Literature DB >> 12614671

Association of ATP synthase alpha-chain with neurofibrillary degeneration in Alzheimer's disease.

N Sergeant1, A Wattez, M Galván-valencia, A Ghestem, J-P David, J Lemoine, P-E Sautiére, J Dachary, J-P Mazat, J-C Michalski, J Velours, R Mena-López, A Delacourte.   

Abstract

Amyloid deposits and neurofibrillary tangles (NFT) are the two hallmarks that characterize Alzheimer's disease (AD). In order to find the molecular partners of these degenerating processes, we have developed antibodies against insoluble AD brain lesions. One clone, named AD46, detects only NFT. Biochemical and histochemistry analyses demonstrate that the labeled protein accumulating in the cytosol of Alzheimer degenerating neurons is the alpha-chain of the ATP synthase. The cytosolic accumulation of the alpha-chain of ATP synthase is observed even at early stages of neurofibrillary degenerating process. It is specifically observed in degenerating neurons, either alone or tightly associated with aggregates of tau proteins, suggesting that it is a new molecular event related to neurodegeneration. Overall, our results strongly suggest the implication of the alpha-chain of ATP synthase in neurofibrillary degeneration of AD that is illustrated by the cytosolic accumulation of this mitochondrial protein, which belongs to the mitochondrial respiratory system. This regulatory subunit of the respiratory complex V of mitochondria is thus a potential target for therapeutic and diagnostic strategies.

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Year:  2003        PMID: 12614671     DOI: 10.1016/s0306-4522(02)00747-9

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  32 in total

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Review 2.  ATP synthase and the actions of inhibitors utilized to study its roles in human health, disease, and other scientific areas.

Authors:  Sangjin Hong; Peter L Pedersen
Journal:  Microbiol Mol Biol Rev       Date:  2008-12       Impact factor: 11.056

3.  Development and characterization of mitochondrial membrane affinity chromatography columns derived from skeletal muscle and platelets for the study of mitochondrial transmembrane proteins.

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Journal:  J Chromatogr B Analyt Technol Biomed Life Sci       Date:  2017-04-13       Impact factor: 3.205

4.  Proteomic identification of specifically carbonylated brain proteins in APP(NLh)/APP(NLh) × PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice model of Alzheimer disease as a function of age.

Authors:  Rukhsana Sultana; Renã A S Robinson; Fabio Di Domenico; Hafiz Mohmmad Abdul; Daret K St Clair; William R Markesbery; Jian Cai; William M Pierce; D Allan Butterfield
Journal:  J Proteomics       Date:  2011-06-25       Impact factor: 4.044

5.  A transcriptional signature of Alzheimer's disease is associated with a metastable subproteome at risk for aggregation.

Authors:  Prajwal Ciryam; Rishika Kundra; Rosie Freer; Richard I Morimoto; Christopher M Dobson; Michele Vendruscolo
Journal:  Proc Natl Acad Sci U S A       Date:  2016-04-11       Impact factor: 11.205

Review 6.  Mitochondrial permeability transition pore is a potential drug target for neurodegeneration.

Authors:  Valasani Koteswara Rao; Emily A Carlson; Shirley Shidu Yan
Journal:  Biochim Biophys Acta       Date:  2013-09-18

Review 7.  Redox proteomics in selected neurodegenerative disorders: from its infancy to future applications.

Authors:  D Allan Butterfield; Marzia Perluigi; Tanea Reed; Tasneem Muharib; Christopher P Hughes; Renã A S Robinson; Rukhsana Sultana
Journal:  Antioxid Redox Signal       Date:  2012-01-18       Impact factor: 8.401

Review 8.  Convergence of amyloid-beta and tau pathologies on mitochondria in vivo.

Authors:  Anne Eckert; Kathrin L Schulz; Virginie Rhein; Jürgen Götz
Journal:  Mol Neurobiol       Date:  2010-03-09       Impact factor: 5.590

Review 9.  Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.

Authors:  Rukhsana Sultana; Marzia Perluigi; D Allan Butterfield
Journal:  Free Radic Biol Med       Date:  2012-10-05       Impact factor: 7.376

10.  Oligomeric and fibrillar species of beta-amyloid (A beta 42) both impair mitochondrial function in P301L tau transgenic mice.

Authors:  Anne Eckert; Susanne Hauptmann; Isabel Scherping; Jessica Meinhardt; Virginie Rhein; Stefan Dröse; Ulrich Brandt; Marcus Fändrich; Walter E Müller; Jürgen Götz
Journal:  J Mol Med (Berl)       Date:  2008-08-16       Impact factor: 4.599

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