Abstract
Alzheimer’s disease (AD) is characterized by the presence of amyloid plaques (aggregates of amyloid-β [Aβ]) and neurofibrillary tangles (aggregates of tau) in the brain, but the underlying mechanisms of the disease are still partially unclear. A growing body of evidence supports mitochondrial dysfunction as a prominent and early, chronic oxidative stress-associated event that contributes to synaptic abnormalities, and, ultimately, selective neuronal degeneration in AD. Using a high-resolution respirometry system, we shed new light on the close interrelationship of this organelle with Aβ and tau in the pathogenic process underlying AD by showing a synergistic effect of these two hallmark proteins on the oxidative phosphorylation capacity of mitochondria isolated from the brain of transgenic AD mice. In the present chapter, we first introduce the principle of the Aβ and tau interaction on mitochondrial respiration, and secondly, we describe in detail the used respiratory protocol.
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Acknowledgements
This work was supported by grants from the Swiss National Science Foundation (Grant SNF 310000–108223), Synapsis and Novartis Foundation for medical-biological research.
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Grimm, A., Schmitt, K., Eckert, A. (2016). Advanced Mitochondrial Respiration Assay for Evaluation of Mitochondrial Dysfunction in Alzheimer’s Disease. In: Castrillo, J., Oliver, S. (eds) Systems Biology of Alzheimer's Disease. Methods in Molecular Biology, vol 1303. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-2627-5_9
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DOI: https://doi.org/10.1007/978-1-4939-2627-5_9
Publisher Name: Humana Press, New York, NY
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