Sleep apnea during pregnancy may increase the risk of brain and behavioral changes associated with autism in males, a new study reports.
Three different autism risk genes affect similar aspects of neural formation and the same types of neurons in the developing human brain.
Inducing massive inflammation resulted in an overexpression of Trpv4. The overexpression led to neural hyperexcitability that resulted in social avoidance behaviors associated with ASD in mouse models.
Study reports 1 in 5 teens and young adults who seek treatment for alcohol and substance use disorders may have previously unrecognized social impairments characteristic of ASD.
When GABA targets are activated, visual processing for people on the autism spectrum becomes more like that of non-autistic people.
Researchers identified molecular signatures of gestational inflammation that appear to be biomarkers for autism risk. The immune signatures were identified in both maternal blood samples during pregnancy and in umbilical cord blood from children later diagnosed with ASD.
Infants and toddlers on the autism spectrum who showed the poorest neural responses to motherese, or baby-talk by parents, also displayed the most severe social symptoms, poorest language outcomes, and greatest impairments in behavioral preference and attention toward motherese. Conversely, neurotypical children showed stronger neural responses and affinity to motherese.
Study reveals symptoms of autism can be detected within the first year of a child's life, and early detection can help with interventions that may significantly reduce the severity of lifelong developmental deviation.
The deletion of the autism-associated Tbx1 gene results in slower cognitive processing and decreased myelin in mouse models.
A new review of almost 200 publications suggests the gut microbiota may play a critical role in modulating brain function, social behavior and other symptoms of autism.
Children with autism have abnormally low levels of the CNTNAP2 protein. The protein, which can be detected in cerebrospinal fluid samples, may serve as a new biomarker for autism and could potentially become a target to treat epilepsy that is commonly associated with ASD.
Gene editing may provide hope for the treatment of Fragile X, the leading genetic cause of autism.
