摘要
背景:阿尔茨海默病(AD)是最常见的神经退行性疾病,主要病理特征为聚集β-淀粉样肽,其存款的老年斑,和tau蛋白,形成神经原纤维缠结。现在普遍认为,炎症是牵连在AD的发病机制。 方法:的确炎症介质,如细胞因子和趋化因子(趋化因子)可以通过影响其表达水平和淀粉样加工和/或β-淀粉样蛋白聚集在阿尔茨海默´的淀粉样前体蛋白的影响。此外,细胞因子和趋化因子能影响激酶的活性,导致tau蛋白磷酸化异常。到目前为止,还没有治愈的广告,但一些治疗策略已针对防止发炎反应。抗炎,而且抗淀粉样物质,如黄酮类化合物被证明有效的一些相关神经退行性疾病的病理事件。 结论:本文综述了细胞因子和趋化因子在AD相关疾病中的作用,并总结了潜在的抗炎治疗方法,旨在预防或延缓疾病进展。
关键词: 炎症反应、细胞因子、趋化因子、淀粉样前体蛋白,β-淀粉样蛋白,tau蛋白
Current Alzheimer Research
Title:Impact of Cytokines and Chemokines on Alzheimer’s Disease Neuropathological Hallmarks
Volume: 14 Issue: 8
关键词: 炎症反应、细胞因子、趋化因子、淀粉样前体蛋白,β-淀粉样蛋白,tau蛋白
摘要: Background: Alzheimer’s disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of β-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles. It is now widely accepted that neuroinflammation is implicated in AD pathogenesis.
Method: Indeed, inflammatory mediators, such as cytokines and chemokines (chemotactic cytokines) can impact on the Alzheimer´s amyloid precursor protein by affecting its expression levels and amyloidogenic processing and/or β -amyloid aggregation. Additionally, cytokines and chemokines can influence kinases’ activities, leading to abnormal TAU phosphorylation. To date there is no cure for AD, but several therapeutic strategies have been directed to prevent neuroinflammation. Anti-inflammatory, but also anti-amyloidogenic compounds, such as flavonoids were shown to favourably modulate some pathological events associated with neurodegeneration. Conclusion: This review focuses on the role of cytokines and chemokines in AD-associated pathologies, and summarizes the potential anti-inflammatory therapeutic approaches aimed at preventing or slowing down disease progression.Export Options
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Cite this article as:
Impact of Cytokines and Chemokines on Alzheimer’s Disease Neuropathological Hallmarks, Current Alzheimer Research 2017; 14 (8) . https://dx.doi.org/10.2174/1567205014666170317113606
DOI https://dx.doi.org/10.2174/1567205014666170317113606 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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