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Int. J. Mol. Sci. 2017, 18(7), 1596;

Autophagy and Human Neurodegenerative Diseases—A Fly’s Perspective

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA
Authors to whom correspondence should be addressed.
Received: 19 June 2017 / Revised: 12 July 2017 / Accepted: 21 July 2017 / Published: 23 July 2017
(This article belongs to the Special Issue Neuronal Protein Homeostasis in Health and Disease)
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Neurodegenerative diseases in humans are frequently associated with prominent accumulation of toxic protein inclusions and defective organelles. Autophagy is a process of bulk lysosomal degradation that eliminates these harmful substances and maintains the subcellular environmental quality. In support of autophagy’s importance in neuronal homeostasis, several genetic mutations that interfere with autophagic processes were found to be associated with familial neurodegenerative disorders. In addition, genetic mutations in autophagy-regulating genes provoked neurodegenerative phenotypes in animal models. The Drosophila model significantly contributed to these recent developments, which led to the theory that autophagy dysregulation is one of the major underlying causes of human neurodegenerative disorders. In the current review, we discuss how studies using Drosophila enhanced our understanding of the relationship between autophagy and neurodegenerative processes. View Full-Text
Keywords: Drosophila; neurodegeneration; autophagy; Alzheimer; Parkinson; Huntington; ataxia; protein aggregate; mitochondrial dysfunction Drosophila; neurodegeneration; autophagy; Alzheimer; Parkinson; Huntington; ataxia; protein aggregate; mitochondrial dysfunction

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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 (CC BY 4.0).

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Kim, M.; Ho, A.; Lee, J.H. Autophagy and Human Neurodegenerative Diseases—A Fly’s Perspective. Int. J. Mol. Sci. 2017, 18, 1596.

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