@article {6156,
	title = {Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer{\textquoteright}s disease.},
	journal = {Nat Genet},
	volume = {45},
	year = {2013},
	month = {2013 Dec},
	pages = {1452-8},
	abstract = {<p>Eleven susceptibility loci for late-onset Alzheimer{\textquoteright}s disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer{\textquoteright}s disease cases and 37,154 controls. In stage 2, 11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer{\textquoteright}s disease cases and 11,312 controls. In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 {\texttimes} 10(-8)) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer{\textquoteright}s disease. </p>},
	keywords = {Age of Onset, Aged, Aged, 80 and over, Alzheimer Disease, Case-Control Studies, Cohort Studies, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide},
	issn = {1546-1718},
	doi = {10.1038/ng.2802},
	author = {Lambert, J C and Ibrahim-Verbaas, C A and Harold, D and Naj, A C and Sims, R and Bellenguez, C and DeStafano, A L and Bis, J C and Beecham, G W and Grenier-Boley, B and Russo, G and Thorton-Wells, T A and Jones, N and Smith, A V and Chouraki, V and Thomas, C and Ikram, M A and Zelenika, D and Vardarajan, B N and Kamatani, Y and Lin, C F and Gerrish, A and Schmidt, H and Kunkle, B and Dunstan, M L and Ruiz, A and Bihoreau, M T and Choi, S H and Reitz, C and Pasquier, F and Cruchaga, C and Craig, D and Amin, N and Berr, C and Lopez, O L and De Jager, P L and Deramecourt, V and Johnston, J A and Evans, D and Lovestone, S and Letenneur, L and Mor{\'o}n, F J and Rubinsztein, D C and Eiriksdottir, G and Sleegers, K and Goate, A M and Fi{\'e}vet, N and Huentelman, M W and Gill, M and Brown, K and Kamboh, M I and Keller, L and Barberger-Gateau, P and McGuiness, B and Larson, E B and Green, R and Myers, A J and Dufouil, C and Todd, S and Wallon, D and Love, S and Rogaeva, E and Gallacher, J and St George-Hyslop, P and Clarimon, J and Lleo, A and Bayer, A and Tsuang, D W and Yu, L and Tsolaki, M and Boss{\`u}, P and Spalletta, G and Proitsi, P and Collinge, J and Sorbi, S and Sanchez-Garcia, F and Fox, N C and Hardy, J and Deniz Naranjo, M C and Bosco, P and Clarke, R and Brayne, C and Galimberti, D and Mancuso, M and Matthews, F and Moebus, S and Mecocci, P and Del Zompo, M and Maier, W and Hampel, H and Pilotto, A and Bullido, M and Panza, F and Caffarra, P and Nacmias, B and Gilbert, J R and Mayhaus, M and Lannefelt, L and Hakonarson, H and Pichler, S and Carrasquillo, M M and Ingelsson, M and Beekly, D and Alvarez, V and Zou, F and Valladares, O and Younkin, S G and Coto, E and Hamilton-Nelson, K L and Gu, W and Razquin, C and Pastor, P and Mateo, I and Owen, M J and Faber, K M and Jonsson, P V and Combarros, O and O{\textquoteright}Donovan, M C and Cantwell, L B and Soininen, H and Blacker, D and Mead, S and Mosley, T H and Bennett, D A and Harris, T B and Fratiglioni, L and Holmes, C and de Bruijn, R F and Passmore, P and Montine, T J and Bettens, K and Rotter, J I and Brice, A and Morgan, K and Foroud, T M and Kukull, W A and Hannequin, D and Powell, J F and Nalls, M A and Ritchie, K and Lunetta, K L and Kauwe, J S and Boerwinkle, E and Riemenschneider, M and Boada, M and Hiltuenen, M and Martin, E R and Schmidt, R and Rujescu, D and Wang, L S and Dartigues, J F and Mayeux, R and Tzourio, C and Hofman, A and N{\"o}then, M M and Graff, C and Psaty, B M and Jones, L and Haines, J L and Holmans, P A and Lathrop, M and Pericak-Vance, M A and Launer, L J and Farrer, L A and van Duijn, C M and Van Broeckhoven, C and Moskvina, V and Seshadri, S and Williams, J and Schellenberg, G D and Amouyel, P}
