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- W1650328097 abstract "Alzheimer's disease (AD) is a neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration." @default.
- W1650328097 created "2016-06-24" @default.
- W1650328097 creator A5007107729 @default.
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- W1650328097 creator A5050126878 @default.
- W1650328097 creator A5055826036 @default.
- W1650328097 creator A5089557922 @default.
- W1650328097 creator A5091600316 @default.
- W1650328097 date "2015-01-01" @default.
- W1650328097 modified "2023-10-05" @default.
- W1650328097 title "Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer’s Disease" @default.
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