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dc.contributor.authorLange, Johannesen_US
dc.contributor.authorLunde, Kristin Aaseren_US
dc.contributor.authorSletten, Camilla Johanneen_US
dc.contributor.authorMøller, Simon Geiren_US
dc.contributor.authorTysnes, Ole-Bjørnen_US
dc.contributor.authorAlves, Guidoen_US
dc.contributor.authorLarsen, Jan Petteren_US
dc.contributor.authorMaple-Grødem, Jodien_US
dc.PublishedParkinson's Disease 2015eng
dc.description.abstractParkinson’s disease (PD) and Alzheimer’s disease (AD) share pathological features, including amyloid-beta pathology. Amyloid-beta peptide is generated by sequential proteolysis of amyloid precursor protein (APP), and genetic variations in the processing pathway genes have been found to increase the risk of AD; however, the contribution in PD is unknown. Methods. The aim of this study was to investigate whether candidate polymorphisms in five genes (ADAM10, BACE1, BACE2, PSEN2, and CLU) involved in the APP processing pathway affect PD risk in a population-based cohort of patients with incident PD and control subjects from the Norwegian ParkWest study. Results. We found an association of rs638405 in BACE1 with increased risk of PD, thus providing a novel link, at the genetic level, between amyloid-beta pathology and PD.en_US
dc.publisherHindawi Publishing Corporationeng
dc.rightsAttribution CC BY 4.0eng
dc.titleAssociation of a BACE1 Gene Polymorphism with Parkinson’s Disease in a Norwegian Populationen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2015 Johannes Lange et al.
dc.subject.nsiVDP::Medisinske Fag: 700en_US

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Attribution CC BY 4.0
Except where otherwise noted, this item's license is described as Attribution CC BY 4.0