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International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 576143, 3 pages
http://dx.doi.org/10.4061/2011/576143
Research Article

Lack of Association between the GPR3 Gene and the Risk for Alzheimer's Disease

1Azienda Ospedaliera Ospedale Civile di Legnano, Ospedale “G.Fornaroli” di Magenta, Via Al Donatore di Sangue 50, 20013 Magenta, Italy
2Section of Biochemistry, Faculty of Medicine, University of Brescia and III Servizio Analisi, Spedali Civili di Brescia, 25123 Brescia, Italy
3Department of Neurological Sciences, “Dino Ferrari” Center University of Milan, Fondazione Cà Granda, IRCSS Ospedale Maggiore Policlinico Fondazione, Via F. Sforza 35, 20122 Milan, Italy

Received 29 November 2010; Accepted 14 February 2011

Academic Editor: Aleister J. Saunders

Copyright © 2011 Roberto Dominici et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Alzheimer's disease is the most frequent form of dementia and its incidence is rapidly increasing. Genetic factors are important determinants of the individual susceptibility to the disease and many efforts have been made to identify loci and markers involved. Recent finding describes the GPR3 gene as a modulator of β-amyloid production, suggesting that perturbation of its activity and function may contribute to the pathogenesis of AD. Furthermore, the gene is located at chromosome 1, in a region proposed as a susceptibility locus for the disease. We searched for nucleotide variations in the coding sequence and in the region 5 prime of it by dHPLC and analysed their distribution in a group of 104 AD patients and 109 age-matched controls. We identified 5 types of variation, two in the putative promoter region (g.27718954A>G and g.27719102A>T) and the others in exon 2 (c.51C>A, c.80C>G, and c.771C>T). All of them were equally represented in the two cohorts of the study, thus suggesting the absence of an association between GPR3 gene and AD in our population.