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

Association of a BACE1 Gene Polymorphism with Parkinson’s Disease in a Norwegian Population

1The Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway
2Centre for Organelle Research, University of Stavanger, 4036 Stavanger, Norway
3Department of Biological Sciences, St. John’s University, New York, NY 11439, USA
4Department of Neurology, Haukeland University Hospital, 5021 Bergen, Norway
5Institute for Clinical Medicine, University of Bergen, 5021 Bergen, Norway
6Department 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.