The loss or delay of language is one of the most common — and most noticeable — features of autism.
Rare or common, inherited or spontaneous, mutations form the core of autism risk.
“I don’t know anything about Williams syndrome”: That isn’t exactly how you’d expect a talk at a meeting on the syndrome to begin, but it happened more than once at a symposium on the disorder last week. Could scientific interchange between Williams syndrome and autism researchers benefit people with either condition?
A mouse model of Williams syndrome pinpoints a genetic region associated with the social behavior seen in the disorder, and may also yield insights into autism, says researcher Uta Francke, professor emeritus of genetics at Stanford University.
Individuals with attention deficit hyperactivity disorder (ADHD) have a higher rate of DNA duplications and deletions, including some in regions linked to autism and schizophrenia, according to a study published 23 October in The Lancet.
A new wave of genetic tests for fragile X syndrome, the leading cause of inherited mental retardation and the most common genetic cause of autism, may make it possible to routinely screen pregnant women and newborns for the syndrome.
A new mouse model of Angelman syndrome that knocks out a large stretch of a key chromosome is clarifying some of the molecular mechanisms underlying the more severe forms of the disorder.
A point mutation in the autism-linked protein neuroligin-3 (NLGN3), seen in individuals with autism, causes the protein to misfold and localize to the wrong site in the cell, according to a study published in September in the Journal of Biological Chemistry.
Two new studies provide clues that may explain sex differences in autism prevalence. Italian researchers have found that injecting estrogen into the brains of young male mice reverses some of the structural and behavioral changes associated with low levels of reelin — a brain protein that has been previously implicated in autism — and the effects endure into adulthood.