ABSTRACT

Identifying common molecular functions among autism-related genes, and common neurobiological correlates of autism-related behaviors, is essential to understanding the nature of autism. This chapter focuses on two such mechanisms that are suggested by a broad range of genetic, neuroanatomical, and clinical evidence in autism: (1) altered connectivity, at both anatomical and functional levels, and (2) altered excitatory–inhibitory balance, particularly affecting the properties of GABAergic circuits that regulate temporal synchrony and feedback. I review important work related to these two components of the basic research and argue that presuming competence is the most important ingredient to understand, research, and treat autism.