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The contribution of epistasis to human disease remains unclear. However, several studies have now identified epistatic interactions between common variants that increase the risk of a neuropsychiatric disorder, while there is growing evidence that genetic interactions contribute to the pathogenicity of rare, multigenic copy-number variants (CNVs) that have been observed in patients. This review discusses the current evidence for epistatic events and genetic interactions in neuropsychiatric disorders, how paradigm shifts in the phenotypic classification of patients would empower the search for epistatic effects, and how network and cellular models might be employed to further elucidate relevant epistatic interactions.

Original publication

DOI

10.1016/j.tig.2017.01.009

Type

Journal article

Journal

Trends Genet

Publication Date

04/2017

Volume

33

Pages

256 - 265

Keywords

autism, bipolar disorder, epistasis, interactions, neuropsychiatric disorders, schizophrenia, Autistic Disorder, Bipolar Disorder, DNA Copy Number Variations, Epistasis, Genetic, Genotype, Humans, Phenotype, Quantitative Trait Loci, Schizophrenia