Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease
作者： P. Hemachandra Reddy , M. Flint Beal
DOI: 10.1016/J.MOLMED.2007.12.002
关键词: Genetically modified mouse 、 Neuroscience 、 Disease 、 Alzheimer's disease 、 Cognitive decline 、 Oxidative stress 、 Biology 、 Pathology 、 Amyloid beta 、 Reactive oxygen species 、 Mitochondrion
摘要: Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic mouse models of AD suggest that oxidative damage, induced by amyloid β (Aβ), is associated with mitochondria early in AD progression. Aβ and amyloid-precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron-transport chain, increase reactive oxygen species production, cause mitochondrial …
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