Difference between revisions of "Grimm 2016 Methods Mol Biol"
(Created page with "{{Publication |title=Grimm A, Schmitt K, Eckert A (2016) Advanced mitochondrial respiration assay for evaluation of mitochondrial dysfunction in alzheimer's disease. Methods M...") |
|||
(One intermediate revision by the same user not shown) | |||
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Grimm A, Schmitt K, Eckert A (2016) Advanced mitochondrial respiration assay for evaluation of mitochondrial dysfunction in | |title=Grimm A, Schmitt K, Eckert A (2016) Advanced mitochondrial respiration assay for evaluation of mitochondrial dysfunction in Alzheimer's disease. Methods Mol Biol 1303:171-83. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/26235066 PMID: 26235066] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/26235066 PMID: 26235066] | ||
|authors=Grimm A, Schmitt K, Eckert A | |authors=Grimm A, Schmitt K, Eckert A | ||
Line 8: | Line 8: | ||
|keywords=Mitochondria, Alzheimer’s disease, Amyloid-β, Tau, Oxygraph, High-resolution respirometry (HRR), Oxidative phosphorylation | |keywords=Mitochondria, Alzheimer’s disease, Amyloid-β, Tau, Oxygraph, High-resolution respirometry (HRR), Oxidative phosphorylation | ||
|editor=[[Plangger M]], | |editor=[[Plangger M]], | ||
|mipnetlab=CH Basel Eckert A | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|diseases=Alzheimer's | |||
|organism=Mouse | |||
|tissues=Nervous system | |||
|preparations=Isolated mitochondria | |||
|couplingstates=LEAK, OXPHOS, ET | |||
|pathways=N, CIV, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels, 2019-08, | |additional=Labels, 2019-08, | ||
}} | }} |
Latest revision as of 14:09, 22 August 2019
Grimm A, Schmitt K, Eckert A (2016) Advanced mitochondrial respiration assay for evaluation of mitochondrial dysfunction in Alzheimer's disease. Methods Mol Biol 1303:171-83. |
Grimm A, Schmitt K, Eckert A (2016) Methods Mol Biol
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. • Keywords: Mitochondria, Alzheimer’s disease, Amyloid-β, Tau, Oxygraph, High-resolution respirometry (HRR), Oxidative phosphorylation • Bioblast editor: Plangger M • O2k-Network Lab: CH Basel Eckert A
Labels: MiParea: Respiration
Pathology: Alzheimer's
Organism: Mouse Tissue;cell: Nervous system Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS, ET
Pathway: N, CIV, ROX
HRR: Oxygraph-2k
Labels, 2019-08