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

Johannes Lange; Kristin Aaser Lunde; Camilla Sletten; Simon Geir Møller; Ole-Bjørn Tysnes; Guido Alves; Jan Petter Larsen; Jodi Maple-Grødem

doi:10.1155/2015/973298

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

Parkinsons Dis. 2015:2015:973298. doi: 10.1155/2015/973298. Epub 2015 Dec 14.

Authors

Johannes Lange¹, Kristin Aaser Lunde², Camilla Sletten³, Simon Geir Møller⁴, Ole-Bjørn Tysnes⁵, Guido Alves⁶, Jan Petter Larsen¹, Jodi Maple-Grødem²

Affiliations

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

Abstract

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.