In conclusion, we identified several novel loci that associate with FTND score. The adjusted model allowed us to isolate ND risk from risk of dependence on alcohol, opioids, and cocaine, important because ND frequently co-occurs with these disorders. The key risk loci that we identified participate, or may participate, in pathways known to be relevant to SD: calcium signaling, dopaminergic function, neuronal differentiation, synapse formation, and cognitive function. None of these SNPs overlap with variants identified as affecting SD risk in our previous studies. However, in some cases, similar pathways are involved (e.g., calcium signaling), and in one case, the same locus, DISC1, is implicated. These results, if replicated, should increase our understanding of the biological mechanisms of ND and may identify novel pharmacologic targets for treatment and biomarkers to identify risk for prevention efforts.
