Targeting neuroinflammation in Alzheimer's disease: from mechanisms to clinical applications

Alzheimer's disease is characterized by sustained neuroinflammation leading to memory loss and cognitive decline. The past decade has witnessed tremendous efforts in Alzheimer's disease research; however, no effective treatment is available to prevent disease progression. An increasing bod...

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Published inNeural regeneration research Vol. 18; no. 4; pp. 708 - 715
Main Authors Si, Zi-Zhen, Zou, Chen-Jun, Mei, Xi, Li, Xiao-Fang, Luo, Hu, Shen, Yao, Hu, Jun, Li, Xing-Xing, Wu, Lun, Liu, Yu
Format Journal Article
LanguageEnglish
Published Mumbai Wolters Kluwer India Pvt. Ltd 01.04.2023
Medknow Publications & Media Pvt. Ltd
Wolters Kluwer - Medknow
Wolters Kluwer Medknow Publications
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Summary:Alzheimer's disease is characterized by sustained neuroinflammation leading to memory loss and cognitive decline. The past decade has witnessed tremendous efforts in Alzheimer's disease research; however, no effective treatment is available to prevent disease progression. An increasing body of evidence suggests that neuroinflammation plays an important role in Alzheimer's disease pathogenesis, alongside the classical pathological hallmarks such as misfolded and aggregated proteins (e.g., amyloid-beta and tau). Firstly, this review summarized the clinical and pathological characteristics of Alzheimer's disease. Secondly, we outlined key aspects of glial cell-associated inflammation in Alzheimer's disease pathogenesis and provided the latest evidence on the roles of microglia and astrocytes in Alzheimer's disease pathology. Then, we revealed the double-edged nature of inflammatory cytokines and inflammasomes in Alzheimer's disease. In addition, the potential therapeutic roles of innate immunity and neuroinflammation for Alzheimer's disease were also discussed through these mechanisms. In the final section, the remaining key problems according to the current research status were discussed.
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Author contributions: ZZS and CJZ prepared the manuscript. XM, XFL, JH, XXL and LW searched the literature. HL and YS edited the manuscript. YL contributed to the definition of intellectual content and manuscript review. All authors approved the final version of the paper.
These two authors contribute equally to this work.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.353484