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A Synergistic Dysfunction of Mitochondrial Fission/Fusion Dynamics and Mitophagy in Alzheimer's Disease

Issue title: Mitochondria and Neurodegenerative Diseases

Guest editors: Xiongwei Zhu, M. Flint Beal, Xinglong Wang, George Perry and Mark A. Smith

Article type: Review Article

Authors: Santos, Renato X.a; b | Correia, Sónia C.a; b | Wang, Xinglongc | Perry, Georgec; d | Smith, Mark A.c | Moreira, Paula I.a; e; * | Zhu, Xiongweic; *

Affiliations: [a] Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, Coimbra, Portugal | [b] Faculty of Sciences and Technology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal | [c] Department of Pathology, Case Western Reserve University, Cleveland, OH, USA | [d] UTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA | [e] Faculty of Medicine, Institute of Physiology, University of Coimbra, Coimbra, Portugal

Correspondence: [*] Correspondence to: Xiongwei Zhu, Ph.D., Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio 44106, USA. Tel.: +1 216 368 5903; Fax: +1 216 368 8964; E-mail: [email protected]. Paula I. Moreira, Ph.D., Center for Neuroscience and Cell Biology, Institute of Physiology- Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, Portugal. Tel.: +351 239480012; Fax: +351 239480034; E-mail: [email protected] or [email protected].

Note: [] Handling Editor: Jesus Avila

Keywords: Alzheimer's disease, fission, fusion, mitochondrial dysfunction, mitophagy

DOI: 10.3233/JAD-2010-100666

Journal: Journal of Alzheimer's Disease, vol. 20, no. s2, pp. S401-S412, 2010

Accepted 29 April 2010
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Published: 3 June 2010
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Abstract

Alzheimer's disease (AD), the most common form of dementia in the elderly, can have a late-onset sporadic or an early-onset familial origin. In both cases, the neuropathological hallmarks are the same: senile plaques and neurofibrillary tangles. Despite AD having a proteinopathic nature, there is strong evidence for an organelle dysfunction-related neuropathology, namely dysfunctional mitochondria. In this regard, dysfunctional mitochondria and associated exacerbated generation of reactive oxygen species are among the earliest events in the progression of the disease. Since the maintenance of a healthy mitochondrial pool is essential given the central role of this organelle in several determinant cellular processes, mitochondrial dysfunction in AD would be predicted to have profound pluripotent deleterious consequences. Mechanistically, recent reports suggest that mitochondrial fission/fusion and mitophagy are altered in AD and in in vitro models of disease, and since both processes are reported to be protective, this review will discuss the role of mitochondrial fission/fusion and mitophagy in the pathogenesis of AD.

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