Affiliations: [a] Department of Pathology, Case Western Reserve University, Cleveland, OH, USA | [b] Department of Neurology, Case Western Reserve University, Cleveland, OH, USA | [c] UTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA
Correspondence:
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Correspondence to: Xiongwei Zhu, Ph.D., Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel.: +1 216 368 5903; Fax: +1 216 368 8964; E-mail: xiongwei.zhu@case.edu.
Note: [†] †
Note: [] †
Abstract: Mitochondrial dysfunction is one of the most early and prominent features in vulnerable neurons in the brain of Alzheimer's disease (AD) patients. Recent studies suggest that mitochondria are highly dynamic organelles characterized by a delicate balance of fission and fusion, a concept that has revolutionized our basic understanding of the regulation of mitochondrial structure and function which has far-reaching significance in studies of health and disease. Tremendous progress has been made in studying changes in mitochondrial dynamics in AD brain and models and the potential underlying mechanisms. This review highlights the recent work demonstrating abnormal mitochondrial dynamics and distribution in AD models and discusses how these abnormalities may contribute to various aspects of mitochondrial dysfunction and the pathogenesis of AD.