}
@article {6597,
	title = {Association of exome sequences with plasma C-reactive protein levels in >9000 participants.},
	journal = {Hum Mol Genet},
	volume = {24},
	year = {2015},
	month = {2015 Jan 15},
	pages = {559-71},
	abstract = {<p>C-reactive protein (CRP) concentration is a heritable systemic marker of inflammation that is associated with cardiovascular disease risk. Genome-wide association studies have identified CRP-associated common variants associated in \~{}25 genes. Our aims were to apply exome sequencing to (1) assess whether the candidate loci contain rare coding variants associated with CRP levels and (2) perform an exome-wide search for rare variants in novel genes associated with CRP levels. We exome-sequenced 6050 European-Americans (EAs) and 3109 African-Americans (AAs) from the NHLBI-ESP and the CHARGE consortia, and performed association tests of sequence data with measured CRP levels. In single-variant tests across candidate loci, a novel rare (minor allele frequency = 0.16\%) CRP-coding variant (rs77832441-A; p.Thr59Met) was associated with 53\% lower mean CRP levels (P = 2.9 {\texttimes} 10(-6)). We replicated the association of rs77832441 in an exome array analysis of 11 414 EAs (P = 3.0 {\texttimes} 10(-15)). Despite a strong effect on CRP levels, rs77832441 was not associated with inflammation-related phenotypes including coronary heart disease. We also found evidence for an AA-specific association of APOE-ε2 rs7214 with higher CRP levels. At the exome-wide significance level (P < 5.0 {\texttimes} 10(-8)), we confirmed associations for reported common variants of HNF1A, CRP, IL6R and TOMM40-APOE. In gene-based tests, a burden of rare/lower frequency variation in CRP in EAs (P <= 6.8 {\texttimes} 10(-4)) and in retinoic acid receptor-related orphan receptor α (RORA) in AAs (P = 1.7 {\texttimes} 10(-3)) were associated with CRP levels at the candidate gene level (P < 2.0 {\texttimes} 10(-3)). This inquiry did not elucidate novel genes, but instead demonstrated that variants distributed across the allele frequency spectrum within candidate genes contribute to CRP levels. </p>},
	keywords = {Adult, African Americans, C-Reactive Protein, Cardiovascular Diseases, Cohort Studies, European Continental Ancestry Group, Exome, Female, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Hepatocyte Nuclear Factor 1-alpha, Humans, Male, Plasma, Polymorphism, Single Nucleotide, Receptors, Interleukin-6, Risk Factors},
	issn = {1460-2083},
	doi = {10.1093/hmg/ddu450},
	author = {Schick, Ursula M and Auer, Paul L and Bis, Joshua C and Lin, Honghuang and Wei, Peng and Pankratz, Nathan and Lange, Leslie A and Brody, Jennifer and Stitziel, Nathan O and Kim, Daniel S and Carlson, Christopher S and Fornage, Myriam and Haessler, Jeffery and Hsu, Li and Jackson, Rebecca D and Kooperberg, Charles and Leal, Suzanne M and Psaty, Bruce M and Boerwinkle, Eric and Tracy, Russell and Ardissino, Diego and Shah, Svati and Willer, Cristen and Loos, Ruth and Melander, Olle and McPherson, Ruth and Hovingh, Kees and Reilly, Muredach and Watkins, Hugh and Girelli, Domenico and Fontanillas, Pierre and Chasman, Daniel I and Gabriel, Stacey B and Gibbs, Richard and Nickerson, Deborah A and Kathiresan, Sekar and Peters, Ulrike and Dupuis, Jos{\'e}e and Wilson, James G and Rich, Stephen S and Morrison, Alanna C and Benjamin, Emelia J and Gross, Myron D and Reiner, Alex P}
}
