Format

Send to:

Choose Destination
See comment in PubMed Commons below
Psychiatry Investig. 2013 Mar;10(1):56-61. doi: 10.4306/pi.2013.10.1.56. Epub 2013 Jan 24.

Association between the BDNF Val66Met Polymorphism and Chronicity of Depression.

Author information

  • 1Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.

Abstract

OBJECTIVE:

Both clinical and biological factors influence the course of depressive disorders. This study tested for associations between the brain-derived neurotrophic factor (BDNF) gene at the Val66Met locus and the course of major depressive disorder (MDD).

METHODS:

Three hundred ten Korean subjects (209 patients, 101 controls) were genotyped for rs6265 at nucleotide 196 (G/A), which produces an amino acid substitution at codon 66 (Val66Met) of the gene for BDNF. Course of illness was evaluated both by chronicity of current episode (episode duration >24 months) and by the lifetime history of recurrences.

RESULTS:

Patients with the Met/Met BDNF genotype had a significantly higher rate of chronic depression than all others. There was a significant dose effect of the Met allele on chronicity. Compared with the Val/Val genotype, the relative risk of chronicity was 1.67 for the Val/Met genotype, and 2.58 for the Met/Met genotype. Lifetime history of recurrent episodes was not related to BDNF genotypes but was significantly associated with younger age of onset and with a history of depression in first degree relatives.

CONCLUSION:

BDNF genotyping may be informative for anticipating chronicity in major depression.

KEYWORDS:

BDNF Val66Met; Brain-derived neurotrophic factor (BDNF); Chronicity; Clinical course; Major depressive disorder; Recurrent depression

PMID:
23482723
[PubMed]
PMCID:
PMC3590431
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Korean Neuropsychiatric Association Icon for PubMed Central
    Loading ...
    Write to the Help Desk