Mitochondrial Aβ A potential cause of metabolic dysfunction in Alzheimer's disease

@article{Chen2006MitochondrialAA,
  title={Mitochondrial A$\beta$ A potential cause of metabolic dysfunction in Alzheimer's disease},
  author={X. Chen and Shi Du Yan},
  journal={IUBMB Life},
  year={2006},
  volume={58}
}
  • X. Chen, S. Yan
  • Published 1 December 2006
  • Biology, Chemistry
  • IUBMB Life
Deficits in mitochondrial function are a characteristic finding in Alzheimer's disease (AD), though the mechanism remains to be clarified. Recent studies revealed that amyloid β peptide (Aβ) gains access into mitochondrial matrix, which was much more pronounced in both AD brain and transgenic mutant APP mice than in normal controls. Aβ progressively accumulates in mitochondria and mediates mitochondrial toxicity. Interaction of mitochondrial Aβ with mitochondrial enzymes such as amyloid… 
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86 Citations
Background Citations
29
Methods Citations
1
Results Citations
1

86 Citations

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It is hypothesized that Aβ-induced and mitochondria-dependent cytotoxic pathways might play an important role in AD pathogenesis and could be a potential therapeutic target.
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Recent studies addressing the following key questions provide new insights into mechanisms of mitochondrial stress related to the pathogenesis of AD and information necessary for developing therapeutic strategy for AD.
Alzheimer's Proteins, Oxidative Stress, and Mitochondrial Dysfunction Interplay in a Neuronal Model of Alzheimer's Disease
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The interplay between beta-amyloid peptide, Tau fragments, oxidative stress, and mitochondria in the neuronal model of cerebellar granule neurons (CGNs) in which the molecular events reminiscent of AD are activated could be helpful to manage the progression of apoptosis in neurodegeneration.
Dysfunction of mitochondria: Implications for Alzheimer's disease.
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  • Biology
    International review of neurobiology
  • 2019
Role of GTPases in the Regulation of Mitochondrial Dynamics in Alzheimer’s Disease and CNS-Related Disorders
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An analysis of the correlation between mitochondria, Alzheimer's disease, and other central nervous system (CNS)-related disorders like the Parkinson’s disease and the autism spectrum disorder is under discussion.
Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment
Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model
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Recognition of the above mentioned complex pathogenesis pathway resulted in novel drug targets in AD research.
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The chemistry and pharmacology of reported ABAD inhibitors are reviewed to highlight the importance of the interaction between Aβ and amyloid-binding alcohol dehydrogenase in Alzheimer's disease.
Interaction between NH2-tau fragment and Aβ in Alzheimer's disease mitochondria contributes to the synaptic deterioration
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