阿尔茨海默病小鼠模型中早期出现的树突棘改变揭示神经退行性变的主要原因
Early-Occurring Dendritic Spines Alterations in Mouse Models of Alzheimer's Disease Inform on Primary Causes of Neurodegeneration.
作者信息
Ammassari-Teule Martine
机构信息
Institute of Biochemistry and Cell Biology, CNR-National Research Council, Rome, Italy.
Laboratory of Psychobiology, IRCCS Santa Lucia Foundation, Rome, Italy.
出版信息
Front Synaptic Neurosci. 2020 Sep 10;12:566615. doi: 10.3389/fnsyn.2020.566615. eCollection 2020.
Abstract
The consensus that synaptic failure is the earliest cause of cognitive deterioration in Alzheimer's disease (AD) has initially led to investigate structural (dendritic spines) and physiological (LTP) synaptic dysfunctions in mouse models of AD with established cognitive alterations. The challenge is now to track down ultra-early alterations in spines to uncover causes rather than disease's symptoms. This review article pinpoints dysregulations of the postsynaptic density (PSD) protein network which alter the morphology and function of spines in pre- and early- symptomatic hAPP mouse models of AD, and, hence, inform on primary causes of neurodegeneration.
摘要
突触功能障碍是阿尔茨海默病（AD）认知衰退的最早原因，这一共识最初促使人们在已出现认知改变的AD小鼠模型中研究结构（树突棘）和生理（长时程增强，LTP）突触功能障碍。现在的挑战是追踪树突棘的超早期改变，以揭示病因而非疾病症状。这篇综述文章指出了突触后致密区（PSD）蛋白网络的失调，这种失调会改变AD症状出现前和早期有症状的人淀粉样前体蛋白（hAPP）小鼠模型中树突棘的形态和功能，从而为神经退行性变的主要原因提供信息。
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2
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Neurobiol Dis. 2020 Jun;139:104787. doi: 10.1016/j.nbd.2020.104787. Epub 2020 Feb 4.
3
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