Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Rhein 2009 Proc Natl Acad Sci U S A"

From Bioblast
Line 1: Line 1:
{{Publication
{{Publication
|title=Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Dröse S, Brandt U, Savaskan E, Czech C, Götz J, Eckert A (2009) Amyloid-beta and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice. Proc Natl Acad Sci U S A 106: 20057-62.
|title=Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Dröse S, Brandt U, Savaskan E, Czech C, Götz J, Eckert A (2009) Amyloid-beta and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice. Proc Natl Acad Sci U S A 106:20057-62.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19897719 PMID:19897719]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19897719 PMID:19897719]
|authors=Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Dröse S, Brandt U, Savaskan E, Czech C, Götz J, Eckert A
|authors=Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Droese S, Brandt U, Savaskan E, Czech C, Gortz J, Eckert A
|year=2009
|year=2009
|journal=Proc Natl Acad Sci U S A
|journal=Proc Natl Acad Sci U S A
Line 13: Line 13:
|organism=Mouse
|organism=Mouse
|tissues=Nervous system
|tissues=Nervous system
|preparations=Isolated Mitochondria
|preparations=Isolated mitochondria
|couplingstates=LEAK, OXPHOS, ETS
|couplingstates=LEAK, OXPHOS, ETS
|substratestates=CI, CIV, ROX
|substratestates=CI, CIV, ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
}}
}}

Revision as of 09:46, 26 February 2015

Publications in the MiPMap
Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Dröse S, Brandt U, Savaskan E, Czech C, Götz J, Eckert A (2009) Amyloid-beta and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice. Proc Natl Acad Sci U S A 106:20057-62.

» PMID:19897719

Rhein V, Song X, Wiesner A, Ittner LM, Baysang G, Meier F, Ozmen L, Bluethmann H, Droese S, Brandt U, Savaskan E, Czech C, Gortz J, Eckert A (2009) Proc Natl Acad Sci U S A

Abstract: Alzheimer's disease (AD) is characterized by amyloid-beta (Abeta)-containing plaques, neurofibrillary tangles, and neuron and synapse loss. Tangle formation has been reproduced in P301L tau transgenic pR5 mice, whereas APP(sw)PS2(N141I) double-transgenic APP152 mice develop Abeta plaques. Cross-breeding generates triple transgenic ((triple)AD) mice that combine both pathologies in one model. To determine functional consequences of the combined Abeta and tau pathologies, we performed a proteomic analysis followed by functional validation. Specifically, we obtained vesicular preparations from (triple)AD mice, the parental strains, and nontransgenic mice, followed by the quantitative mass-tag labeling proteomic technique iTRAQ and mass spectrometry. Within 1,275 quantified proteins, we found a massive deregulation of 24 proteins, of which one-third were mitochondrial proteins mainly related to complexes I and IV of the oxidative phosphorylation system (OXPHOS). Notably, deregulation of complex I was tau dependent, whereas deregulation of complex IV was Abeta dependent, both at the protein and activity levels. Synergistic effects of Abeta and tau were evident in 8-month-old (triple)AD mice as only they showed a reduction of the mitochondrial membrane potential at this early age. At the age of 12 months, the strongest defects on OXPHOS, synthesis of ATP, and reactive oxygen species were exhibited in the (triple)AD mice, again emphasizing synergistic, age-associated effects of Abeta and tau in perishing mitochondria. Our study establishes a molecular link between Abeta and tau protein in AD pathology in vivo, illustrating the potential of quantitative proteomics. Keywords: amyloid-beta peptide, electron transport chain, energy metabolism, � mitochondrial complexes, � tau protein

O2k-Network Lab: CH Basel Eckert A


Labels: MiParea: Respiration, Genetic knockout;overexpression 


Organism: Mouse  Tissue;cell: Nervous system  Preparation: Isolated mitochondria 


Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Oxygraph-2k