In this review paper, we present current theories about the inflammatory etiopathogenesis of
schizophrenia. We mentioned the biopsychosocial etiological model of the disease and stressed the
importance of neuroinflammation and neurodegeneration in its biological basis.
We searched the literature about innate immunity, Toll-like receptors, inflammation, and
neurodegeneration, and we summarized their role in the etiopathogenetic mechanisms of schizophrenia.
We also found studies on available antipsychotics that can regulate the expression of Toll-like receptors
and modulate innate inflammatory mechanisms. Despite the effective properties of antipsychotics in
reducing psychotic symptoms, their role in inflammatory mechanisms remains imprecise and underresearched.
More specific information about how antipsychotics affect neuroinflammation could lead to the
development of a wider range of possible drugs that could keep inflammatory processes working properly
and improve mental abilities and, ultimately, the quality of life
