Study maps genetic variability in autism brains
The first effort to sequence genes tied to autism in postmortem brain tissue reveals a range of harmful mutations in people with the condition.
The first effort to sequence genes tied to autism in postmortem brain tissue reveals a range of harmful mutations in people with the condition.
An online catalog helps clarify the roles of thousands of spontaneous mutations in four neuropsychiatric disorders, including autism.
Analyzing the sequences of more than 20,000 people, researchers have unearthed the largest and most robust list of autism genes so far, they reported today in Nature.
Researchers have sequenced the whole genomes of 1,000 people with autism and their parents, they announced yesterday at the American Society of Human Genetics Annual Meeting in San Diego. These sequences, and another 1,000 that are on the way, will eventually be freely available online.
Much of the genetic risk for autism may reside in regulatory regions of the genome, hidden from traditional methods of sequence analysis. That’s the upshot of preliminary results from three studies presented yesterday at the American Society of Human Genetics Annual Meeting in San Diego.
A new method of statistical analysis can predict whether a rare mutation identified in someone with autism has a meaningful association with the disorder or was found only by chance, researchers reported in the September issue of Nature Genetics.
Now that genetic studies have implicated several hundred genes in autism, researchers are turning their attention to where and when in the healthy young brain these genes are expressed. The first two studies to tackle these questions appear today in Cell.
Spontaneous mutations are elevated in people with autism, but only in those who also have intellectual disability, according to unpublished data presented yesterday at a conference in Cambridge, Massachusetts.
The first sizable study to use whole-genome sequencing to investigate autism has shown its mettle, revealing new mutations and candidate genes for the disorder, according to a report published 11 July in the American Journal of Human Genetics.