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Autophagy Balances Neuroinflammation in Alzheimer’s Disease

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Abstract

Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as intracellular pathogens for energy and survival. Dysfunction of autophagy has been associated with the pathologies of Alzheimer’s disease (AD), including Aβ plaques and neurofibrillary tangles. Recently, the presence of sustained immune response in the brain has been considered a new core pathology in AD. Accumulating evidence suggests that autophagy activation may suppress inflammation response through degrading inflammasomes or pro-inflammatory cytokines and improving immune system function in both clinical trials and preclinical studies. This review provides an overview of updated information on autophagy and inflammation and their potential mediators in AD. In summary, we believe that understanding the relationship between autophagy and inflammation will provide insightful knowledge for future therapeutic implications in AD.

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The work was funded by Shanghai TCM special department (special disease) alliance project (HWZG (2021) No. 13).

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XC and YW are co-first authors of the article. XC and YW participated in the conception of the study, wrote the paper, drew pictures and designed the framework of the paper. ZQ searched and assembled relevant literature. LH contributed to revision and final review of the manuscript.

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Correspondence to Li Han.

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Cheng, X., Wei, Y., Qian, Z. et al. Autophagy Balances Neuroinflammation in Alzheimer’s Disease. Cell Mol Neurobiol 43, 1537–1549 (2023). https://doi.org/10.1007/s10571-022-01269-6

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  • DOI: https://doi.org/10.1007/s10571-022-01269-6

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