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衰老和阿尔茨海默病进展中的神经炎症分子机制。

Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression.

机构信息

Department of Psycho-Neurosciences and Rehabilitation, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania.

Department of Preclinical Sciences, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania.

出版信息

Int J Mol Sci. 2023 Jan 18;24(3):1869. doi: 10.3390/ijms24031869.

Abstract

Aging is the most prominent risk factor for late-onset Alzheimer's disease. Aging associates with a chronic inflammatory state both in the periphery and in the central nervous system, the evidence thereof and the mechanisms leading to chronic neuroinflammation being discussed. Nonetheless, neuroinflammation is significantly enhanced by the accumulation of amyloid beta and accelerates the progression of Alzheimer's disease through various pathways discussed in the present review. Decades of clinical trials targeting the 2 abnormal proteins in Alzheimer's disease, amyloid beta and tau, led to many failures. As such, targeting neuroinflammation via different strategies could prove a valuable therapeutic strategy, although much research is still needed to identify the appropriate time window. Active research focusing on identifying early biomarkers could help translating these novel strategies from bench to bedside.

摘要

衰老是迟发性阿尔茨海默病的最主要危险因素。衰老与外周和中枢神经系统的慢性炎症状态有关,目前正在讨论其证据和导致慢性神经炎症的机制。尽管如此,淀粉样蛋白-β的积累显著增强了神经炎症,并通过本综述中讨论的各种途径加速了阿尔茨海默病的进展。几十年来,针对阿尔茨海默病中两种异常蛋白——淀粉样蛋白-β和 tau 的临床试验都以失败告终。因此,通过不同策略靶向神经炎症可能是一种有价值的治疗策略,尽管仍需要大量研究来确定合适的时间窗。目前正在积极研究确定早期生物标志物,这有助于将这些新策略从实验室转化到临床。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38b0/9915182/4bc5fa82da81/ijms-24-01869-g001.jpg

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