Association study between the neurexin-1 gene and tardive dyskinesia.

OBJECTIVE: Tardive dyskinesia (TD) is a motor side effect that may develop after long-term antipsychotic treatment. Schizophrenia has recently been associated with the Neurexin-1 (NRXN1) gene that codes for a cell adhesion molecule in synaptic communication. METHODS: This study examined five NRXN1 single-nucleotide polymorphisms (SNPs) for possible association with the occurrence and severity of TD in 178 schizophrenia patients of European ancestry. RESULTS: We did not find these SNPs to be significantly associated with TD. CONCLUSIONS: More research is needed with additional SNPs and in bigger samples before we can completely rule out the role of NRXN1 in TD.

Pharmacogenetics of tardive dyskinesia: an updated review of the literature.

Tardive dyskinesia (TD) is a serious and potentially irreversible side effect of long-term exposure to antipsychotic medication characterized by involuntary trunk, limb and orofacial muscle movements. Various mechanisms have been proposed for the etiopathophysiology of antipsychotic-induced TD in schizophrenia patients with genetic factors playing a prominent role. Earlier association studies have focused on polymorphisms in CYP2D6, dopamine-, serotonin-, GABA- and glutamate genes. This review highlights recent advances in the genetic investigation of TD. Recent promising findings were obtained with the HSPG2, DPP6, MTNR1A, SLC18A2, PIP5K2A and CNR1 genes. More research, including collection of well-characterized samples, enhancement of genome-wide strategies, gene-gene interaction and epigenetic analyses, is needed before genetic tests with clinical utility can be made available for TD.