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• W4366525376 endingPage "147437" @default.
• W4366525376 startingPage "147437" @default.
• W4366525376 abstract "Cellular senescence increases with aging. While senescence is associated with an exit of the cell cycle, there is ample evidence that post-mitotic cells including neurons can undergo senescence as the brain ages, and that senescence likely contributes significantly to the progression of neurodegenerative diseases (ND) such as Alzheimer's Disease (AD) and Amyotrophic Lateral Sclerosis (ALS). Stress granules (SGs) are stress-induced cytoplasmic biomolecular condensates of RNA and proteins, which have been linked to the development of AD and ALS. The SG seeding hypothesis of NDs proposes that chronic stress in aging neurons results in static SGs that progress into pathological aggregates Alterations in SG dynamics have also been linked to senescence, though studies that link SGs and senescence in the context of NDs and the aging brain have not yet been performed. In this Review, we summarize the literature on senescence, and explore the contribution of senescence to the aging brain. We describe senescence phenotypes in aging neurons and glia, and their links to neuroinflammation and the development of AD and ALS. We further examine the relationships of SGs to senescence and to ND. We propose a new hypothesis that neuronal senescence may contribute to the mechanism of SG seeding in ND by altering SG dynamics in aged cells, thereby providing additional aggregation opportunities within aged neurons." @default.
• W4366525376 created "2023-04-22" @default.
• W4366525376 creator A5082468349 @default.
• W4366525376 creator A5083710474 @default.
• W4366525376 date "2023-06-01" @default.
• W4366525376 modified "2023-10-16" @default.
• W4366525376 title "Connecting the dots: Neuronal senescence, stress granules, and neurodegeneration" @default.
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