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- W3132389598 abstract "Abstract ɑ-synuclein (ɑ-syn) progressively accumulates in age related neurodegenerative diseases such as Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB). Although ɑ-syn spreading has been extensively investigated, the role of aging in the manifestation of disease remains unclear. Thus, we explored the role of aging in the pathogenesis of synucleinopathies in a mouse model of DLB/PD initiated by intrastiatal injection of ɑ-syn preformed fibrils (pff). We found that aged mice showed more extensive accumulation of ɑ-syn and behavioral deficits that was associated with greater infiltration of T cells and microgliosis. Microglial inflammatory gene expression induced by ɑ-syn-pff injection in young mice had hallmarks of aged microglia, indicating that enhanced age-associated pathologies may result from inflammatory synergy between aging and the effects of ɑ-syn aggregation. We propose that aging related inflammation influences outcomes of pathological spreading of ɑ-syn and suggests that targeting immune responses might be important in developing treatments for DLB/PD." @default.
- W3132389598 created "2021-03-01" @default.
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- W3132389598 date "2021-02-19" @default.
- W3132389598 modified "2023-09-27" @default.
- W3132389598 title "Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits a mouse model of DLB/PD" @default.
- W3132389598 doi "https://doi.org/10.21203/rs.3.rs-211252/v1" @default.
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