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自闭症谱系障碍中的树突棘肌动蛋白细胞骨架。

Dendritic spine actin cytoskeleton in autism spectrum disorder.

机构信息

Minerva Foundation Institute for Medical Research, 00290 Helsinki, Finland; Clem Jones Centre for Ageing Dementia Research, The University of Queensland, Brisbane, Queensland 4072, Australia; Queensland Brain Institute, The University of Queensland, Brisbane, Queensland 4072, Australia.

Clem Jones Centre for Ageing Dementia Research, The University of Queensland, Brisbane, Queensland 4072, Australia; Queensland Brain Institute, The University of Queensland, Brisbane, Queensland 4072, Australia.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 2018 Jun 8;84(Pt B):362-381. doi: 10.1016/j.pnpbp.2017.08.023. Epub 2017 Sep 1.

Abstract

Dendritic spines are small actin-rich protrusions from neuronal dendrites that form the postsynaptic part of most excitatory synapses. Changes in the shape and size of dendritic spines correlate with the functional changes in excitatory synapses and are heavily dependent on the remodeling of the underlying actin cytoskeleton. Recent evidence implicates synapses at dendritic spines as important substrates of pathogenesis in neuropsychiatric disorders, including autism spectrum disorder (ASD). Although synaptic perturbations are not the only alterations relevant for these diseases, understanding the molecular underpinnings of the spine and synapse pathology may provide insight into their etiologies and could reveal new drug targets. In this review, we will discuss recent findings of defective actin regulation in dendritic spines associated with ASD.

摘要

树突棘是神经元树突上富含肌动蛋白的小突起,构成大多数兴奋性突触的突触后部分。树突棘的形状和大小的变化与兴奋性突触的功能变化相关,并严重依赖于基础肌动蛋白细胞骨架的重塑。最近的证据表明,树突棘上的突触是神经精神疾病发病机制的重要底物,包括自闭症谱系障碍(ASD)。尽管突触扰动不是这些疾病唯一的改变,但了解棘突和突触病理学的分子基础可能有助于深入了解其病因,并可能揭示新的药物靶点。在这篇综述中,我们将讨论与 ASD 相关的树突棘中肌动蛋白调节缺陷的最新发现。

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