Schizophrenia is a complex neurodevelopmental disorder affecting around 19. 8 million people worldwide. The etiology of the disorder is due to many interacting genetic and environmental factors, with no one element causing the full spectrum of disease symptoms. Amongst these factors, maternal immune activation (MIA) acting during specific gestational timings has been implicated in increasing schizophrenia risk in offspring. Epidemiological studies have provided the rationale for this link with prevalence of maternal infection correlating to increased risk, but these studies have been unable to prove causality due to lack of control of confounding factors like genetic susceptibility and inability to identify specific cellular and molecular mechanisms. Animal models have proved significantly more useful in establishing the extent to which MIA can predispose an individual to schizophrenia, displaying how maternal infection alone can directly result in behavioral abnormalities in rodent offspring. Alongside information from genome wide association studies (GWAS), animal models have been able to identify the role of complement proteins, particularly C4, and display how alterations in this system can cause development of schizophrenia-associated neuropathology and behavior. This article will review the current literature in order to assess whether schizophrenia can, therefore, be viewed as an immune priming disorder.
Keywords: complement; immune; maternal; neurodevelopment; schizophrenia.
Copyright © 2021 Choudhury and Lennox.