| Literature DB >> 29222989 |
Carla Em Golden1, Joseph D Buxbaum2, Silvia De Rubeis3.
Abstract
Autism spectrum disorder (ASD) and intellectual disability (ID) are caused by a wide range of genetic mutations, a significant fraction of which reside in genes important for synaptic function. Studies have found that sensory, prefrontal, hippocampal, cerebellar, and striatal regions, as well as the circuits that connect them, are perturbed in mouse models of ASD and ID. Dissecting the disruptions in morphology and activity in these neural circuits might help us to understand the shared risk between the two disorders as well as their clinical heterogeneity. Treatments that target the balance between excitation and inhibition in these regions are able to reverse pathological phenotypes, elucidating this deficit as a commonality across models and opening new avenues for intervention.Entities:
Mesh:
Year: 2017 PMID: 29222989 PMCID: PMC5825272 DOI: 10.1016/j.conb.2017.11.006
Source DB: PubMed Journal: Curr Opin Neurobiol ISSN: 0959-4388 Impact factor: 6.627