Chronic depression is associated with a pronounced decrease in serum brain-derived neurotrophic factor over time

Chronic depression is associated with a pronounced decrease in serum brain-derived neurotrophic factor over time
复制标题

DOI:
10.1038/mp.2014.83
复制
发表时间:
2015-05-01
影响因子:
11
通讯作者:
Voshaar, R. C. O.
Voshaar, R. C. O.
中科院分区:
医学1区
文献类型:
--
作者:
Bus, B. A. A.;Molendijk, M. L.;Voshaar, R. C. O.

文献摘要

被引文献

相似文献

关于抑郁症的主要神经生物学假说之一指出,脑源性神经营养因子(BDNF)的表达减少有助于抑郁症。与非抑郁对照组相比,抑郁症患者血清BDNF水平较低,这一一致的发现支持了这一点。尽管人们普遍认为这是抑郁症的一种状态特征,但关于状态或特质效应的强有力推论需要纵向研究设计。为了研究血清BDNF与抑郁症之间的纵向联系,我们测定了血清BDNF,基线和2年后1751例受试者(包括发生事件的患者(n = 153))的(当前和既往)抑郁状态、抗抑郁药使用情况和所有潜在协变量,缓解组(n = 420)、持续性抑郁组(n = 310)和非抑郁对照组(n = 868)。我们分析了这四组血清BDNF的变化/差异,并对协变量和基线BDNF值进行了协方差分析,以及开始和停止抗抑郁治疗的影响。我们的分析显示,抑郁症病程组的差异有统计学意义(P = 0.007)。与非抑郁症对照组相比,持续性抑郁症和缓解期患者的脑源性神经营养因子水平随着时间的推移下降幅度更大(分别为-1.33(P = 0.001)和-0.97 ng ml(-1(P = 0.011),而抑郁症患者的脑源性神经营养因子水平下降幅度与健康对照组相似。抗抑郁药的开始或停用与BDNF的变化无关(P = 0.72)。这些发现表明,BDNF不仅有助于抑郁症,但抑郁症反过来也可能有助于低BDNF。
One of the leading neurobiological hypotheses on depression states that decreased expression of brain-derived neurotrophic factor (BDNF) contributes to depression. This is supported by consistent findings of low serum BDNF levels in depressed patients compared with non-depressed controls. Whereas it has been generally assumed that this is a state characteristic of depression, strong inferences about state or trait effects require a longitudinal study design. To investigate the longitudinal association between serum BDNF and depression, we measured serum BDNF, (current and past) depression status, use of antidepressants, and all potential covariates at baseline and after 2 years in 1751 individuals, consisting of patients with an incident (n = 153), remitted (n = 420) and persistent depression (n = 310) and non-depressed controls (n = 868). We analyzed change/differences in serum BDNF across these four groups with analyses of covariance adjusted for covariates and baseline BDNF value, together with the effects of starting and stopping antidepressant treatment. Our analyses revealed a significant difference for the depression course groups (P = 0.007). Compared with non-depressed controls, persistently depressed and remitted patients had a steeper decrease of BDNF levels over time (-1.33 (P = 0.001) and -0.97 ng ml(-1) (P = 0.011), respectively), whereas BDNF reductions in patients with incident depression were similar to those in healthy controls. Initiation or discontinuation of antidepressants was not associated with BDNF change (P = 0.72). These findings suggest that BDNF not only contributes to depression, but that depression in turn may also contribute to low BDNF.