Choi Myoung-Jin, Kang Rhee-Hun, Lim Se-Won, Oh Kang-Seob, Lee Min-Soo
Depression Center, Korea University, Seoul, Republic of Korea.
Brain Res. 2006 Nov 6;1118(1):176-82. doi: 10.1016/j.brainres.2006.08.012. Epub 2006 Sep 18.
The brain-derived neurotrophic factor (BDNF) gene is a candidate gene for influencing the clinical response to treatment with antidepressants. The purpose of this study was to determine the relationship between the Val66Met polymorphism in the BNDF gene and the response to citalopram in a Korean population with major depressive disorder (MDD). Citalopram was administered for 8 weeks to the 83 patients who completed this study. We found that the genotype, allele, and allele-carrier distributions for the Val66Met polymorphism differed significantly between responders (Rp) and nonresponders (Non-Rp). The frequency of M-allele carriers (VM+MM) was higher in Rp than in Non-Rp (chi(2)=8.926, p=0.003, OR=4.375, 95%CI=1.609-11.892), as was the M-allele frequency (chi(2)=6.879, p=0.009, OR=2.500, 95%CI=1.249-5.005). There were also significant differences in the core (p=0.012) and activity (p=0.008) scores. Patients carrying the M-allele had a lower score. Also, patients carrying the M-allele tended to have lower psychic anxiety (p=0.072). The percentage change in the total HAM-D score was higher for M-allele carriers (VM+MM allele) than for noncarriers (p=0.034) after 8 weeks of medication. We found that the genotype, allele, and allele-carrier distributions did not differ significantly between MDD patients and normal controls. These results suggest that the Val66Met polymorphism of BDNF is associated with citalopram efficacy, with M-allele carriers responding better to citalopram treatment. Moreover, the Val66Met polymorphism was correlated with improvements in core, activity, and psychic anxiety symptoms.
脑源性神经营养因子(BDNF)基因是影响抗抑郁药治疗临床反应的候选基因。本研究的目的是确定韩国重度抑郁症(MDD)患者中BDNF基因Val66Met多态性与西酞普兰反应之间的关系。对完成本研究的83例患者给予西酞普兰治疗8周。我们发现,Val66Met多态性的基因型、等位基因和等位基因携带者分布在反应者(Rp)和无反应者(Non-Rp)之间存在显著差异。Rp中M等位基因携带者(VM+MM)的频率高于Non-Rp(χ²=8.926,p=0.003,OR=4.375,95%CI=1.609-11.892),M等位基因频率也是如此(χ²=6.879,p=0.009,OR=2.500,95%CI=1.249-5.005)。核心(p=0.012)和活动(p=0.008)评分也存在显著差异。携带M等位基因的患者得分较低。此外,携带M等位基因的患者往往有较低的精神焦虑(p=0.072)。用药8周后,M等位基因携带者(VM+MM等位基因)的总汉密尔顿抑郁量表(HAM-D)评分变化百分比高于非携带者(p=0.034)。我们发现,MDD患者和正常对照之间的基因型、等位基因和等位基因携带者分布没有显著差异。这些结果表明,BDNF的Val66Met多态性与西酞普兰疗效相关,M等位基因携带者对西酞普兰治疗反应更好。此外,Val66Met多态性与核心、活动和精神焦虑症状的改善相关。