TPH2 polymorphisms may modify clinical picture in treatment-resistant depression

Neurosci Lett. 2009 Oct 16;464(1):43-6. doi: 10.1016/j.neulet.2009.08.018. Epub 2009 Aug 11.

Abstract

The association of two tryptophan hydroxylase 2 (TPH2) polymorphisms and treatment response in electroconvulsive therapy (ECT) and the risk of depression was studied. The patient sample consisted of 119 subjects with treatment-resistant major depressive disorder who were treated with ECT. Treatment response was assessed by the Montgomery and Asberg Depression Rating Scale (MADRS) scores. Patients who had <8 scores in post-treatment MADRS were considered remitters; scores >15 indicated non-response. The polymorphisms studied (rs1386494 and rs1843809) were not associated with treatment response to ECT. However, TPH2 rs1386494 A/A genotype carrying patients had significantly higher MADRS scores before ECT than A/G+G/G genotype carriers (p<0.001). A/A genotype carriers also had a greater decline in MADRS scores than A/G+G/G genotype carriers during the course of ECT treatment (p=0.03). This polymorphism may be associated with the severity of treatment-resistant depression. ECT may able to counteract a putative genetically driven worse depressive phenotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Depressive Disorder, Major / genetics*
  • Depressive Disorder, Major / therapy
  • Electroconvulsive Therapy*
  • Female
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Polymorphism, Genetic
  • Tryptophan Hydroxylase / genetics*

Substances

  • TPH2 protein, human
  • Tryptophan Hydroxylase