The purpose of this review is to correlate autism with autoimmune dysfunction in the absence
of an explanation for the etiology of autism spectrum disorder. The anti-N-methyl-Daspartate
receptor (anti-NMDAR) autoantibody is a typical synaptic protein that can bind to
synaptic NMDA glutamate receptors, leading to dysfunctional glutamate neurotransmission
in the brain that manifests as psychiatric symptoms (psychosis, hallucinations, and
personality changes). Detection of autoantibodies, cytokines, decreased lymphocytes,
serum immunoglobulin level imbalance, T-cell mediated immune profile, maternal infection
history, and children’s infection history can all be vital biological markers of autoimmune
autism. Diagnosing autoimmune encephalitis sooner can increase the effectiveness of
curative treatments—such as immune therapy or immune modulatory therapy—that may
prevent the long-term consequence of being misdiagnosed with autism spectrum disorder.
Glutamate therapy primarily normalizes glutamate neurotransmission and can be a new
add-on intervention alongside antipsychotics for treating autoimmune autism.