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Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease

Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease

October 2009 | Denise Harold, Richard Abraham, Paul Hollingworth, Rebecca Sims, Amy Gerrish, Marian L Hamshere, Jaspreet Singh Pahwa, Valentina Moskvina, Kimberley Dowzell, Amy Williams, Nicola Jones, Charlene Thomas, Alexandra Stretton, Angharad R Morgan, Simon Lovestone, John Powell, Petroula Protiis, Michelle K Lupton, Carol Brayne, David C Rubinsztstein, Michael Gill, Brian Lawlor, Aoibhinn Lynch, Kevin Morgan, Kristelle S Brown, Peter A Passmore, David Craig, Bernadette McGuinness, Stephen Todd, Clive Holmes, David Mann, A David Smith, Seth Love, Patrick G Kehoe, John Hardy, Simon Mead, Nick Fox, Martin Rossor, John Collinge, Wolfgang Maier, Frank Jessen, Britta Schürmann, Hendrik van den Bussche, Isabella Heuser, Johannes Kornhuber, Jens Wiltfang, Martin Dichgans, Lutz Fröhlich, Harald Hampel, Michael Hüll, Dan Rujescu, Alison M Goate, John S K Kauwe, Carlos Cruchaga, Petra Nowotny, John C Morris, Kevin Mayo, Kristel Sleegers, Karolien Bettens, Sebastiaan Engelborghs, Peter P De Deyn, Christine Van Broeckhoven, Gill Livingston, Nicholas J Bass, Hugh Gurling, Andrew McQuillin, Rhiann Guilliam, Panagiotis Deloukas, Ammar Al-Chalabi, Christopher E Shaw, Magda Tsolaki, Andrew B Singleton, Rita Guerreiro, Thomas W Mühleisen, Markus M Nöthen, Susanne Moebus, Karl-Heinz Jöckel, Norman Klopp, H-Erich Wichmann, Minerva M Carrasquillo, V Shane Pankratz, Steven G Younkin, Peter A Holmans, Michael O'Donovan & Julie Williams
A genome-wide association study (GWAS) identified genetic variants at the CLU and PICALM genes associated with Alzheimer's disease (AD). The study involved over 16,000 individuals, making it the most powerful AD GWAS to date. In the first stage, the study replicated the association with the APOE locus and found genome-wide significant associations with SNPs at CLU and PICALM. These associations were confirmed in the second stage, providing strong evidence for their association with AD. The study found that variants at CLU (rs11136000) and PICALM (rs3851179) were significantly associated with AD, with odds ratios of 0.86 and 0.86, respectively. These findings suggest that CLU and PICALM may play a role in the development of AD. The study also identified other genes associated with AD, including CR1, BIN1, and DAB1. The study highlights the importance of large-scale GWAS in identifying genetic risk factors for complex diseases like AD. The results suggest that susceptibility genes are not randomly distributed through functional pathways, and that further research is needed to understand the mechanisms underlying these associations. The study was conducted by a collaborative consortium of researchers from Europe and the United States, and involved a two-stage study design. The study used a combination of genotyping platforms and quality control measures to ensure the reliability of the results. The findings contribute to the understanding of the genetic basis of AD and may lead to the development of new therapeutic strategies.A genome-wide association study (GWAS) identified genetic variants at the CLU and PICALM genes associated with Alzheimer's disease (AD). The study involved over 16,000 individuals, making it the most powerful AD GWAS to date. In the first stage, the study replicated the association with the APOE locus and found genome-wide significant associations with SNPs at CLU and PICALM. These associations were confirmed in the second stage, providing strong evidence for their association with AD. The study found that variants at CLU (rs11136000) and PICALM (rs3851179) were significantly associated with AD, with odds ratios of 0.86 and 0.86, respectively. These findings suggest that CLU and PICALM may play a role in the development of AD. The study also identified other genes associated with AD, including CR1, BIN1, and DAB1. The study highlights the importance of large-scale GWAS in identifying genetic risk factors for complex diseases like AD. The results suggest that susceptibility genes are not randomly distributed through functional pathways, and that further research is needed to understand the mechanisms underlying these associations. The study was conducted by a collaborative consortium of researchers from Europe and the United States, and involved a two-stage study design. The study used a combination of genotyping platforms and quality control measures to ensure the reliability of the results. The findings contribute to the understanding of the genetic basis of AD and may lead to the development of new therapeutic strategies.
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