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The complement system: a gateway to gene–environment interactions in schizophrenia pathogenesis
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The complement system: a gateway to gene–environment interactions in schizophrenia pathogenesis
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Journal Article
The complement system: a gateway to gene–environment interactions in schizophrenia pathogenesis
2017
Overview
The pathogenesis of schizophrenia is considered to be multi-factorial, with likely gene–environment interactions (GEI). Genetic and environmental risk factors are being identified with increasing frequency, yet their very number vastly increases the scope of possible GEI, making it difficult to identify them with certainty. Accumulating evidence suggests a dysregulated complement pathway among the pathogenic processes of schizophrenia. The complement pathway mediates innate and acquired immunity, and its activation drives the removal of damaged cells, autoantigens and environmentally derived antigens. Abnormalities in complement functions occur in many infectious and autoimmune disorders that have been linked to schizophrenia. Many older reports indicate altered serum complement activity in schizophrenia, though the data are inconclusive. Compellingly, recent genome-wide association studies suggest repeat polymorphisms incorporating the complement 4A (
C4A
) and 4B (
C4B)
genes as risk factors for schizophrenia. The
C4A/C4B
genetic associations have re-ignited interest not only in inflammation-related models for schizophrenia pathogenesis, but also in neurodevelopmental theories, because rodent models indicate a role for complement proteins in synaptic pruning and neurodevelopment. Thus, the complement system could be used as one of the ‘staging posts’ for a variety of focused studies of schizophrenia pathogenesis. They include GEI studies of the
C4A/C4B
repeat polymorphisms in relation to inflammation-related or infectious processes, animal model studies and tests of hypotheses linked to autoimmune diseases that can co-segregate with schizophrenia. If they can be replicated, such studies would vastly improve our understanding of pathogenic processes in schizophrenia through GEI analyses and open new avenues for therapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 59/57
/ 631/208
/ 64/60
/ Analysis
/ Animals
/ Complement Activation - genetics
/ Complement Activation - immunology
/ Complement Pathway, Classical - immunology
/ Complement Pathway, Classical - physiology
/ Gene-Environment Interaction
/ Genome-wide association studies
/ Genome-Wide Association Study - methods
/ Genomes
/ Humans
/ Medicine
