title: Advanced Mitochondrial Respiration Assay for Evaluation of Mitochondrial Dysfunction in Alzheimer's Disease.
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.
authors.affiliation: Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, University of Basel, Transfaculty Research Platform, Molecular & Cognitive Neurosciences, Wilhelm Klein-Strasse 27, 4012, Basel, Switzerland.
authors.forename: Amandine
authors.initials: A
authors.lastname: Grimm
authors.forename: Karen
authors.initials: K
authors.lastname: Schmitt
authors.forename: Anne
authors.initials: A
authors.lastname: Eckert
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D019069:Cell Respiration; D003584:Cytological Techniques / Q000379:methods*; D051379:Mice; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins