Author(s)

Ziqi Wang

Corresponding Author

Ziqi Wang

ABSTRACT

Autism spectrum disorder (ASD) is one of the most common neural disorders typified by social ability impairments, communicative defects, and repetitive/restricted behaviors. Gene components strongly contribute to the possible pathology of ASD. And evidence shows key risk genes converge at common cell pathways at synapse. These studies also attempted to explain the common etiology of heterogenous ASD phenotypes using genomic analysis and animal models from different perspectives. This review tries to incorporate ASD mechanisms on molecular and cellular level into two main aspects: synaptic dysfunctions and under-pruning resulted from dysregulated mTOR pathway. Future devotion in this direction should ultimately focus on increasing pruning efficiency by targeting downstream of mTOR-autophagy signaling, therefore providing clues for novel ASD treatments.

KEYWORDS

Autism spectrum disorder, synapse, mTOR, SHANK3, autophagy