Cellular senescence at the crossroads of inflammation and Alzheimer's disease. Issue 9 (September 2021)

• Record Type: Journal Article
• Authors: Guerrero, Ana; De Strooper, Bart; Arancibia-Cárcamo, I. Lorena
• Is Part Of: Trends in neurosciences. Volume 44:Issue 9(2021)
• Page Start: 714
• Page End: 727
• Publication Date: 2021-09
• Subjects: aging -- neuroinflammation -- microglia -- astrocytes -- neurodegeneration -- SASP; Neurology -- Periodicals; Neurophysiology -- Periodicals; Neurobiology -- Periodicals; 612.8
• DOI: 10.1016/j.tins.2021.06.007
• Languages: English
• ISSNs: 0166-2236

Abstract

Abstract : Aging is a key risk factor for Alzheimer's disease (AD), but the reasons for this association are not well understood. Senescent cells accumulate in aged tissues and have been shown to play causal roles in age-related pathologies through their proinflammatory secretome. The question arises whether senescence-induced inflammation might contribute to AD and bridge the gap between aging and AD. Here, we highlight the role of cellular senescence as a driver of the aging phenotype, and discuss the current evidence that connects senescence with AD and neurodegeneration. Highlights: Senescent cells accumulate in aged tissues and often play a causal role in age-related pathologies, partly due to their proinflammatory secretome. In mouse models of neurodegeneration, clearance of senescent glial cells alleviates tau-dependent neurodegeneration and decreases inflammation as well as β-amyloid plaque size. Senescence emerges as a pivotal player in the complex cellular landscape of Alzheimer's disease (AD). The senescence secretome constitutes a promising therapeutic target to balance neuroinflammation during AD progression.