Summary What is known and objective Obsessive‐compulsive disorder (OCD) is a chronic neuropsychiatric disorder. Selective serotonin reuptake inhibitors (SSRIs) are the first line of medication for OCD treatment; however, 40%‐60% of patients with OCD do not respond to SSRIs adequately. There are growing pieces of evidence which suggest a significant role for the glutamatergic system in the genesis of OCD and its consequent treatment. In the present study, we aimed to assess the association of SLC1A1 polymorphisms (rs301430, rs2228622 and rs3780413) with OCD and its clinical characteristics, as well as the importance of these SNPs in the response of OCD patients to SSRI pharmacotherapy. Methods Sample study consisted of 243 OCD cases and 221 control subjects. Patients were treated 12 weeks with fluvoxamine (daily dose: 150‐300 mg). Based on the reduction in obsessive and compulsive severity scores using Y‐BOCS severity scale, patients were classified as responders, non‐responders and refractory. A total of 239, 228 and 215 patients were genotyped for rs301430, rs2228622 and rs3780413, respectively, by the means of PCR‐RFLP. Results and discussion No association was detected between SLC1A1 SNPs and OCD, except an association between the familial form of the disease in males with rs2228622 (P = 0.033). The results of pharmacogenetic studies revealed the associations of two SLC1A1 SNPs, rs2228622 (P = 0.031) and rs3780413 (P = 0.008), with treatment response. What is new and conclusion Results of the current study suggest a role for the glutamate transporter in OCD treatment response with SSRIs which should encourage researchers to further investigate the importance of glutamate transporter in OCD pharmacogenetics.
Obsessive–compulsive disorder (OCD) is a chronic neuropsychiatric disorder with complex genetic inheritance. Findings suggest a role for brain-derived neurotrophic factor (BDNF) in OCD, but reports are limited. Here we studied the association of BDNF polymorphisms rs6265 and rs2883187 with OCD and its clinical characteristics in Iranian patients as well as the fluvoxamine-treatment outcome of OCD patients. Iranian OCD patients who were diagnosed according to DSM–IV–TR entered the study. DNAs were extracted from blood samples and were genotyped by means of PCR-RFLP. A total of 200 OCD cases and 225 controls for rs6265 and 219 cases and 224 controls for rs2883187 were studied in the genetic association analysis. Pharmacotherapy was defined as 12 weeks treatment with fluvoxamine (daily dose: 150–300 mg), and patients were classified into 3 groups (responders, nonresponders, and refractory) based on the reduction in their Y-BOCS severity scores. Data of 94 patients for rs6265 and 106 patients for rs2883187 was analyzed to evaluate the association of these single nucleotide polymorphism (SNPs) with treatment response. A significant association was detected between the BDNF polymorphism rs2883187 and OCD (p = .00). The other BDNF polymorphism, rs6265, was not associated with OCD, but a weak association with the cleaning-contamination subtype was detected (p = .038). No association was detected between BDNF SNPs and sex, age of onset, and family history. None of the studied BDNF SNPs or their haplotypes were associated with fluvoxamine treatment response. Results propose BDNF SNP, rs2883187, as a candidate genetic factor in OCD but not in OCD treatment response with fluvoxamine.
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