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

被引:15
作者
Lange, Johannes [1 ]
Lunde, Kristin Aaser [1 ,2 ]
Sletten, Camilla [2 ]
Moller, Simon Geir [3 ]
Tysnes, Ole-Bjorn [4 ,5 ]
Alves, Guido [1 ,6 ]
Larsen, Jan Petter [1 ]
Maple-Grodem, Jodi [1 ,2 ]
机构
[1] Stavanger Univ Hosp, Norwegian Ctr Movement Disorders, N-4011 Stavanger, Norway
[2] Univ Stavanger, Ctr Organelle Res, N-4036 Stavanger, Norway
[3] St Johns Univ, Dept Biol Sci, New York, NY 11439 USA
[4] Haukeland Hosp, Dept Neurol, N-5021 Bergen, Norway
[5] Univ Bergen, Inst Clin Med, N-5021 Bergen, Norway
[6] Stavanger Univ Hosp, Dept Neurol, N-4011 Stavanger, Norway
关键词
ALZHEIMERS-DISEASE; CEREBROSPINAL-FLUID; AMYLOID-BETA; CLINICAL-FEATURES; PRECURSOR PROTEIN; DEMENTIA; APOE; DEGRADATION; MUTATIONS; BURDEN;
D O I
10.1155/2015/973298
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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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页数:5
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