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- W2369737041 abstract "The β-amyloid protein (Aβ) has long been considered to associate with Alzheimer's disease (AD). In addition, groups of evidence show that the soluble intracellular Aβ plays an important role in the disease development. The mitochondrial dysfunction induced by Aβ accumulation is a main pathologic process in early stage of AD. Matured Aβ is imported into the mitochondria through an unclear route. Once inside the mitochondria, Aβ is able to interact with a number of targets, including amyloid-binding alcohol dehydrogenase (ABAD) and cyclophilin D (CypD), which is a component of the mitochondrial permeability transition pore. Interference with the normal functions of these proteins results in mitochondrial injury, such as energy dyshomeostasis, production of reactive oxygen species, membrane permeability alteration and so on. This review explores the Aβ generation and location in mitochondria. The mitochondrial injury induced by the interaction between Aβ and its targets are also discussed." @default.
- W2369737041 created "2016-06-24" @default.
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- W2369737041 date "2010-01-01" @default.
- W2369737041 modified "2023-09-26" @default.
- W2369737041 title "Advances in mitochondria injury by Aβ in Alzheimer's disease" @default.
- W2369737041 hasPublicationYear "2010" @default.
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