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dc.contributor.authorRocha, Emily Men_US
dc.contributor.authorSmith, Gaynor Aen_US
dc.contributor.authorPark, Ericen_US
dc.contributor.authorCao, Hongmeien_US
dc.contributor.authorBrown, Eilishen_US
dc.contributor.authorHallett, Penelopeen_US
dc.contributor.authorIsacson, Oleen_US
dc.date.accessioned2015-05-04T15:28:12Z
dc.date.issued2015en_US
dc.identifier.citationRocha, Emily M, Gaynor A Smith, Eric Park, Hongmei Cao, Eilish Brown, Penelope Hallett, and Ole Isacson. 2015. “Progressive decline of glucocerebrosidase in aging and Parkinson's disease.” Annals of Clinical and Translational Neurology 2 (4): 433-438. doi:10.1002/acn3.177. http://dx.doi.org/10.1002/acn3.177.en
dc.identifier.issn2328-9503en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:15035072
dc.description.abstractThe principal risk factor for developing most adult onset neurodegenerative diseases is aging, with incidence rising significantly after age 50. Despite research efforts, the causes of Parkinson's disease (PD) remain unknown. As neurons age, they show signs of diminished lysosomal and mitochondrial function, including increased oxidative stress and accumulation of misfolded proteins, and these changes become exacerbated PD. We show that activity of the lysosomal hydrolase glucocerebrosidase gradually diminishes with age in the substantia nigra and putamen of healthy controls. This reduction is comparable to glucocerebrosidase activity in GBA1-mutation carrier PD patients. These data, demonstrate for the first time that an age-dependent reduction in glucocerebrosidase activity may lower the threshold for developing PD.en
dc.language.isoen_USen
dc.publisherBlackWell Publishing Ltden
dc.relation.isversionofdoi:10.1002/acn3.177en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402088/pdf/en
dash.licenseLAAen_US
dc.titleProgressive decline of glucocerebrosidase in aging and Parkinson's diseaseen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalAnnals of Clinical and Translational Neurologyen
dash.depositing.authorHallett, Penelopeen_US
dc.date.available2015-05-04T15:28:12Z
dc.identifier.doi10.1002/acn3.177*
dash.contributor.affiliatedHallett, Penelope
dash.contributor.affiliatedIsacson, Ole


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