Abstract
Accumulating evidence suggests that the glutamatergic system plays a major role in the pathophysiology of obsessive compulsive disorder (OCD) and empathic processing. Particularly, genetic influence of glutamate transporter gene (SLC1A1) on OCD has been frequently replicated in previous studies, but several studies did not replicate the result. Therefore, we aimed to replicate the associations between the SLC1A1 and OCD in a Korean population. In addition, we investigated the influence of SLC1A1 on trait empathy, impairments in which are characteristic of OCD. Six single-nucleotide polymorphisms (SNP) of SLC1A1 were genotyped in 615 patients with OCD and 508 healthy controls. The interpersonal reactivity index (IRI)—which consists of four subscales (perspective taking, PT; fantasy seeking, FS; empathic concern, EC; personal distress, PD)—was assessed from 277 patients with OCD and 395 controls. There were no significant associations between OCD and SNPs or haplotypes of SLC1A1. Patients with OCD exhibited significantly lower PT and higher PD scores than controls. The C-T-G haplotype at rs301430-rs301434-rs3087879 of SLC1A1 was significantly associated with higher PD scores after adjusted for age, sex, and OCD status. Our results suggest that six common SNPs of SLC1A1 may not contribute to the development of OCD, but may contribute to certain aspect of trait empathy such as personal distress. However, insufficient sample size and limited number of SLC1A1 SNPs may have reduced the likelihood of detecting significant associations. Therefore, further studies with larger sample size and more tag SNPs of the SLC1A1 gene were warranted.
Highlights
The causes of obsessive compulsive disorder (OCD) are not fully understood, accumulating evidence indicates that the underlying bases of OCD are neurochemical [1]
We identified no significant associations between six single-nucleotide polymorphisms (SNP) or haplotypes of SLC1A1 and OCD in a sample of Korean probands and controls
SLC1A1 has received attention as a promising candidate gene for OCD, as two independent studies have suggested a linkage between OCD and 9p24, on which SLC1A1 is located [8,9]
Summary
The causes of obsessive compulsive disorder (OCD) are not fully understood, accumulating evidence indicates that the underlying bases of OCD are neurochemical [1]. Research has demonstrated that the serotonin system is closely interrelated with other neurotransmitter systems in the brain [1], indicating that other neurotransmitters may play a role in the pathophysiology of OCD. Several lines of evidence have suggested that alterations in glutamate neurotransmission contribute to OCD pathophysiology. Additional studies have reported increased levels of glutamate in the cerebrospinal fluid of patients with OCD [4]. The potential therapeutic benefits of some glutamate modulating agents such as memantine [5], N-acetyl cysteine, riluzole [6], and ketamine [7] have been demonstrated in patients with OCD
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