Two new analyses help to explain why mutations to the chromosomal region 16p11.2 can lead to autism, intellectual disability or language difficulties.
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Parents of children with rare autism-linked mutations are banding together for support and to join forces with scientists, accelerating the pace of research.
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Music therapy proves ineffective for autism, brain structures differ with 16p11.2 duplications and deletions, and mice missing NLGN3 may influence the sociability of their littermates.
Children missing a stretch of DNA on chromosome 16 show worsening motor and social skills in the first eight years of life; those with an extra copy of the region do not show this decline.
An autism-linked rearrangement on chromosome 16 often occurs on the copy of the chromosome inherited from the mother.
People with an extra copy of the autism-linked chromosomal region 16p11.2 have a range of characteristics, suggesting that other genetic factors are at play.
Cell biologist Nicholas Katsanis explains why zebrafish have been key in studying a chromosomal region linked to autism.
Deletion and duplication of the 16p11.2 chromosomal region have opposite effects on brain size, but produce similar alterations in the brain’s processing of sound. Researchers reported these and other unpublished findings at the 2013 Society for Neuroscience annual meeting in San Diego, painting a complex picture of the region’s role in autism.