New clues about brain changes in autism
Autism spectrum disorder (ASD) refers to a group of complex neurodevelopment disorders that cause significant social, communication and behavioral challenges. Now, a new study reports on a potential drug target that increases social interaction in ASD. The study was carried out by researchers at the University of Pennsylvania School of Medicine, and was published in the journal Biological Psychiatry.
We already have drugs to address specific symptoms of ASD, including behavioral issues, anxiety or depression, mood swings, obsessive compulsive disorder, attentional issues, and hyperactivity. However, no drug can cure the core social interaction deficits in ASD, in part because the brain basis of these social interaction problems remains largely unknown. Study senior author Edward S. Brodkin said that their research could extend the understanding of the mechanism of ASD and facilitate the development of therapeutics for it.
Abnormal connections between neurons are part of the reason for behavioral problems in people with ASD. However, the molecular mechanism of ASD-associated behavioral and brain physiology is not entirely understood. It has been reported that a gene termed Protocadherin 10 (PCDH10)
is implicated in ASD. This gene belongs to the protocadherin gene family, a subfamily of the cadherin superfamily. The PCDH10 protein is important to the maintenance of synapses, which are functional connections between neurons. Certain brain regions like the amygdala express high levels of PCDH10. The amygdala is essential for encoding emotions. And this structure is associated with social deficits in ASD.
The researchers created mice that lacked one copy of PCDH10 (Pcdh10+/–), and found that male Pcdh10+/– mice had decreased social approach behavior, as well as anomalies in the structure and function of amygdala circuitry. When the researchers treated these mice with a drug termed d-cycloserine, their social approach deficits were reversed.