AffiliationDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
Banner Sun Health Research Institute and Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, 10515 W. Santa Fe Drive, Sun City, AZ 85351, USA
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CitationOrr and Oddo Alzheimer's Research & Therapy 2013, 5:53 http://alzres.com/content/5/5/53
JournalAlzheimer's Research & Therapy
Rights© 2013 BioMed Central Ltd.
Collection InformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at email@example.com.
AbstractAutophagy serves as the sole catabolic mechanism for degrading organelles and protein aggregates. Increasing evidence implicates autophagic dysfunction in Alzheimer's disease (AD) and other neurodegenerative diseases associated with protein misprocessing and accumulation. Under physiologic conditions, the autophagic/lysosomal system efficiently recycles organelles and substrate proteins. However, reduced autophagy function leads to the accumulation of proteins and autophagic and lysosomal vesicles. These vesicles contain toxic lysosomal hydrolases as well as the proper cellular machinery to generate amyloid-beta, the major component of AD plaques. Here, we provide an overview of current research focused on the relevance of autophagic/lysosomal dysfunction in AD pathogenesis as well as potential therapeutic targets aimed at restoring autophagic/lysosomal pathway function.
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