Abstract
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-D-aspartate 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.
Highlights
Autism spectrum disorder (ASD) is characterized by symptoms of impaired communication, stereotyped behavior, difficulty with social interaction, and certain repetitive or unusual behaviors
Earlier diagnosis of autoimmune encephalitis increases the potential of curative treatments by enabling provision of timely immune therapy or immune modulatory therapy, which can prevent long-term consequences, such as being misdiagnosed with autism [16]
An immunophenotyped patient with symptoms of autism may need to obtain a diagnosis of autoimmune encephalitis to avoid being misdiagnosed with ASD
Summary
Autism spectrum disorder (ASD) is characterized by symptoms of impaired communication, stereotyped behavior, difficulty with social interaction, and certain repetitive or unusual behaviors. At the beginning of the 1980s, researchers began to apply the “immune hypothesis of schizophrenia” to explain immune-dysfunction– induced neuroinflammation as a cause for the symptoms of schizophrenia [2]. The so-called “anti-brain autoantibody” may damage fetal or children’s brain cells, eventually leading to children falling into an autistic or regressive state. Such brain-reactive antibodies causing autistic symptoms may elucidate the exploration of autism’s etiology and suggest practical anti-inflammatory management protocols for children with ASD [7]. This review introduces the potential pathogenicity of autism, which could explain why autoimmune dysfunction leads to autistic symptoms (indicated as “autoimmune autism”). Through a literature review, we review four hypothetical pathways that correlate autism with dysfunctional autoimmunity
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