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首页> 外文期刊>Neuropathology and applied neurobiology >Mechanisms underlying synaptic vulnerability and degeneration in neurodegenerative disease
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Mechanisms underlying synaptic vulnerability and degeneration in neurodegenerative disease

机译：神经退行性疾病中突触脆弱性和变性的潜在机制

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摘要

Recent developments in our understanding of events underlying neurodegeneration across the central and peripheral nervous systems have highlighted the critical role that synapses play in the initiation and progression of neuronal loss. With the development of increasingly accurate and versatile animal models of neurodegenerative disease it has become apparent that disruption of synaptic form and function occurs comparatively early, preceding the onset of degenerative changes in the neuronal cell body. Yet, despite our increasing awareness of the importance of synapses in neurodegeneration, the mechanisms governing the particular susceptibility of distal neuronal processes are only now becoming clear. In this review we bring together recent developments in our understanding of cellular and molecular mechanisms regulating synaptic vulnerability. We have placed a particular focus on three major areas of research that have gained significant interest over the last few years: (i) the contribution of synaptic mitochondria to neurodegeneration; (ii) the contribution of pathways that modulate synaptic function; and (iii) regulation of synaptic degeneration by local posttranslational modifications such as ubiquitination. We suggest that targeting these organelles and pathways may be a productive way to develop synaptoprotective strategies applicable to a range of neurodegenerative conditions.
机译：我们对横跨中枢神经系统和周围神经系统的神经退行性事件的了解的最新进展突显了突触在神经元丢失的发生和发展中所起的关键作用。随着神经退行性疾病的越来越精确和通用的动物模型的发展，已经很明显，突触形式和功能的破坏发生在神经元细胞体内发生变性变化之前比较早。然而，尽管我们对突触在神经退行性变中的重要性的认识不断提高，但控制远端神经元突触的特殊敏感性的机制现在才变得清晰起来。在这篇综述中，我们汇集了对调节突触脆弱性的细胞和分子机制的最新进展。在过去的几年中，我们特别关注了三个主要研究领域：（i）突触线粒体对神经变性的贡献; （ii）调节突触功能的途径的贡献; （iii）通过局部翻译后修饰如泛素化来调节突触变性。我们建议针对这些细胞器和途径可能是开发适用于一系列神经退行性疾病的突触保护策略的有效途径。

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