小心!脑震荡诱导的神经变性中淀粉样变性和轴突转运通路的相互联系。

IF 2.9 Q2 NEUROSCIENCES
Neuroscience Insights Pub Date : 2022-10-17 eCollection Date: 2022-01-01 DOI:10.1177/26331055221129641
Angels Almenar-Queralt, Rodrigo Dos Santos Chaves, Ester J Kwon, Sameer B Shah
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引用次数: 1

摘要

轻度创伤性脑损伤(mTBI)是一种大脑功能被机械力短暂破坏的情况,是发展为阿尔茨海默病(AD)和其他神经退行性疾病的主要危险因素。在这篇评论中,我们总结了诱导多能干细胞衍生的人类神经元的最新发现,详细介绍了轻度损伤后可能导致未来神经退行性变的早期神经元事件。特别地,我们讨论了mTBI与几种可能导致AD进展的生物学途径之间的相互联系,包括淀粉样蛋白前体蛋白(APP)的淀粉样蛋白分裂、轴突运输损伤以及APP相关轴突肿胀的发展。我们还描述了这些发现对未来的机制和转化研究的意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Heads Up! Interlinked Amyloidogenic and Axonal Transport Pathways in Concussion-Induced Neurodegeneration.

Heads Up! Interlinked Amyloidogenic and Axonal Transport Pathways in Concussion-Induced Neurodegeneration.

Heads Up! Interlinked Amyloidogenic and Axonal Transport Pathways in Concussion-Induced Neurodegeneration.

Mild traumatic brain injury (mTBI), a condition in which brain function is transiently disrupted by a mechanical force, is a major risk factor for developing Alzheimer's disease (AD) and other neurodegenerative conditions. In this commentary, we summarize recent findings in human neurons derived from induced pluripotent stem cells, detailing early neuronal events following mild injury that may seed future neurodegeneration. In particular, we discuss interlinked relationships between mTBI and several biological pathways hypothesized to underlie AD progression, including amyloidogenic cleavage of amyloid precursor protein (APP), impairment of axonal transport, and the development of APP-associated axonal swellings. We also describe the implications of these findings for future mechanistic and translational studies.

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来源期刊
Neuroscience Insights
Neuroscience Insights Neuroscience-Neuroscience (all)
CiteScore
6.10
自引率
0.00%
发文量
24
审稿时长
9 weeks
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