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- W2968767455 abstract "Summary The linear cause-consequence relationship linking amyloid-β peptide (Aβ) accumulation to neuronal dysfunction in Alzheimer disease (AD) is gradually replaced by the concept that Aβ initiates complex inflammatory-like cellular alterations that progressively become Aβ independent and lead to brain dyshomeostasis. Little is known about the pathophysiology of this cellular phase of AD. We use here two orthogonal technologies, Spatial Transcriptomics and in situ sequencing, to analyse the transcriptome changes in cells in the amyloid-β plaque niche in a knock-in mouse model for AD. We identify a multicellular co-expressed gene network of 57 Plaque-Induced Genes (PIGs) that define a series of co-ordinated and spatially restricted microglia, astroglia and oligodendrocyte responses to progressing amyloid plaques encompassing complement, oxidative stress and inflammation. A separate oligodendrocyte network suggests abnormal myelination. Spatial Transcriptomics provides an unprecedented approach to untangle the dysregulated cellular network in the vicinity of pathogenic hallmarks of AD and other brain diseases." @default.
- W2968767455 created "2019-08-22" @default.
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- W2968767455 date "2019-08-12" @default.
- W2968767455 modified "2023-09-30" @default.
- W2968767455 title "Spatial and temporal transcriptomics reveal microglia-astroglia crosstalk in the amyloid-β plaque cell niche of Alzheimer’s disease" @default.
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- W2968767455 doi "https://doi.org/10.1101/719930" @default.
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