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Table 1 BSC models of Aβ physiology and pathophysiology

From: Organotypic brain slice cultures to model neurodegenerative proteinopathies

Human PathologySlice Culture PathologyReference(s)
Increased levels of Aβ productionBSCs from 3xTg-AD mice produce increased amounts of Aβ42 after 4 weeks in culture. BSCs from CRND8 mice also show elevated levels of Aβ42 from 2 weeks in culture. APP overexpression in non-transgenic rat cultures shows increased Aβ production by 3 days in culture.[13, 38, 44]
Thioflavin S positive plaquesBSCs treated with APP23 or APPPS1 brain and supplemented with Aβ1–40 show Thioflavin S positive plaques. BSCs from adult APPSwDI show preserved Thioflavin S plaques in culture.[20, 45]
Dystrophic neuritesBSCs treated with APP23 or APPPS1 brain and supplemented with Aβ1–40 develop dystrophic neurites.[45]
GliosisBSCs from adult APPSwDI show preserved gliosis in culture.[20]
Synapse lossCRND8 BSCs develop synapse loss by 6 weeks in culture.[38]