炎症在阿尔茨海默病的发病机制中起主要作用吗?

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2023-09-01 Epub Date: 2023-04-07 DOI:10.1007/s12017-023-08741-6
Benita Wiatrak, Paulina Jawień, Adam Szeląg, Izabela Jęśkowiak-Kossakowska
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引用次数: 2

摘要

阿尔茨海默病(AD)是一种导致痴呆的神经退行性疾病,目前尚无有效的药物治疗。目前,治疗的目标只是减缓疾病不可避免的进展,减少一些症状。AD导致具有Aβ和tau病理结构的蛋白质积累,并诱导大脑中神经的炎症,从而导致神经元死亡。活化的小胶质细胞产生促炎细胞因子,诱导慢性炎症反应并介导突触损伤和神经元死亡。神经炎症一直是正在进行的AD研究中一个经常被忽视的方面。越来越多的科学论文将神经炎症纳入AD发病机制,尽管对于合并症或性别差异的影响还没有明确的结果。本出版物基于我们自己使用模型细胞培养和其他研究人员进行的体外研究结果,对炎症在AD进展中的作用进行了批判性的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Does Inflammation Play a Major Role in the Pathogenesis of Alzheimer's Disease?

Alzheimer's disease (AD) is a neurodegenerative disease leading to dementia for which no effective medicine exists. Currently, the goal of therapy is only to slow down the inevitable progression of the disease and reduce some symptoms. AD causes the accumulation of proteins with the pathological structure of Aβ and tau and the induction of inflammation of nerves in the brain, which lead to the death of neurons. The activated microglial cells produce pro-inflammatory cytokines that induce a chronic inflammatory response and mediate synapse damage and the neuronal death. Neuroinflammation has been an often ignored aspect of ongoing AD research. There are more and more scientific papers taking into account the aspect of neuroinflammation in the pathogenesis of AD, although there are no unambiguous results regarding the impact of comorbidities or gender differences. This publication concerns a critical look at the role of inflammation in the progression of AD, based on the results of our own in vitro studies using model cell cultures and other researchers.

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4.30%
发文量
567
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