Objective: Genes involved in inflammation, oxidative stress and calcium signaling may be involved in Bipolar disorder (BD). Comorbidity for substance use disorders (SUD) is frequent in BD, and shared genetic mechanics may be hypothesized. In the present study we preliminarily investigated polymorphisms within Interleukin 1-beta (IL1b), neuronal Nitric oxide adaptor protein (NOS1AP) and Transient receptor potential cation channel 2 (TRPM2) in BD and comorbidity for SUD. Method: One-hundred and thirty-one (131) BD patients (66 comorbid for SUD) and 64 healthy controls were genotyped for rs1143634, rs1143627, rs16944, rs1143623 (IL1b), rs12742393 (NOS1AP) and rs1556314 (TRPM2). Results: Genetic variants were not found associated to BD, while rs1143627 and a haplotype in IL1b showed significant associations with SUD, both comparing SUD subjects with healthy controls and to non-comorbid BD patients. Conclusions: The present study has several limitations, mainly linked to the small sample size and the naturalistic characterization of the study design. Taking into account these limitations and the preliminary nature of the study, present data do not support a role of IL1b, NOS1AP and TRPM2 in BD, though ILb1 may play a role in SUD.
|Number of pages||7|
|Publication status||Published - 2011|
- bipolar depression
- substance-related disorders