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

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

Author information

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.

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