Glycosylation and other PTMs alterations in neurodegenerative diseases: Current status and future role in neurotrauma.
Glycosylation and other PTMs alterations in neurodegenerative diseases: Current status and future role in neurotrauma.
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DOI：
10.1002/elps.201500585
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发表时间：
2016-06
期刊：
影响因子：
2.9
通讯作者：
Kobeissy F
中科院分区：
文献类型：
--
作者：
Abou-Abbass H;Abou-El-Hassan H;Bahmad H;Zibara K;Zebian A;Youssef R;Ismail J;Zhu R;Zhou S;Dong X;Nasser M;Bahmad M;Darwish H;Mechref Y;Kobeissy F
创伤性脑损伤（TBI）是影响世界各国的主要公共卫生威胁。随着受 TBI 折磨的患者数量预计会增加，我们更有必要加深对 TBI 病理生理机制的了解。已知 TBI 会增加罹患多种神经退行性疾病 (ND) 的风险，例如阿尔茨海默病 (AD) 和帕金森病 (PD)。因此，可以合理地假设，ND 的病理生理学与 TBI 的病理生理学有共同的机制基础。通过这篇综述，我们的目的是确定与 ND 和 TBI 发病机制有关的蛋白质-蛋白质相互作用、差异蛋白质表达和 PTM（主要是糖基化）。 OVID 和 PubMed 经过严格检索，以确定利用先进蛋白质组学平台（基于 MS）和系统生物学工具来揭示 ND 背后机制的研究，试图揭示损伤后发生的神秘生物过程。已发现 TBI 和 AD 之间存在多种 PTM 共同点，但 TBI 和 PD 之间没有发现相似之处。磷酸化 tau 蛋白、糖基化淀粉样前体蛋白和许多其他修饰似乎在 TBI 和 AD 中都很常见。 PTM、差异蛋白谱和改变的生物途径似乎通过以类似于 TBI 的方式干扰 ND 的病理状况，在 ND 过程中发挥关键作用。为了开发更好的诊断工具、治疗方法和更有利的预后，迫切需要推进与 ND 和 TBI 相关的糖蛋白组学研究。
Traumatic brain injuries (TBIs) present a chief public health threat affecting nations worldwide. As numbers of patients afflicted by TBI are expected to rise, the necessity to increase our understanding of the pathophysiological mechanism(s) as a result of TBI mounts. TBI is known to augment the risk of developing a number of neurodegenerative diseases (NDs) such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Hence, it is rational to assume that a common mechanistic ground links the pathophysiology of NDs to that of TBIs. Through this review, we aim to identify the protein–protein interactions, differential proteins expression, and PTMs, mainly glycosylation, that are involved in the pathogenesis of both ND and TBI. OVID and PubMed have been rigorously searched to identify studies that utilized advanced proteomic platforms (MS based) and systems biology tools to unfold the mechanism(s) behind ND in an attempt to unveil the mysterious biological processes that occur postinjury. Various PTMs have been found to be common between TBI and AD, whereas no similarities have been found between TBI and PD. Phosphorylated tau protein, glycosylated amyloid precursor protein, and many other modifications appear to be common in both TBI and AD. PTMs, differential protein profiles, and altered biological pathways appear to have critical roles in ND processes by interfering with their pathological condition in a manner similar to TBI. Advancement in glycoproteomic studies pertaining to ND and TBI is urgently needed in order to develop better diagnostic tools, therapies, and more favorable prognoses.