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Exploring the Genetic Architecture of Parkinson's Disease in a Southern Spanish Population
Sara Bandrés Ciga1, Clara Ruz1, Francisco J Barrero2, Francisco Escamilla Sevilla2, Javier Pelegrina2, Manuel Ramírez3, Francisco Vives1and Raquel Duran1*1Department of Physiology and Institute of Neurosciences Federico Olóriz, Biomedical Research Centre (BRC), University of Granada, 18016, Granada, Spain
2Movement Disorders Unit, Service of Neurology, Hospital of Health Technology Park (PTS), 18016, Granada, Spain
3Unit of Physiology, Department of Health Sciences, University of Jaén, Paraje Las Lagunillas s/n, Jaén, Spain
- *Corresponding Author:
- Raquel Duran
Department of Physiology and Institute of Neurosciences
Federico Olóriz, Biomedical Research Centre (BRC)
University of Granada, 18016, Granada, Spain
Tel: + 34 958243521
E-mail: rduran@ugr.es
Received date: June 21, 2017; Accepted date: July 11, 2017; Published date: July 18, 2017
Citation: Ciga SB, Ruz C, Barrero FJ, Sevilla FE, Pelegrina J, et al. (2017) Exploring the Genetic Architecture of Parkinson's Disease in a Southern Spanish Population. J Alzheimers Dis Parkinsonism 7:351. doi:10.4172/2161-0460.1000351
Copyright: © 2017 Ciga SB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Abstract
In the recent years, the emergence of new technologies has revolutionized our concepts to identify genetic mechanisms implicated in Parkinson's disease (PD). Genome-wide association studies (GWAS) have been key in such enormous advance. To the best of our knowledge we have conducted the first GWAS of PD in a Spanish population. We replicated the association of 5 reported PD-related loci at nominal p-value, and our cumulative risk score was consistent with studies performed in other European populations. We did not manage to identify any novel rare variant through single variant and gene-based tests and we assume that there may be structural genomic variation conferring risk for PD poorly covered or undetectable by the array. We conclude that in complex genetic disorders such as PD, collaboration drives progress and real advances can only be made by large consortiums cooperating with collaborative spirit. In the years to come, interpretation of the risk in the context of disease pathogenesis will be the main goal to reach.
