Mechanism of autism

The mechanisms of autism are the molecular and cellular processes believed to cause or contribute to the symptoms of autism. Multiple processes are hypothesized to explain different autism spectrum features. These hypotheses include defects in synapse structure and function, reduced synaptic plasticity, disrupted neural circuit function, gut–brain axis dyshomeostasis, neuroinflammation, and altered brain structure or connectivity. Autism symptoms stem from maturation-related changes in brain systems. The mechanisms of autism are divided into two main areas: pathophysiology of brain structures and processes, and neuropsychological linkages between brain structures and behaviors, with multiple pathophysiologies linked to various autism behaviors.

Evidence suggests gut–brain axis abnormalities may contribute to autism. Studies propose that immune, gastrointestinal inflammation, autonomic nervous system dysfunction, gut microbiota alterations, and dietary metabolites may contribute to brain neuroinflammation and dysfunction. Additionally, enteric nervous system abnormalities could play a role in neurological disorders by allowing disease pathways from the gut to impact the brain.

Synaptic dysfunction also appears to be implicated in autism, with some mutations disrupting synaptic pathways involving cell adhesion. Evidence points to teratogens affecting the early developmental stages, suggesting autism arises very early, possibly within the first eight weeks after conception.

Neuroanatomical studies support that autism may involve abnormal neuronal growth and pruning, leading to brain enlargement in some areas and reduction in others. Functional neuroimaging studies show reduced activation in somatosensory cortices during theory of mind tasks in autistic individuals and highlight potential imbalances in neurotransmitters like glutamate and Γ-aminobutyric acid that may underlie autism's behavioral manifestations.