their child with ASD to be tested for autism mutation risk when their sister or brother is under two years old. Post-graduation needs of young people with high-functioning autism Abstract: The post-graduation living environment and service needs of older adolescents and adults with high-functioning autism who reside in Queensland, Australia, are described. Respondents were 95 parent pairs. Results showed that the majority of young people were not employed and lived at home. Of those who were offered jobs, 56% were in jobs that required a relatively low level of skill. The assessment found that they would spend more time on separate, technology-based activities and less time on employment or social aspects. Parents ranked employment support first in importance, followed by continuing education support, high school to adult transition support and social skills training.