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Parkinson’s Disease - Volume 2015 2015, Article ID 973298, 5 pages -

Research Article

The Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway

Centre for Organelle Research, University of Stavanger, 4036 Stavanger, Norway

Department of Biological Sciences, St. John’s University, New York, NY 11439, USA

Department of Neurology, Haukeland University Hospital, 5021 Bergen, Norway

Institute for Clinical Medicine, University of Bergen, 5021 Bergen, Norway

Department of Neurology, Stavanger University Hospital, 4011 Stavanger, Norway

Received 5 October 2015; Accepted 29 November 2015

Academic Editor: Antonio Pisani

Copyright © 2015 Johannes Lange et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Parkinson’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.

Autor: Johannes Lange, Kristin Aaser Lunde, Camilla Sletten, Simon Geir Møller, Ole-Bjørn Tysnes, Guido Alves, Jan Petter Larsen,



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