Proteoglycans and glycosaminoglycans in misfolded proteins formation in Alzheimer's disease.
Proteoglycans and glycosaminoglycans in misfolded proteins formation in Alzheimer's disease.
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阿尔茨海默病中错误折叠蛋白质形成中的蛋白聚糖和糖胺聚糖。
DOI：
10.2174/0929866521666140626095145
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发表时间：
2014
影响因子：
1.6
通讯作者：
K. Ding
中科院分区：
文献类型：
--
作者：
Peipei Wang;K. Ding
错折叠蛋白淀粉样β蛋白（Aβ）和tau蛋白是阿尔茨海默病（AD）的两个重要标志，是治疗AD的重要靶点。对这两种蛋白诱导神经元功能障碍机制的研究为AD的治疗提供了新的策略，包括抑制Aβ的产生和聚集，加速Aβ的清除以及减少tau蛋白的过度磷酸化。蛋白聚糖（PG）由核心蛋白和糖胺聚糖（GAG）链组成，由于核心蛋白、GAG链的数量以及硫酸化的程度和位置的变化而具有巨大的结构多样性。大量证据表明PGs和GAGs在Aβ和tau蛋白的加工过程中发挥重要作用。许多糖胺聚糖及其类似物在AD中具有潜在的治疗作用。在这篇综述中，我们重点介绍了PG和GAG与AD中错误折叠蛋白的关系及其潜在的治疗意义。
Misfolded protein amyloid-beta protein (Aβ) and tau protein are two high hallmarks of Alzheimer's disease (AD), representing significant targets in treating AD. Researches on mechanisms of the two proteins inducing neuron dysfunctions provide therapeutic strategies of AD, including inhibition of Aβ production and aggregation, acceleration of Aβ clearance as well as reduction of tau hyperphosphorylation. Proteoglycans (PGs) consist of a core protein and glycosaminoglycans (GAGs) chains, with enormous structural diversity due to variation in the core protein, the number of GAGs chains as well as extent and position of sulfation. Considerable evidences have indicated that PGs and GAGs play important roles in Aβ and tau processing. Numbers of GAGs and analogues have potential therapeutic function in AD. In this Review, we focus on the relationship of PGs and GAGs with misfolded proteins in AD and their potential therapeutic implications.