Monthly Archives: February 2016


Adult mice recover Shank3-related deficits

Autism and autism spectrum conditions comprise a spectrum, in which most cases cannot be attributed to a single cause. In some cases, however, autism diagnoses have known genetic roots. Mutations in the Shank3 gene, which encodes an important synaptic protein, account for approximately 1% of autism cases. The Simons Center […]


Neuroscientists reverse autism symptoms

Neuroscientists reverse autism symptoms Turning on a gene later in life can restore typical behavior in mice. Source [Anne Trafton | MIT News Office, February 17, 2016] Autism has diverse genetic causes, most of which are still unknown. About 1 percent of people with autism are missing a gene called Shank3, […]


Mouse-hosted cells for developmental studies

Human cells integrate and function after injection into fetal mice The invasive study of cellular and molecular pathogenesis in humans is in most cases impossible. Patient-derived and other human cells can, however, be studied intensively in host animals, enabling researchers to observe cell- and organ-specific phenotypes at close range and […]


Novel gene analysis shows promise

New Approaches Yield Insights into Details of Complex Disorder Most autism spectrum disorders differ from syndromic autisms, in which patient phenotype follows from inheritance of or de novo mutation at a single genetic locus. Occurrence of these non-syndromic autisms has been linked to multiple mutations at different genetic loci, with […]


A link between immune signaling and ASD

Maternal immune activation acts through interleukin-17a to promote ASD-like phenotypes in mice Interleukin-17a (IL-17a) is a protein produced by activated T cells as part of the immune system’s response to infection. It promotes inflammation, and is associated with rheumatoid arthritis and psoriasis. Elevated IL-17a levels have been found in autistic […]