Researchers have discovered an enzyme that lowers brain levels of FMRP, the protein missing in people with fragile X syndrome. Blocking the enzyme may ease fragile X symptoms in people with the disorder who have low levels of FMRP and mild symptoms.

An autism-linked mutation in the SHANK3 gene alters the protein skeleton of mouse neurons. Repairing the scaffold eases the animals’ social deficits.

Children who are diagnosed with autism after drastically and suddenly losing cognitive abilities may actually have a distinct disorder, according to data presented yesterday at the 2015 International Meeting for Autism Research in Salt Lake City, Utah.

Blocking an enzyme involved in learning and memory corrects brain abnormalities and improves memory in fly and mouse models of fragile X syndrome.

Pivotal response treatment, an effective form of behavioral therapy for autism, normalizes brain activity in children with the disorder, according to a small study published earlier this month in Brain Imaging and Behavior. This suggests that brain imaging can signal early responses to autism treatments.

Oxytocin may influence social behavior by priming brain circuits in a region of the hippocampus important for social memory, according to preliminary results presented yesterday at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

The SHANK family of proteins, some of which are strong autism candidates, work together to facilitate brain signaling, according to unpublished results presented yesterday at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

Mice with an extra copy of the autism-linked gene UBE3A show abnormal social behavior after experiencing recurrent seizures. The findings, presented Tuesday at the Autism Consortium Research Symposium in Boston, provide one possible explanation for why seizures and autism often go hand in hand.