Deciphering microbiome and neuroactive immune gene interactions in schizophrenia

摘要: The body's microbiome represents an actively regulated network of novel mechanisms that potentially underlie the etiology and pathophysiology a wide range diseases. For complex brain disorders such as schizophrenia, understanding cellular molecular pathways intersect bidirectional gut-brain axis is anticipated to lead new methods treatment. means by which might differ across neuropsychiatric neurological are not known. Brain diverse major depression, Parkinson's disease multiple sclerosis appear share common pathology imbalanced community commensal microbiota, often measured in terms leaky gut phenotype accompanied low level systemic inflammation. While environmental factors associated with these states contribute intestinal pathologies, products from perturbed may also directly promote specific signs, symptoms etiologies individual disorders. We hypothesize it putatively unique susceptibility related genes modulate immune system pleiotropy leads particularly neuropathological response when challenged dysbiosis. Consequences exposure this dysbiosis occur during pre- or post-natal time periods thus interfere normal neurodevelopment those who genetically predisposed. Here, we review evidence literature supports idea intersection gene schizophrenia relevant etiologically for progression. Figuring prominently at both ends points between proteins encoded found histocompatibility (MHC), including select MHC well non-MHC complement pathway genes.