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Mitochondria, Cognitive Impairment, and Alzheimer's Disease

To date, the beta amyloid (Aβ) cascade hypothesis remains the main pathogenetic model of Alzheimer's disease (AD), but its role in the majority of sporadic AD cases is unclear. The “mitochondrial cascade hypothesis” could explain many of the biochemical, genetic, and pathological features of sp...

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Autores principales: Mancuso, M., Calsolaro, V., Orsucci, D., Carlesi, C., Choub, A., Piazza, S., Siciliano, G.
Formato: Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925259/
https://www.ncbi.nlm.nih.gov/pubmed/20798880
http://dx.doi.org/10.4061/2009/951548
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author Mancuso, M.
Calsolaro, V.
Orsucci, D.
Carlesi, C.
Choub, A.
Piazza, S.
Siciliano, G.
author_facet Mancuso, M.
Calsolaro, V.
Orsucci, D.
Carlesi, C.
Choub, A.
Piazza, S.
Siciliano, G.
author_sort Mancuso, M.
collection PubMed
description To date, the beta amyloid (Aβ) cascade hypothesis remains the main pathogenetic model of Alzheimer's disease (AD), but its role in the majority of sporadic AD cases is unclear. The “mitochondrial cascade hypothesis” could explain many of the biochemical, genetic, and pathological features of sporadic AD. Somatic mutations in mitochondrial DNA (mtDNA) could cause energy failure, increased oxidative stress, and accumulation of Aβ, which in a vicious cycle reinforce the mtDNA damage and the oxidative stress. Despite the evidence of mitochondrial dysfunction in AD, no causative mutations in the mtDNA have been detected so far. Indeed, results of studies on the role of mtDNA haplogroups in AD are controversial. In this review we discuss the role of the mitochondria, and especially of the mtDNA, in the cascade of events leading to neurodegeneration, dementia, and AD.
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spelling pubmed-29252592010-08-26 Mitochondria, Cognitive Impairment, and Alzheimer's Disease Mancuso, M. Calsolaro, V. Orsucci, D. Carlesi, C. Choub, A. Piazza, S. Siciliano, G. Int J Alzheimers Dis Review Article To date, the beta amyloid (Aβ) cascade hypothesis remains the main pathogenetic model of Alzheimer's disease (AD), but its role in the majority of sporadic AD cases is unclear. The “mitochondrial cascade hypothesis” could explain many of the biochemical, genetic, and pathological features of sporadic AD. Somatic mutations in mitochondrial DNA (mtDNA) could cause energy failure, increased oxidative stress, and accumulation of Aβ, which in a vicious cycle reinforce the mtDNA damage and the oxidative stress. Despite the evidence of mitochondrial dysfunction in AD, no causative mutations in the mtDNA have been detected so far. Indeed, results of studies on the role of mtDNA haplogroups in AD are controversial. In this review we discuss the role of the mitochondria, and especially of the mtDNA, in the cascade of events leading to neurodegeneration, dementia, and AD. SAGE-Hindawi Access to Research 2009-07-06 /pmc/articles/PMC2925259/ /pubmed/20798880 http://dx.doi.org/10.4061/2009/951548 Text en Copyright © 2009 M. Mancuso et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Mancuso, M.
Calsolaro, V.
Orsucci, D.
Carlesi, C.
Choub, A.
Piazza, S.
Siciliano, G.
Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title_full Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title_fullStr Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title_full_unstemmed Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title_short Mitochondria, Cognitive Impairment, and Alzheimer's Disease
title_sort mitochondria, cognitive impairment, and alzheimer's disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925259/
https://www.ncbi.nlm.nih.gov/pubmed/20798880
http://dx.doi.org/10.4061/2009/951548
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