No impact of eight NTRK2 genetic polymorphisms on 6-month antidepressant efficacy in depressed patients

Pharmacogenomics. 2017 Mar;18(4):349-357. doi: 10.2217/pgs-2016-0165. Epub 2017 Feb 17.

Abstract

Aim: NTRK2 is the main receptor of the brain derived neurotrophic factor, which is involved in antidepressant efficacy. We assessed the impact of eight NTRK2 SNPs pertaining to response and remission after antidepressant treatment in depressed patients.

Patients & methods: In a naturalistic study, 569 patients with a major depressive episode requiring a new antidepressant treatment were genotyped for eight NTRK2 SNPs (rs1187352, rs1439050, rs1778933 rs2289656, rs2289657, rs2289658, rs3824519, rs56142442) and prospectively assessed for response and remission after 6 months of treatment.

Results: No association was shown between the NTRK2 SNPs and response/remission.

Conclusion: There is no benefit to assess these eight TRKB SNPs to predict response/remission after antidepressant treatment in depressed patients.

Keywords: NTRK2; TRKB; antidepressant; genetic polymorphism; major depressive disorder; major depressive episode; pharmacogenetics; remission; response.

MeSH terms

  • Adult
  • Antidepressive Agents / therapeutic use*
  • Depressive Disorder, Major / diagnosis
  • Depressive Disorder, Major / drug therapy*
  • Depressive Disorder, Major / genetics*
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Membrane Glycoproteins / genetics*
  • Middle Aged
  • Polymorphism, Single Nucleotide / genetics*
  • Prospective Studies
  • Protein-Tyrosine Kinases / genetics*
  • Receptor, trkB
  • Time Factors
  • Treatment Outcome

Substances

  • Antidepressive Agents
  • Membrane Glycoproteins
  • Protein-Tyrosine Kinases
  • Receptor, trkB
  • tropomyosin-related kinase-B, human