1 Bioinformatics Research Centre (BiRC), Science and Technology, Aarhus University2 Department of Biomedicine - Forskning og uddannelse, Øst, Department of Biomedicine, Health, Aarhus University3 Department of Clinical Medicine - Translational Neuropsychiatry Unit, Department of Clinical Medicine, Health, Aarhus University4 Center for Translational Social Neuroscience, Emory University, Atlanta, GA, USA5 Department of Biomedicine - Forskning og uddannelse, Øst, Department of Biomedicine, Health, Aarhus University
In recent years, good progress has been made in uncovering the genetic underpinnings of schizophrenia. Even so, as a polygenic disorder, schizophrenia has a complex etiology that is far from understood. Meanwhile, data are being collected enabling the study of interactions between genes and the environment. A confluence of data from genetic and environmental exposure studies point to the role of infections and immunity in the pathophysiology of schizophrenia. In a recent study by Børglum et al., a single nucleotide polymorphism (SNP) in the gene CTNNA3 was identified that may provide clues to gene-environment interactions. The carriers of the minor allele for the SNP had a fivefold risk of later developing schizophrenia if their mothers were CMV positive, while the children not carrying the allele had no excess risk from maternal CMV. In the current paper, we summarize recent advances to clarify a possible mechanism of such interactions between the host genotype and infection in schizophrenia risk.
Current Behavioral Neuroscience Reports, 2014, Vol 1, Issue 4, p. 215-223