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Int J Clin Exp Pathol 2010;3(6):570-581
Review Article
Alzheimer’s disease: diverse aspects of mitochondrial malfunctioning
Renato X. Santos, Sónia C. Correia, Xinglong Wang, George Perry, Mark A. Smith, Paula I. Moreira, Xiongwei Zhu
Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, Coimbra, Portugal; Faculty of Sciences and Technology,
Department of Life Sciences, University of Coimbra, Coimbra, Portugal; Department of Pathology, Case Western Reserve University, Cleveland,
Ohio, USA; UTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, Texas, USA; Faculty of
Medicine, Institute of Physiology, University of Coimbra, Coimbra, Portugal.
Received June 13, 2010, accepted June 21, 2010, available online June 25, 2010
Abstract: Alzheimer’s disease is a progressive neurodegenerative disorder, either assuming a sporadic, age-associated, late-onset form, or a
familial form, with early onset, in a smaller fraction of the cases. Whereas in the familial cases several mutations have been identified in genes
encoding proteins related with the pathogenesis of the disease, for the sporadic form several causes have been proposed and are currently
under debate. Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of
Alzheimer’s disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen
species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that
mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to
its onset and progression. (IJCEP1006004).
Key words: Alzheimer’s disease, mitochondria, mitochondrial dysfunction, mitochondrial dynamics
Full text PDF
Address all correspondence to:
Xiongwei Zhu, PhD
Department of Pathology
Case Western Reserve University
2103 Cornell Road
Cleveland, Ohio 44106, USA
Tel: 216-368-5903, Fax: 216-368-8964
Email: xiongwei.zhu@case.edu
Review Article
Alzheimer’s disease: diverse aspects of mitochondrial malfunctioning
Renato X. Santos, Sónia C. Correia, Xinglong Wang, George Perry, Mark A. Smith, Paula I. Moreira, Xiongwei Zhu
Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, Coimbra, Portugal; Faculty of Sciences and Technology,
Department of Life Sciences, University of Coimbra, Coimbra, Portugal; Department of Pathology, Case Western Reserve University, Cleveland,
Ohio, USA; UTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, Texas, USA; Faculty of
Medicine, Institute of Physiology, University of Coimbra, Coimbra, Portugal.
Received June 13, 2010, accepted June 21, 2010, available online June 25, 2010
Abstract: Alzheimer’s disease is a progressive neurodegenerative disorder, either assuming a sporadic, age-associated, late-onset form, or a
familial form, with early onset, in a smaller fraction of the cases. Whereas in the familial cases several mutations have been identified in genes
encoding proteins related with the pathogenesis of the disease, for the sporadic form several causes have been proposed and are currently
under debate. Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of
Alzheimer’s disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen
species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that
mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to
its onset and progression. (IJCEP1006004).
Key words: Alzheimer’s disease, mitochondria, mitochondrial dysfunction, mitochondrial dynamics
Full text PDF
Address all correspondence to:
Xiongwei Zhu, PhD
Department of Pathology
Case Western Reserve University
2103 Cornell Road
Cleveland, Ohio 44106, USA
Tel: 216-368-5903, Fax: 216-368-8964
Email: xiongwei.zhu@case.edu
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