Two-hit wonder
We know that carrying one specific DNA variant can increase your risk of autism. What if you carry two?
We know that carrying one specific DNA variant can increase your risk of autism. What if you carry two?
Several genetic and animal studies in the past year have found intriguing ties between autism and DISC1, one of the oldest candidate genes for psychiatric disorders.
Individuals who carry a large and rare deletion on chromosome 16 that is associated with autism are likely to have developmental delays, be obese or both, according to two studies published last week in Nature.
Scientists have for the first time found direct evidence that defects in the GABA receptor sometimes give rise to autism, according to research published 24 November in Molecular Psychiatry.
Deletions or duplications of chromosomal segment 16p11.2 — previously reported as a key autism region — are seen in people with developmental delays and speech and behavioral problems, but not necessarily autism. That’s the finding from two large studies published last week of people carrying these rare genetic variations.
The Psychiatric GWAS Consortium has released its first batch of analyses, identifying several significant common variations associated with schizophrenia. The results were presented Sunday at the World Congress of Psychiatric Genetics in San Diego.
Variations linked to autism and schizophrenia crop up in people with a large variety of conditions, including bipolar disorder, seizures and obsessive-compulsive disorder, as well as in healthy people. This notion gained new support from unpublished data presented at the World Congress for Psychiatric Genetics in San Diego.
A new mutation in the neuroligin-4 (NLGN4) gene, one of the few genes convincingly tied to autism, has been found in two brothers with autism, further implicating the gene in the disorder, scientists reported in the Journal of Neuroscience.
Mice lacking a gene located in the chromosomal region 22q13 — which has been linked to autism — have motor learning and social deficits reminiscent of the disorder, according to unpublished findings presented in a poster session yesterday at the Society for Neuroscience meeting in Chicago.
After a Monday afternoon poster session at the Society for Neuroscience meeting in Chicago, Noboru Hiroi talked about the challenges of following up human genetic findings in the mouse.