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Your search keyword '"Mancuso, Michelangelo"' showing total 7 results
Start Over Author "Mancuso, Michelangelo" Journal neurobiology of aging
7 results on '"Mancuso, Michelangelo"'

4. Absence of angiogenic genes modification in Italian ALS patients

Author

Del Bo, Roberto, Scarlato, Marina, Ghezzi, Serena, Martinelli-Boneschi, Filippo, Corti, Stefania, Locatelli, Federica, Santoro, Domenico, Prelle, Alessandro, Briani, Chiara, Nardini, Martina, Siciliano, Gabriele, Mancuso, Michelangelo, Murri, Luigi, Bresolin, Nereo, and Comi, Giacomo Pietro

Published
2008
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5. No major progranulin genetic variability contribution to disease etiopathogenesis in an ALS Italian cohort

Author

Del Bo, Roberto, primary, Corti, Stefania, additional, Santoro, Domenico, additional, Ghione, Isabella, additional, Fenoglio, Chiara, additional, Ghezzi, Serena, additional, Ranieri, Michela, additional, Galimberti, Daniela, additional, Mancuso, Michelangelo, additional, Siciliano, Gabriele, additional, Briani, Chiara, additional, Murri, Luigi, additional, Scarpini, Elio, additional, Schymick, Jennifer C., additional, Traynor, Bryan J., additional, Bresolin, Nereo, additional, and Comi, Giacomo P., additional

Published
2011
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6. Evidence of the association of BIN1 and PICALM with the AD risk in contrasting European populations

Author

Lambert, Jean-Charles, primary, Zelenika, Diana, additional, Hiltunen, Mikko, additional, Chouraki, Vincent, additional, Combarros, Onofre, additional, Bullido, Maria J., additional, Tognoni, Gloria, additional, Fiévet, Nathalie, additional, Boland, Anne, additional, Arosio, Beatrice, additional, Coto, Eliecer, additional, Zompo, Maria Del, additional, Mateo, Ignacio, additional, Frank-Garcia, Ana, additional, Helisalmi, Seppo, additional, Porcellini, Elisa, additional, Pilotto, Alberto, additional, Forti, Paola, additional, Ferri, Raffaele, additional, Delepine, Marc, additional, Scarpini, Elio, additional, Siciliano, Gabriele, additional, Solfrizzi, Vincenzo, additional, Sorbi, Sandro, additional, Spalletta, Gianfranco, additional, Ravaglia, Giovanni, additional, Valdivieso, Fernando, additional, Alvarez, Victoria, additional, Bosco, Paolo, additional, Mancuso, Michelangelo, additional, Panza, Francesco, additional, Nacmias, Benedetta, additional, Bossù, Paola, additional, Piccardi, Paola, additional, Annoni, Giorgio, additional, Seripa, Davide, additional, Galimberti, Daniela, additional, Licastro, Federico, additional, Lathrop, Mark, additional, Soininen, Hilkka, additional, and Amouyel, Philippe, additional

Published
2011
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7. Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer’s disease

Author

Bosetti, Francesca, Brizzi, Francesca, Barogi, Silvia, Mancuso, Michelangelo, Siciliano, Gabriele, Tendi, Elisabetta A., Murri, Luigi, Rapoport, Stanley I., and Solaini, Giancarlo

Subjects
*ALZHEIMER'S disease, *MITOCHONDRIAL pathology
Abstract

Evidence suggests that mitochondrial dysfunction is prominent in Alzheimer’s disease (AD). A failure of one or more of the mitochondrial electron transport chain enzymes or of F1F0-ATPase (ATP synthase) could compromise brain energy stores, generate damaging reactive oxygen species (ROS), and lead to neuronal death. In the present study, cytochrome c oxidase (COX) and F1F0-ATPase activities of isolated mitochondria from platelets and postmortem motor cortex and hippocampus from AD patients and age-matched control subjects were assayed. Compared with controls, COX activity was decreased significantly in platelets (-30%, P < 0.01, n = 20) and hippocampus (-35 to -40%, P < 0.05, n = 6), but not in motor cortex from the AD patients. In contrast, in AD platelets and brain tissues, F1F0-ATP hydrolysis activity was not significantly changed. Moreover, the ATP synthesis rate was similar in mitochondria of platelets from AD patients and controls. These results demonstrate that COX but not F1F0-ATPase is a mitochondrial target in AD, in both a brain association area and in platelets. A reduced COX activity may make the tissue vulnerable to excitotoxicity or reduced oxygen availability. Abbreviations: Aβ: amyloid beta; AD: Alzheimer’s disease; COX: cytochrome oxidase; OS-ATPase: oligomycin-sensitive ATPase; ROS: reactive oxygen species. [Copyright &y& Elsevier]

Published
2002
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