Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease

By J. Lambert, S. Heath, G. Even, D. Campion, K. Sleegers, M. Hiltunen, O. Combarros, D. Zélénika, M. Bullido, B. Tavernier and 40 more. Nature Genetics, 2009

1,386 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5e2893b44d977eaa784dd5bec7efb4ecfc662b25

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Citations in the corpus

• The ENIGMA Consortium: large-scale collaborative analyses of neuroimaging and genetic data (2014, neutral): “Many common polymorphisms have now been found that increase genetic risk for AD (Harold et al. 2009; Lambert et al. 2009; Naj et al. 2011), age-related cognitive decline (Davies et al. 2012), schizophrenia (Almasy et al. 2008; Stefansson et al. 2009; Ripke et al. 2011; Rietschel et al. 2012),…”
• Eliminating microglia in Alzheimer's mice prevents neuronal loss without modulating amyloid-β pathology. (2016, methodology): “Counts for target genes were normalized to house-keeping genes (Eef1g, G6pdx, Hprt, Polr1b, Polr2a, Ppia, Rpl19, Sdha, and Tbp) to account for variability in the RNA content.”
• A blood–brain barrier overview on structure, function, impairment, and biomarkers of integrity (2020, background): “Different studies have shown that any mutation to the PICALM gene resulting in decreased expression in ECs may affect disease progression and is considered as a genetic risk factor for Alzheimer’s disease [209].”
• A statistical framework for cross-tissue transcriptome-wide association analysis (2018, background): “Two independent association peaks at this locus, one at CLU and the other at PTK2B , have previously been identified in GWAS ( Supplementary Figure 5 ) [37, 47].”
• Common variants in ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer’s disease (2011, neutral): “A second independent AD GWAS by Lambert and colleagues 4 using the EADI1 sample (European Alzheimer’s Disease Initiative 1) showed genome-wide significant evidence for association with CLU (P=7.5×10 −9 ) and CR1 (P=3.7×10 −9 ), and support for PICALM (P=3×10 −3 ).”
• Alzheimer's disease risk genes and mechanisms of disease pathogenesis (2014, neutral): “The SNPs 50 to PICALM rs3851179 and rs541458 are associated with reduced LOAD risk (3,6,13).”
• Epidemiology of Alzheimer Disease (2012, neutral): “Genome-wide association (GWA) studies have identified variants in CLU, PICALM, CR1, and BIN1 as putative susceptibility loci (Harold et al. 2009; Lambert et al. 2009; Seshadri et al. 2010).”
• Discovering causal interactions using Bayesian network scoring and information gain (2016, background): “By investigating single-locus associations, researchers have identified over 150 risk loci associated with 60 common diseases and traits [10 – 13].”