The complement system in schizophrenia: where are we now and what's next?

Mol Psychiatry

Tanenbaum Centre for Pharmacogenetics, Campbell Family Mental Health Research Institute, Center for Addiction and Mental Health, 250 College Street, Toronto, ON, M5T 1R8, Canada.

Published: January 2020

AI Article Synopsis

  • The complement system plays a crucial role in the immune response and has been linked to central nervous system diseases, including schizophrenia, with recent studies showing elevated complement pathway activity in affected individuals.
  • Recent genetic research has identified complement component 4 (C4) and CUB and Sushi Multiple Domains 1 (CSMD1) as potential markers for schizophrenia, with evidence suggesting specific deficiencies and expressions in patients.
  • Limitations in current studies, such as small sample sizes and inconsistent methodologies, highlight the need for further research into the complement system's role in schizophrenia and the potential for developing targeted therapies.

Article Abstract

The complement system is a set of immune proteins involved in first-line defense against pathogens and removal of waste materials. Recent evidence has implicated the complement cascade in diseases involving the central nervous system, including schizophrenia. Here, we provide an up-to-date narrative review and critique of the literature on the relationship between schizophrenia and complement gene polymorphisms, gene expression, protein concentration, and pathway activity. A literature search identified 23 new studies since the first review on this topic in 2008. Overall complement pathway activity appears to be elevated in schizophrenia. Recent studies have identified complement component 4 (C4) and CUB and Sushi Multiple Domains 1 (CSMD1) as potential genetic markers of schizophrenia. In particular, there is some evidence of higher rates of C4B/C4S deficiency, reduced peripheral C4B concentration, and elevated brain C4A mRNA expression in schizophrenia patients compared to controls. To better elucidate the additive effects of multiple complement genotypes, we also conducted gene- and gene-set analysis through MAGMA which supported the role of Human Leukocyte Antigen class (HLA) III genes and, to a lesser extent, CSMD1 in schizophrenia; however, the HLA-schizophrenia association was likely driven by the C4 gene. Lastly, we identified several limitations of the literature on the complement system and schizophrenia, including: small sample sizes, inconsistent methodologies, limited measurements of neural concentrations of complement proteins, little exploration of the link between complement and schizophrenia phenotype, and lack of studies exploring schizophrenia treatment response. Overall, recent findings highlight complement components-in particular, C4 and CSMD1-as potential novel drug targets in schizophrenia. Given the growing availability of complement-targeted therapies, future clinical studies evaluating their efficacy in schizophrenia hold the potential to accelerate treatment advances.

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Source
http://dx.doi.org/10.1038/s41380-019-0479-0DOI Listing

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