Published: July 22, 2024
Background: Neuroinflammation has long been implicated in the progression of amyloid beta (Aβ) accumulation and decline cognitive function Alzheimer's disease (AD). Currently, many transcription factors, downstream signaling pathways, molecular mechanisms that regulate polarization microglia have explored. Furthermore, may also exert a complex role AD through transformation Aβ plaques or debris clearance, reflected phagocytosis. One mediators neuroinflammation is activated microglia. Therefore, regulation microglial be key to successfully treating AD. Methods: This review article. PubMed, Embase, Scopus, research meeting abstracts were searched up 2024 for studies Disease. Systematic information retrieval was performed appropriate isolated based on important available studies. The from each articles un-derstood extracted form database. Results: similar neuropathological results between several animals cases show possibility implement microglia-related changes as an earlier diagnostic marker humans. gene sets identified various transcriptomic further foster this avenue by offering potential targets therapeutic development. Multiple suggest microglia-associated at special stage could protective, there-fore, intervention should delicate so beneficial response retained. Conclusion: phenotype balance A1 (toxic) A2 (safe) phenotypes toxic illness become hot topic present. Substantial evidence, both vitro vivo, suggested loss normal activation contribute neurodegeneration Promoting restoring mi-croglia towards thus represent effective strategy ame-liorating progressive neurocognitive impairments.
Language: Английский