Electroconvulsive therapy selectively enhances amyloid β 1-42 in the cerebrospinal fluid of patients with major depression: A prospective pilot study
Electroconvulsive therapy selectively enhances amyloid β 1-42 in the cerebrospinal fluid of patients with major depression: A prospective pilot study
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DOI：
10.1016/j.euroneuro.2016.11.004
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发表时间：
2016-12-01
影响因子：
5.6
通讯作者：
Sartorius, Alexander
中科院分区：
文献类型：
--
作者：
Kranaster, Laura;Aksay, Suna Su;Sartorius, Alexander
β-淀粉样蛋白（A β）、阿尔茨海默病（AD）和重度抑郁症（MDD）之间的复杂相互作用表明，MDD患者的大脑A β代谢发生改变，患AD的风险增加。为了阐明抗抑郁治疗与人类A β代谢之间的关系，我们对MDD患者在电休克治疗（ECT）作为有效的抗抑郁治疗期间的脑脊液（CSF）中的A β肽进行了研究。我们检测了12例MDD患者ECT治疗前后CSF中A β（1-42）、A β（1-40）和tau蛋白的水平。与基线相比，ECT治疗后A β（1-42）显著升高，而其他肽和蛋白质如A β（1-40）、A β比率、总tau蛋白或其磷酸化形式没有发现差异。最显著的发现是，在所有对治疗有临床反应的患者中发现ECT后A β（1-42）增加，但在那些没有反应的患者中没有发现。每例反应患者的ECT疗程数与CSF中A β（1-42）的增加相关。我们的数据指向一种特定的抗抑郁机制，该机制不是基于A β的普遍增加，而是似乎仅涉及A β（1-42），具有最高淀粉样蛋白生成潜力的亚型。我们提出了第一项在人类中的研究，证明了对ECT治疗有反应的抑郁症患者的CSF中A β（1-42）的孤立动员。(C)2016 Elsevier B.V.和ECNP。All rights reserved.
A complex interplay between beta-amyloid (A beta), Alzheimer's disease (AD) and major depression disorder (MDD) suggests that patients with MDD have an altered cerebral A beta metabolism and an increased risk of developing AD. In order to elucidate the relationship between antidepressant treatment and A beta metabolism in humans, we performed a study on A beta peptides in the cerebrospinal fluid (CSF) in patients with MDD during electroconvulsive therapy (ECT) as an effective antidepressant treatment. We measured the levels of A beta(1-42), A beta(1-40) and of tau proteins in the CSF in 12 patients with MDD before and after a course of ECT. A beta(1-42) was significantly elevated after the ECT treatment compared to baseline, whereas no difference was found for other peptides and proteins such as A beta(1-40), A beta ratio, total tau protein or its phosphorylated form. The most salient finding was, that the increase of A beta(1-42) after ECT was found in all patients with clinical response to the treatment, but not in those who did not respond. The number of ECT sessions of each responding patient correlated with the increase of A beta(1-42) in the CSF. Our data point towards to a specific antidepressant mechanism which is not based on a general increase of A beta, but seems to involve merely A beta(1-42), the isoform with highest amyloidogenic potential. We present the first study in humans demonstrating an isolated mobilization of A beta(1-42) in the CSF of patients with depression who respond to an ECT treatment. (C) 2016 Elsevier B.V. and ECNP. All rights reserved.