TAOK2, a gene in the autism-associated 16p11.2 chromosomal region, is part of a signaling pathway that builds neuronal connections during development, according to a study published 10 June in Nature Neuroscience.
Studying tuberous sclerosis provides researchers with a unique opportunity to find a common pathway among the various genetic causes of autism, says neurologist Mustafa Sahin.
Mice lacking the autism-associated gene SHANK2 show autism-like behaviors similar to those seen in mice lacking SHANK3, another member of the same gene family. But SHANK2 and SHANK3 mice have distinct alterations at neuronal junctions, according to a report published 29 April in Nature.
Mutations in more than 100 autism-associated genes lead to shared neurobiological deficits in mice, including alterations in the shape of their brains and changes to the electrical properties of neurons, according to a study published 20 February in Molecular Autism.
By screening the genomes of hundreds of people with autism and analyzing the effects of newly identified mutations in cultured neurons, researchers have clarified the disorder’s link to the SHANK2 gene.
A new microscope allows researchers to capture the movement of tiny signal-receiving branches in the brains of adult mice at the nanoscale level. The results were published 3 February in Science.
Neurobeachin, or NBEA, an autism–associated gene, may regulate the transport of signaling molecules to neuronal branches, according to a study published 22 November in Nature Communications.
Researchers have uncovered cellular abnormalities in Timothy syndrome by regenerating neurons from individuals with the rare autism-related disorder, according to a study published 27 November in Nature Medicine.
The etiology of autism may be best understood as an impairment of neuronal circuits, specifically interneurons that dampen signals in the brain, says neuroscientist Gordon Fishell.
Wenbao Gan describes the technique he has devised to track the development of neurons in live mouse brains.