| Literature DB >> 20847397 |
Jean-Charles Lambert1, Kristel Sleegers, Antonio González-Pérez, Martin Ingelsson, Gary W Beecham, Mikko Hiltunen, Onofre Combarros, Maria J Bullido, Nathalie Brouwers, Karolien Bettens, Claudine Berr, Florence Pasquier, Florence Richard, Steven T Dekosky, Didier Hannequin, Jonathan L Haines, Gloria Tognoni, Nathalie Fiévet, Jean-François Dartigues, Christophe Tzourio, Sebastiaan Engelborghs, Beatrice Arosio, Elicer Coto, Peter De Deyn, Maria Del Zompo, Ignacio Mateo, Merce Boada, Carmen Antunez, Jesus Lopez-Arrieta, Jacques Epelbaum, Brit-Maren Michaud Schjeide, Ana Frank-Garcia, Vilmentas Giedraitis, Seppo Helisalmi, Elisa Porcellini, Alberto Pilotto, Paola Forti, Raffaele Ferri, Marc Delepine, Diana Zelenika, Mark Lathrop, Elio Scarpini, Gabriele Siciliano, Vincenzo Solfrizzi, Sandro Sorbi, Gianfranco Spalletta, Giovanni Ravaglia, Fernando Valdivieso, Saila Vepsäläinen, Victoria Alvarez, Paolo Bosco, Michelangelo Mancuso, Francesco Panza, Benedetta Nacmias, Paola Bossù, Olivier Hanon, Paola Piccardi, Giorgio Annoni, David Mann, Philippe Marambaud, Davide Seripa, Daniela Galimberti, Rudolph E Tanzi, Lars Bertram, Corinne Lendon, Lars Lannfelt, Federico Licastro, Dominique Campion, Margaret A Pericak-Vance, Hilkka Soininen, Christine Van Broeckhoven, Annick Alpérovitch, Agustin Ruiz, M Ilyas Kamboh, Philippe Amouyel.
Abstract
The only established genetic determinant of non-Mendelian forms of Alzheimer's disease (AD) is the ε4 allele of the apolipoprotein E gene (APOE). Recently, it has been reported that the P86L polymorphism of the calcium homeostasis modulator 1 gene (CALHM1) is associated with the risk of developing AD. In order to independently assess this association, we performed a meta-analysis of 7,873 AD cases and 13,274 controls of Caucasian origin (from a total of 24 centers in Belgium, Finland, France, Italy, Spain, Sweden, the UK, and the USA). Our results indicate that the CALHM1 P86L polymorphism is likely not a genetic determinant of AD but may modulate age of onset by interacting with the effect of the ε4 allele of the APOE gene.Entities:
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Year: 2010 PMID： 20847397 PMCID： PMC2964875 DOI： 10.3233/JAD-2010-100933
Source DB: PubMed Journal: J Alzheimers Dis ISSN： 1387-2877 Impact factor: 4.472