Autophagy Balances Neuroinflammation in Alzheimer’s Disease

• Published in: Cellular and molecular neurobiology Vol. 43; no. 4; pp. 1537 - 1549
• Main Authors: Cheng, Xuehua, Wei, Yong, Qian, Zijun, Han, Li
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.05.2023; Springer Nature B.V
• Subjects: Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Autophagy; Biomedical and Life Sciences; Biomedicine; Cell Biology; Clinical trials; Evolutionary conservation; Humans; Immune response; Inflammasomes; Inflammasomes - metabolism; Inflammation; Inflammation - pathology; Macromolecules; Microglia - metabolism; Mitochondria; Neurobiology; Neurodegenerative diseases; Neurofibrillary tangles; Neuroinflammatory Diseases; Neurosciences; Organelles; Review Paper; Senile plaques; Inflammation; NLRP3 inflammasomes; Genetic factors; Alzheimer’s disease; Autophagy; Microglia
• ISSN: 0272-4340; 1573-6830
• DOI: 10.1007/s10571-022-01269-6

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.