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- W2094795235 abstract "The molecular alterations that induce tau pathology in Alzheimer disease (AD) are not known, particularly whether this is an amyloid-β (Aβ)-dependent or -independent event. We addressed this issue in the 3xTg-AD mice using both genetic and immunological approaches. We show that a selective decrease in Aβ42 markedly delays the progression of tau pathology. The mechanism underlying this effect involves alterations in the levels of carboxyl terminus of heat shock protein70-interacting protein (CHIP) as we show that Aβ accumulation decreases CHIP expression and increases tau levels. We show that the Aβ-induced effects on tau were rescued by overexpressing CHIP. Our findings have profound clinical implications as they indicate that preventing Aβ accumulation will significantly alter AD progression. These data highlight the critical role CHIP plays as a link between Aβ and tau and identify CHIP as a new target not for neurodegenerative disorder characterized by tau accumulation." @default.
- W2094795235 created "2016-06-24" @default.
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- W2094795235 date "2008-07-01" @default.
- W2094795235 modified "2023-10-16" @default.
- W2094795235 title "O2-02-06: Blocking Aβ42 accumulation delays the onset and progression of Tau pathology and cognitive decline via CHIP: A mechanistic link between Aβ and Tau pathology" @default.
- W2094795235 doi "https://doi.org/10.1016/j.jalz.2008.05.318" @default.
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