Eckert 2008 J Mol Med: Difference between revisions

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|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential
|instruments=Oxygraph-2k, Method, Theory
|instruments=Oxygraph-2k, Method, Theory
|articletype=Protocol; Manual
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Revision as of 17:08, 23 December 2010

Publications in the MiPMap
Eckert A, Hauptmann S, Scherping I, Meinhardt J, Rhein V, DrΓΆse S, Brandt U, FΓ€ndrich M, MΓΌller WE, GΓΆtz J (2008) Oligomeric and fibrillar species of beta-amyloid (Abeta42) both impair mitochondrial function in P301L tau transgenic mice. J. Mol. Med. 86: 1255-1267.

Β» PMID: 18709343

Eckert A, Hauptmann S, Scherping I, Meinhardt J, Rhein V, Droese S, Brandt U, Faendrich M, Mueller WE, Goetz J (2008) J. Mol. Med.

Abstract: We recently provided evidence for a mitochondrial dysfunction in P301L tau transgenic mice, a strain modeling the tau pathology of Alzheimer’s disease (AD) and frontotemporal dementia (FTD). In addition to tau aggregates, the AD brain is further characterized by AΞ² peptide-containing plaques. When we addressed the role of AΞ², this indicated a synergistic action of tau and AΞ² pathology on the mitochondria. In the present study, we compared the toxicity of different AΞ²42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar AΞ² might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated (mainly monomeric) AΞ²42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301L tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301L tau mitochondria either with oligomeric or fibrillar preparations of AΞ²42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric AΞ²42 damage indicating that oligomeric and fibrillar AΞ²42 are both toxic, but exert different degrees of toxicity. β€’ Keywords: Alzheimer’s disease, Amyloid aggregates, Amyloid Ξ²-peptide, Amyloid toxicity, Fibrils, Frontotemporal dementia, Globulomer, Mitochondria, Oligomer, Protein aggregation, Respiration, Tau - Transgenic mice

β€’ O2k-Network Lab: CH_Basel_EckertA, DE_Frankfurt_BrandtU


Labels:

Stress:Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Mouse  Tissue;cell: Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. 


Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Coupling; Membrane Potential"Coupling; Membrane Potential" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k, Method"Method" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property., Theory 


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