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支架破裂:细胞骨架功能障碍在重度抑郁症发病机制中的可能作用。

A breach in the scaffold: the possible role of cytoskeleton dysfunction in the pathogenesis of major depression.

机构信息

Neurodysfunction Research Laboratory, Department of Psychiatry, LKS Faculty of Medicine, Hong Kong Special Administrative Region, China.

出版信息

Ageing Res Rev. 2013 Jan;12(1):67-75. doi: 10.1016/j.arr.2012.08.004. Epub 2012 Sep 17.

Abstract

Depression is one of the most common psychiatric disorders with inadequately understood disease mechanisms. It has long been considered that dendritic regression and decrease in the number of dendritic spines are involved in depression. Dendrites made up of microtubules and actin filaments form synapses with neighboring neurons, which come together as an important communication network. Cytoskeletal proteins undergo post-translational modifications to define their structure and function. In depression and other psychiatric disorders, post-translational modifications may be disrupted that can result in altered cytoskeletal functions. The disruption of microtubule and actin in terms of morphology and functions may be a leading cause of dendritic regression and decrease in dendritic spine in depression.

摘要

抑郁症是一种最常见的精神障碍疾病,其发病机制尚未完全被理解。长期以来,人们一直认为树突萎缩和树突棘数量减少与抑郁症有关。由微管和肌动蛋白丝组成的树突与邻近神经元形成突触,这些神经元聚集在一起形成一个重要的通讯网络。细胞骨架蛋白发生翻译后修饰以定义其结构和功能。在抑郁症和其他精神障碍中,翻译后修饰可能会被破坏,从而导致细胞骨架功能改变。微管和肌动蛋白在形态和功能上的破坏可能是导致抑郁症中树突萎缩和树突棘减少的主要原因。

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