| Affiliation: | 1. Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA;2. Biostatistics Unit, Mayo Clinic College of Medicine, Jacksonville, FL, USA;3. Department of Neurology, St. Olav’s Hospital, Trondheim, Norway;4. Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway;5. Department of Neurology, Royal Victoria Hospital, Belfast, Ireland;6. Department of Neurology, Mater Misericordiae Hospital, Dublin, Ireland;7. University College Dublin Conway Neuroscience Investigator, Dublin, Ireland;8. Department of Neurology, Medical University of Silesia, Katowice, Poland;9. Department of Neurology, Collegium Medicum, Jagiellonian University, Krakow, Poland;10. Department of Neurodegenerative Disorders, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland;11. Department of Neurology, MSWiA Hospital, Warsaw, Poland;12. Department of Neurology, Mayo Clinic College of Medicine, Jacksonville, FL, USA |
| Abstract: | Background and purpose: Calcium levels have been proposed to play an important role in the selective vulnerability of nigrostriatal dopaminergic neurons in Parkinson’s disease (PD). Recently, an association was reported between the calcium buffer, calbindin (rs1805874) and risk of PD in a Japanese patient–control series. Methods: We genotyped rs1805874 in four independent Caucasian patient–control series (1543 PD patients, 1771 controls). Results: There was no evidence of an association between rs1805874 and disease risk in individual populations or in the combined series (odds ratio: 1.04, 95% CI: 0.82–1.31, P = 0.74). Discussion: Our study shows there is no association between rs1805874 and risk for PD in four Caucasian populations. This suggests the effect of calbindin on PD risk displays population specificity. |
