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Modeling the cooperativity of schizophrenia risk genes

Nature Genetics volume 51, pages 1434–1436 (2019)Cite this article

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Common genetic variants increase the risk of schizophrenia, but the downstream biological mechanisms are largely unknown. A new study demonstrates that schizophrenia risk genes cause neuronal dysfunction and have synergistic effects on gene expression.

A plethora of common genetic variants are currently being identified, each of which slightly increases the risk of complex genetic disorders such as schizophrenia, type 2 diabetes and coronary heart disease1,2,3. However, the mechanisms by which these variants interact and cause disease remain largely unknown. Schrode et al.4 now describe that disease-relevant expression changes in schizophrenia risk genes lead to pre- and postsynaptic neuronal deficits in human cells and that simultaneous perturbation of multiple risk genes leads to more extreme changes than expected on the basis of separate studies of each gene. Although their approach is focused on only a very small subset of the hundreds of risk genes in schizophrenia, their prioritized and combinational approach should be applicable to more genes and other complex disorders.

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Fig. 1: A genetics-anchored multifaceted approach to study the biological etiopathogenesis of schizophrenia.

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Authors and Affiliations

  1. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Center for Genomics and Personalized Medicine, Center for Integrative Sequencing, iSEQ and Department of Biomedicine, Aarhus University, Aarhus, Denmark

    Jane H. Christensen & Anders D. Børglum

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  1. Jane H. Christensen
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  2. Anders D. Børglum
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Correspondence to Jane H. Christensen or Anders D. Børglum.

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The authors declare no competing interests.

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Christensen, J.H., Børglum, A.D. Modeling the cooperativity of schizophrenia risk genes. Nat Genet 51, 1434–1436 (2019). https://doi.org/10.1038/s41588-019-0508-6

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  • DOI: https://doi.org/10.1038/s41588-019-0508-6

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