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).
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: email@example.com