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Article: Autophagy deregulation in neurodegenerative diseases - Recent advances and future perspectives

TitleAutophagy deregulation in neurodegenerative diseases - Recent advances and future perspectives
Authors
KeywordsSpecies Index: Animalia
Issue Date2011
PublisherBlackwell Publishing Ltd
Citation
Journal Of Neurochemistry, 2011, v. 118 n. 3, p. 317-325 How to Cite?
AbstractAutophagy is an evolutionarily conserved homeostatic process for the turnover of cellular contents, organelles and misfolded proteins through the lysosomal machinery. Recently, the involvement of autophagy in the pathophysiology of neurodegenerative diseases has attracted considerable interest because autophagy deregulation has been linked to some of these neurodegenerative disorders. This interest is further heightened by the demonstration that various autophagic pathways, including macroautophagy and chaperone-mediated autophagy, are implicated in the turnover of proteins that are prone to aggregation in cellular or animal disease models. These observations have stimulated new awareness in the pivotal role of the autophagic pathways in neurodegenerative disease pathophysiology, and have sparked extensive research aimed at deciphering the mechanisms by which autophagy is altered in these disorders. Here, we summarize the latest advances in our understanding of the role of autophagy deregulation in Parkinson's, Alzheimer's and Huntington's disease. © 2011 International Society for Neurochemistry.
Persistent Identifierhttp://hdl.handle.net/10722/145834
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKUST 661007
661109
660309
660210
1/06C
6/CRF/08
University Grants CommitteeAoE/B-15/01
Funding Information:

We apologize to the authors whose work was not cited because of space limitation. We thank Ka-Chun Lok for his excellent help in preparing the figure. The study of N.Y. Ip and Z. H. Cheung was supported in part by the Research Grants Council of Hong Kong (HKUST 661007, 661109, 660309, 660210, 1/06C and 6/CRF/08) and the Area of Excellence Scheme of the University Grants Committee (AoE/B-15/01). N.Y. Ip and Z. H. Cheung were Croucher Foundation Senior Research Fellow and Croucher Foundation Fellow, respectively.

References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorIp, NYen_HK
dc.date.accessioned2012-03-23T09:49:54Z-
dc.date.available2012-03-23T09:49:54Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Neurochemistry, 2011, v. 118 n. 3, p. 317-325en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145834-
dc.description.abstractAutophagy is an evolutionarily conserved homeostatic process for the turnover of cellular contents, organelles and misfolded proteins through the lysosomal machinery. Recently, the involvement of autophagy in the pathophysiology of neurodegenerative diseases has attracted considerable interest because autophagy deregulation has been linked to some of these neurodegenerative disorders. This interest is further heightened by the demonstration that various autophagic pathways, including macroautophagy and chaperone-mediated autophagy, are implicated in the turnover of proteins that are prone to aggregation in cellular or animal disease models. These observations have stimulated new awareness in the pivotal role of the autophagic pathways in neurodegenerative disease pathophysiology, and have sparked extensive research aimed at deciphering the mechanisms by which autophagy is altered in these disorders. Here, we summarize the latest advances in our understanding of the role of autophagy deregulation in Parkinson's, Alzheimer's and Huntington's disease. © 2011 International Society for Neurochemistry.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltden_US
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.subjectSpecies Index: Animaliaen_US
dc.subject.meshAlzheimer Disease - pathologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAutophagy - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHuntington Disease - pathologyen_HK
dc.subject.meshNeurodegenerative Diseases - pathologyen_HK
dc.subject.meshParkinson Disease - pathologyen_HK
dc.subject.meshSignal Transduction - physiologyen_HK
dc.titleAutophagy deregulation in neurodegenerative diseases - Recent advances and future perspectivesen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1471-4159.2011.07314.xen_HK
dc.identifier.pmid21599666-
dc.identifier.scopuseid_2-s2.0-79960308079en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960308079&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume118en_HK
dc.identifier.issue3en_HK
dc.identifier.spage317en_HK
dc.identifier.epage325en_HK
dc.identifier.eissn1471-4159-
dc.identifier.isiWOS:000292654300002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridIp, NY=35899235100en_HK
dc.identifier.citeulike9345529-

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