Altered expression of neurotrophic factors in patients with major depression
Altered expression of neurotrophic factors in patients with major depression
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DOI：
10.1016/j.jpsychires.2008.01.010
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发表时间：
2008-10-01
影响因子：
4.8
通讯作者：
Watanabe, Yoshifumi
中科院分区：
文献类型：
--
作者：
Otsuki, Koji;Uchida, Shusaku;Watanabe, Yoshifumi
有大量证据表明，神经营养因子表达水平的改变与神经精神疾病的病理生理有关。尽管死后脑研究表明情绪障碍患者神经营养因子表达水平的改变，但尚不清楚这些改变是状态依赖还是特征依赖。在这项研究中，我们采用实时荧光定量PCR方法检测了神经胶质细胞系来源的神经营养因子（GDNF）家族成员（GDNF、artemin （ARTN）、neurturin和persephin）、脑源性神经营养因子、神经生长因子、神经营养因子-3 （NT-3）和神经营养因子-4 mrna在重度抑郁症和双相情感障碍患者当前抑郁和缓解状态下的外周血中的表达水平。GDNF、ARTN和NT-3 mrna的表达水平在重度抑郁症患者处于当前抑郁状态，而非缓解状态。在双相情感障碍患者中未发现这些mrna的表达改变。我们的研究结果提示GDNF、ARTN和NT-3 mrna表达水平的变化可能是状态依赖性的，并与重度抑郁症的病理生理有关。(C) 2008 Elsevier Ltd版权所有。
There is an abundance of evidence suggesting the involvement of altered levels of expression of neurotrophic factors in the pathophysiology of neuropsychiatric disorders. Although postmortem brain studies have indicated the alterations in the expression levels of neurotrophic factors in mood disorder patients, it is unclear whether these changes are state- or trait-dependent. In this study, we examined the expression levels of the members of the glial cell line-derived neurotrophic factor (GDNF) family (GDNF, artemin (ARTN), neurturin, and persephin), brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3 (NT-3), and neurotrophin-4 mRNAs by using quantitative real-time PCR method in peripheral blood cells of patients with major depressive and bipolar disorders in both a current depressive and a remissive states. Reduced expression levels of GDNF, ARTN, and NT-3 mRNAs were found in patients with major depressive disorder in a current depressive state, but not in a remissive state. Altered expressions of these mRNAs were not found in patients with bipolar disorder. Our results suggest that the changes in the expression levels of GDNF, ARTN, and NT-3 mRNAs might be state-dependent and associated with the pathophysiology of major depression. (C) 2008 Elsevier Ltd. All rights reserved.