The nature of the mutation that leads to Angelman syndrome — a disorder characterized by speech impairment and developmental delays — affects the disorder’s presentation, reports a study published 19 March in Research in Developmental Disabilities.

Autism, schizophrenia and intellectual disability share underlying deficits in pathways that regulate how the brain encodes new experiences, says Jason Shepherd.

A small fragment of RNA may regulate the expression of RORA, a gene implicated in many autism-related pathways, according to a study published 6 February in Scientific Reports.

Long pieces of RNA that do not code for protein have diverse and important roles in the cell and may contribute to autism risk, say Nikolaos Mellios and Mriganka Sur.

Mutations in TRIM33, a protein that is part of the cell’s cleanup crew, may up the risk for autism, according to a study published 5 November in Molecular Psychiatry.

Mutations in a single gene in 15q11.13 — a chromosomal region linked to multiple neurological disorders — may increase the risk of autism, according a study published in November in Nature Genetics.

Tune in for daily updates and reactions from attendees at the 2013 Society for Neuroscience meeting in San Diego, California.

A gene’s length may influence its expression, and this has implications for autism, which tends to be linked to particularly long genes, says Mark Zylka. 

Researchers have uncovered the mechanism by which a candidate drug for Angelman syndrome activates UBE3A, the gene that is silenced in the syndrome, according to a study published 20 August in the Proceedings of the National Academy of Sciences.

Neurons derived from individuals who carry extra copies of an autism-linked chromosomal region have gene expression patterns that are unexpectedly similar to those of neurons with deletions of the region. The unpublished findings were presented Thursday at the Dup15q Alliance Scientific Meeting in Sacramento, California.