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脑源性神经营养因子与电休克治疗的抗抑郁作用:临床前和临床文献的系统评价与荟萃分析

Brain-Derived Neurotrophic Factor and Antidepressive Effect of Electroconvulsive Therapy: Systematic Review and Meta-Analyses of the Preclinical and Clinical Literature.

作者信息

Polyakova M, Schroeter M L, Elzinga B M, Holiga S, Schoenknecht P, de Kloet E R, Molendijk M L

机构信息

Max Planck Institute for Human Cognitive and Brain Sciences & Clinic for Cognitive Neurology, University Hospital, Leipzig, Germany; University Hospital Leipzig, Department of Psychiatry and Psychotherapy, Leipzig, Germany.

Max Planck Institute for Human Cognitive and Brain Sciences & Clinic for Cognitive Neurology, University Hospital, Leipzig, Germany.

出版信息

PLoS One. 2015 Nov 3;10(11):e0141564. doi: 10.1371/journal.pone.0141564. eCollection 2015.

DOI:10.1371/journal.pone.0141564
PMID:26529101
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4631320/
Abstract

Emerging data suggest that Electro-Convulsive Treatment (ECT) may reduce depressive symptoms by increasing the expression of Brain-Derived Neurotrophic Factor (BDNF). Yet, conflicting findings have been reported. For this reason we performed a systematic review and meta-analysis of the preclinical and clinical literature on the association between ECT treatment (ECS in animals) and changes in BDNF concentrations and their effect on behavior. In addition, regional brain expression of BDNF in mouse and human brains were compared using Allen Brain Atlas. ECS, over sham, increased BDNF mRNA and protein in animal brain (effect size [Hedge's g]: 0.38-0.54; 258 effect-size estimates, N = 4,284) but not in serum (g = 0.06, 95% CI = -0.05-0.17). In humans, plasma but not serum BDNF increased following ECT (g = 0.72 vs. g = 0.14; 23 effect sizes, n = 281). The gradient of the BDNF increment in animal brains corresponded to the gradient of the BDNF gene expression according to the Allen brain atlas. Effect-size estimates were larger following more ECT sessions in animals (r = 0.37, P < .0001) and in humans (r = 0.55; P = 0.05). There were some indications that the increase in BDNF expression was associated with behavioral changes in rodents, but not in humans. We conclude that ECS in rodents and ECT in humans increase BDNF concentrations but this is not consistently associated with changes in behavior.

摘要

新出现的数据表明,电休克治疗(ECT)可能通过增加脑源性神经营养因子(BDNF)的表达来减轻抑郁症状。然而,也有相互矛盾的研究结果报道。因此,我们对关于ECT治疗(动物中的电惊厥休克[ECS])与BDNF浓度变化及其对行为的影响之间关联的临床前和临床文献进行了系统综述和荟萃分析。此外,使用艾伦脑图谱比较了小鼠和人类大脑中BDNF的区域脑表达。与假手术相比,ECS增加了动物脑中BDNF的mRNA和蛋白质水平(效应大小[Hedge's g]:0.38 - 0.54;258个效应大小估计值,N = 4284),但血清中未增加(g = 0.06,95% CI = -0.05 - 0.17)。在人类中,ECT后血浆BDNF增加,但血清BDNF未增加(g = 0.72对g = 0.14;23个效应大小,n = 281)。根据艾伦脑图谱,动物脑中BDNF增加的梯度与BDNF基因表达的梯度相对应。在动物(r = 0.37,P <.0001)和人类(r = 0.55;P = 0.05)中,ECT疗程越多,效应大小估计值越大。有一些迹象表明,BDNF表达的增加与啮齿动物的行为变化有关,但与人类无关。我们得出结论,啮齿动物中的ECS和人类中的ECT会增加BDNF浓度,但这与行为变化并不总是相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0583/4631320/818b581f24bf/pone.0141564.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0583/4631320/704e464e5123/pone.0141564.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0583/4631320/818b581f24bf/pone.0141564.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0583/4631320/704e464e5123/pone.0141564.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0583/4631320/818b581f24bf/pone.0141564.g002.jpg

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