The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease.
The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease.
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DOI：
10.3389/fneur.2020.570711
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发表时间：
2020
影响因子：
3.4
通讯作者：
Ulland TK
中科院分区：
文献类型：
--
作者：
Hanslik KL;Ulland TK
阿尔茨海默病（AD）是最普遍的迟发性痴呆形式。AD影响着美国和全世界数百万人的健康。目前，还没有批准的治疗方法可以阻止或逆转AD的临床进展。传统上，AD的特征首先是淀粉样蛋白-β（Aβ）斑块的出现，随后是由过度磷酸化的tau（p-tau）组成的神经元内神经元缠结（NFT）的形成。这些损伤与突触丧失和最终的认知障碍有关。此外，小神经胶质细胞增生始终存在于AD病理学的大脑区域中。小胶质细胞在AD发病和进展中的作用尚不清楚。最近的一些报道表明，被称为NOD、LRR和含pyrin-domain 3（Nlrp 3）炎性体的多蛋白复合物通过小胶质细胞的组装导致含有CARD（Asc）specs的凋亡spec-like蛋白的形成，其然后使新的Aβ斑块成核，从而放大Aβ相关的病理。NFT还可以激活Nlrp 3炎性体，导致增强的tau相关病理学。本文就小胶质细胞和炎性小体在AD先天免疫应答中的作用作一综述。
Alzheimer's disease (AD) is the most prevalent form of late-onset dementia. AD affects the health of millions of people in the United States and worldwide. Currently, there are no approved therapies that can halt or reverse the clinical progression of AD. Traditionally, AD is characterized first by the appearance of amyloid-β (Aβ) plaques followed by the formation of intraneuronal neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (p-tau). These lesions are linked to synapse loss and eventual cognitive impairment. Additionally, microgliosis is consistently found in regions of the brain with AD pathology. The role of microglia in AD onset and progression remains unclear. Several recent reports indicate that the assembly of the multi-protein complex known as the NOD, LRR, and pyrin-domain containing 3 (Nlrp3) inflammasome by microglia results in apoptosis spec-like protein containing a CARD (Asc) spec formation, which then nucleates new Aβ plaques, thus amplifying Aβ-associated pathology. NFTs can also activate the Nlrp3 inflammasome leading to enhanced tau-associated pathology. Here, we will review the role of microglia and the activation of the inflammasome in the innate immune response to AD.
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