5HT1A and 5HT2A receptor genes in treatment response phenotypes in major depressive disorder


Noro M., Antonijevic I., Forray C., Kasper S., Kocabas N. A., Lecrubier Y., ...Daha Fazla

INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY, cilt.25, sa.4, ss.228-231, 2010 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 25 Sayı: 4
  • Basım Tarihi: 2010
  • Doi Numarası: 10.1097/yic.0b013e328338bcf4
  • Dergi Adı: INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.228-231
  • Anahtar Kelimeler: antidepressant treatment, major depressive disorder, phenotype, serotonin receptor, single nucleotide polymorphism, treatment resistant depression, TREATMENT-RESISTANT DEPRESSION, SEROTONIN TRANSPORTER GENES, ANTIDEPRESSANT RESPONSE, ELECTROCONVULSIVE-THERAPY, PROMOTER POLYMORPHISM, JAPANESE PATIENTS, 5-HT1A RECEPTOR, MOOD DISORDERS, 2A, ASSOCIATION
  • Gazi Üniversitesi Adresli: Hayır

Özet

The 5HT2A (5HTR2A) and 5HT1A receptor (5HTR1A) genes are plausible candidate genes for major depressive disorders. Two single nucleotide polymorphisms, the rs7997012 in 5HTR2A and the -1019C/G in 5HTR1A, were analyzed in 206 patients with Diagnostic and Statistical Manual of Mental Disorders, fourth edition major depressive disorder. Patients were retrospectively characterized for clinical response to antidepressant treatment. We found a significant difference in the rs7997012 allele frequency between resistant and nonresistant patients. However, following the Bonferroni correction we could not find any association between this single nucleotide polymorphism and treatment resistance phenotype. Nevertheless, given the limited power of our analysis, we are not able to conclude that these results reflect a lack of association. Additional studies are needed to confirm or to disprove our result. Int Clin Psychopharmacol 25: 228-231 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.