In this study, we applied a pooled sample 454 sequencing strategy, to explore the contribution of genetic variation in DISC1 and 10 of its interaction partners (ATF5, Grb2, FEZ1, LIS-1, PDE4B, NDE1, NDEL1, TRAF3IP1, YWHAE, and ZNF365) to schizophrenia susceptibility in an isolated northern Swedish population.
No associations were observed for DBZ with schizophrenia or with bipolar disorder; further, there was no significant difference between the DBZ mRNA levels of control, schizophrenia and bipolar postmortem brains.
In schizophrenia with DISC1 translocation carrier, the DISC1-Fez1 and DISC1-DBZ interaction is disrupted, and it is likely that neural circuit formation remains immature, suggesting that schizophrenia is a neurodevelopmental disease.