Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders that develop in early life due to interaction between several genetic and environmental factors and lead to alterations in brain function and structure. During the last decades, several mechanisms have been placed to explain the pathogenesis of autism. Unfortunately, these are reported in several studies and reviews which make it difficult to follow by the reader. In addition, some recent molecular mechanisms related to ASD have been unrevealed. This paper revises and highlights the major common molecular mechanisms responsible for the clinical symptoms seen in people with ASD, including the roles of common genetic factors and disorders, neuroinflammation, GABAergic signaling, and alterations in Ca ⁺² signaling. Besides, it covers the major molecular mechanisms and signaling pathways involved in initiating the epileptic seizure, including the alterations in the GABAergic and glutamate signaling, vitamin and mineral deficiency, disorders of metabolism, and autoimmunity. Finally, this review also discusses sleep disorder patterns and the molecular mechanisms underlying them.

A graphical abstract: Various mechanisms involves in the development of autism spectrum disorders. DIA-1: deleted in autism-1 gene (DIA-1); NGLs: neuroligins; NRXNs: neurexins; PCDH: protocadherin; UBE3A: ubiquitin 3 CoA ligase; TSC1/2: tuberous sclerosis complex; RELN: Reelin; FXS: fragile X syndrome; Rett: Rett syndrome; MECP2: methyl-CpG-binding protein 2; BDNF: brain-derived neurotrophic factor; and P5P: pyridoxal-5-phosphate.