Autophagic/lysosomal dysfunction in Alzheimer's disease

Persistent Link:
http://hdl.handle.net/10150/610220
Title:
Autophagic/lysosomal dysfunction in Alzheimer's disease
Author:
Orr, Miranda; Oddo, Salvatore
Affiliation:
Department 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
Issue Date:
2013
Publisher:
BioMed Central
Citation:
Orr and Oddo Alzheimer's Research & Therapy 2013, 5:53 http://alzres.com/content/5/5/53
Journal:
Alzheimer's Research & Therapy
Rights:
© 2013 BioMed Central Ltd.
Collection Information:
This 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 repository@u.library.arizona.edu.
Abstract:
Autophagy 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.
EISSN:
1758-9193
DOI:
10.1186/alzrt217
Version:
Final published version
Additional Links:
http://alzres.com/content/5/5/53

Full metadata record

DC FieldValue Language
dc.contributor.authorOrr, Mirandaen
dc.contributor.authorOddo, Salvatoreen
dc.date.accessioned2016-05-20T09:01:25Z-
dc.date.available2016-05-20T09:01:25Z-
dc.date.issued2013en
dc.identifier.citationOrr and Oddo Alzheimer's Research & Therapy 2013, 5:53 http://alzres.com/content/5/5/53en
dc.identifier.doi10.1186/alzrt217en
dc.identifier.urihttp://hdl.handle.net/10150/610220-
dc.description.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.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://alzres.com/content/5/5/53en
dc.rights© 2013 BioMed Central Ltd.en
dc.titleAutophagic/lysosomal dysfunction in Alzheimer's diseaseen
dc.typeArticleen
dc.identifier.eissn1758-9193en
dc.contributor.departmentDepartment 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, USAen
dc.contributor.departmentBanner 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, USAen
dc.identifier.journalAlzheimer's Research & Therapyen
dc.description.collectioninformationThis 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 repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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