Schizophrenia risk from complex variation of complement component 4 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-02

AUTHORS

Aswin Sekar, Allison R. Bialas, Heather de Rivera, Avery Davis, Timothy R. Hammond, Nolan Kamitaki, Katherine Tooley, Jessy Presumey, Matthew Baum, Vanessa Van Doren, Giulio Genovese, Samuel A. Rose, Robert E. Handsaker, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Mark J. Daly, Michael C. Carroll, Beth Stevens, Steven A. McCarroll

ABSTRACT

Schizophrenia is a heritable brain illness with unknown pathogenic mechanisms. Schizophrenia's strongest genetic association at a population level involves variation in the major histocompatibility complex (MHC) locus, but the genes and molecular mechanisms accounting for this have been challenging to identify. Here we show that this association arises in part from many structurally diverse alleles of the complement component 4 (C4) genes. We found that these alleles generated widely varying levels of C4A and C4B expression in the brain, with each common C4 allele associating with schizophrenia in proportion to its tendency to generate greater expression of C4A. Human C4 protein localized to neuronal synapses, dendrites, axons, and cell bodies. In mice, C4 mediated synapse elimination during postnatal development. These results implicate excessive complement activity in the development of schizophrenia and may help explain the reduced numbers of synapses in the brains of individuals with schizophrenia. More... »

PAGES

177

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature16549

    DOI

    http://dx.doi.org/10.1038/nature16549

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1004538257

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26814963


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