@article {9391,
	title = {{Exome-Derived Adiponectin-Associated Variants Implicate Obesity and Lipid Biology},
	journal = {Am J Hum Genet},
	volume = {105},
	year = {2019},
	month = {Sep},
	pages = {670{\textendash}671},
	author = {Spracklen, C. N. and Karaderi, T. and Yaghootkar, H. and Schurmann, C. and Fine, R. S. and Kutalik, Z. and Preuss, M. H. and Lu, Y. and Wittemans, L. B. L. and Adair, L. S. and Allison, M. and Amin, N. and Auer, P. L. and Bartz, T. M. and her, M. and Boehnke, M. and Borja, J. B. and Bork-Jensen, J. and Broer, L. and Chasman, D. I. and Chen, Y. I. and Chirstofidou, P. and Demirkan, A. and van Duijn, C. M. and Feitosa, M. F. and Garcia, M. E. and Graff, M. and Grallert, H. and Grarup, N. and Guo, X. and Haesser, J. and Hansen, T. and Harris, T. B. and Highland, H. M. and Hong, J. and Ikram, M. A. and Ingelsson, E. and Jackson, R. and Jousilahti, P. and nen, M. and Kizer, J. R. and Kovacs, P. and Kriebel, J. and Laakso, M. and Lange, L. A. and ki, T. and Li, J. and Li-Gao, R. and Lind, L. and Luan, J. and inen, L. P. and MacGregor, S. and Mackey, D. A. and Mahajan, A. and Mangino, M. and {\"o}, S. and McCarthy, M. I. and McKnight, B. and Medina-Gomez, C. and Meigs, J. B. and Molnos, S. and Mook-Kanamori, D. and Morris, A. P. and de Mutsert, R. and Nalls, M. A. and Nedeljkovic, I. and North, K. E. and Pennell, C. E. and Pradhan, A. D. and Province, M. A. and Raitakari, O. T. and Raulerson, C. K. and Reiner, A. P. and Ridker, P. M. and Ripatti, S. and Roberston, N. and Rotter, J. I. and Salomaa, V. and rate, A. A. and Sitlani, C. M. and Spector, T. D. and Strauch, K. and Stumvoll, M. and Taylor, K. D. and Thuesen, B. and njes, A. and Uitterlinden, A. G. and Venturini, C. and Walker, M. and Wang, C. A. and Wang, S. and Wareham, N. J. and Willems, S. M. and Willems van Dijk, K. and Wilson, J. G. and Wu, Y. and Yao, J. and Young, K. L. and Langenberg, C. and Frayling, T. M. and inen, T. O. and Lindgren, C. M. and Loos, R. J. F. and Mohlke, K. L.}
}
@article {9374,
	title = {{Exome-Derived Adiponectin-Associated Variants Implicate Obesity and Lipid Biology},
	journal = {Am J Hum Genet},
	volume = {105},
	year = {2019},
	month = {Jul},
	pages = {15{\textendash}28},
	abstract = {) with at least one obesity or lipid trait. Candidate genes include PRKAR2A, PTH1R, and HDAC9, which have been suggested to play roles in adipocyte differentiation or bone marrow adipose tissue. Taken together, these findings provide further insights into the processes that influence circulating adiponectin levels.},
	author = {Spracklen, C. N. and Karaderi, T. and Yaghootkar, H. and Schurmann, C. and Fine, R. S. and Kutalik, Z. and Preuss, M. H. and Lu, Y. and Wittemans, L. B. L. and Adair, L. S. and Allison, M. and Amin, N. and Auer, P. L. and Bartz, T. M. and her, M. and Boehnke, M. and Borja, J. B. and Bork-Jensen, J. and Broer, L. and Chasman, D. I. and Chen, Y. I. and Chirstofidou, P. and Demirkan, A. and van Duijn, C. M. and Feitosa, M. F. and Garcia, M. E. and Graff, M. and Grallert, H. and Grarup, N. and Guo, X. and Haesser, J. and Hansen, T. and Harris, T. B. and Highland, H. M. and Hong, J. and Ikram, M. A. and Ingelsson, E. and Jackson, R. and Jousilahti, P. and nen, M. and Kizer, J. R. and Kovacs, P. and Kriebel, J. and Laakso, M. and Lange, L. A. and ki, T. and Li, J. and Li-Gao, R. and Lind, L. and Luan, J. and inen, L. P. and MacGregor, S. and Mackey, D. A. and Mahajan, A. and Mangino, M. and {\"o}, S. and McCarthy, M. I. and McKnight, B. and Medina-Gomez, C. and Meigs, J. B. and Molnos, S. and Mook-Kanamori, D. and Morris, A. P. and de Mutsert, R. and Nalls, M. A. and Nedeljkovic, I. and North, K. E. and Pennell, C. E. and Pradhan, A. D. and Province, M. A. and Raitakari, O. T. and Raulerson, C. K. and Reiner, A. P. and Ridker, P. M. and Ripatti, S. and Roberston, N. and Rotter, J. I. and Salomaa, V. and rate, A. A. and Sitlani, C. M. and Spector, T. D. and Strauch, K. and Stumvoll, M. and Taylor, K. D. and Thuesen, B. and njes, A. and Uitterlinden, A. G. and Venturini, C. and Walker, M. and Wang, C. A. and Wang, S. and Wareham, N. J. and Willems, S. M. and Willems van Dijk, K. and Wilson, J. G. and Wu, Y. and Yao, J. and Young, K. L. and Langenberg, C. and Frayling, T. M. and inen, T. O. and Lindgren, C. M. and Loos, R. J. F. and Mohlke, K. L.}
}
@article {8518,
	title = {{Genome-Wide Association Study of Apparent Treatment-Resistant Hypertension in the CHARGE Consortium: The CHARGE Pharmacogenetics Working Group},
	journal = {Am J Hypertens},
	volume = {32},
	year = {2019},
	month = {11},
	pages = {1146{\textendash}1153},
	abstract = {{Only a handful of genetic discovery efforts in apparent treatment-resistant hypertension (aTRH) have been described.\ We conducted a case-control genome-wide association study of aTRH among persons treated for hypertension, using data from 10 cohorts of European ancestry (EA) and 5 cohorts of African ancestry (AA). Cases were treated with 3 different antihypertensive medication classes and had blood pressure (BP) above goal (systolic BP {\^a}{\textperthousand}{\textyen} 140 mm Hg and/or diastolic BP {\^a}{\textperthousand}{\textyen} 90 mm Hg) or 4 or more medication classes regardless of BP control (nEA = 931},
	author = {Irvin, M. R. and Sitlani, C. M. and Floyd, J. S. and Psaty, B. M. and Bis, J. C. and Wiggins, K. L. and Whitsel, E. A. and Sturmer, T. and Stewart, J. and Raffield, L. and Sun, F. and Liu, C. T. and Xu, H. and Cupples, A. L. and Tanner, R. M. and Rossing, P. and Smith, A. and Zilh?o, N. R. and Launer, L. J. and Noordam, R. and Rotter, J. I. and Yao, J. and Li, X. and Guo, X. and Limdi, N. and Sundaresan, A. and Lange, L. and Correa, A. and Stott, D. J. and Ford, I. and Jukema, J. W. and Gudnason, V. and Mook-Kanamori, D. O. and Trompet, S. and Palmas, W. and Warren, H. R. and Hellwege, J. N. and Giri, A. and O{\textquoteright}Donnell, C. and Hung, A. M. and Edwards, T. L. and Ahluwalia, T. S. and Arnett, D. K. and Avery, C. L.}
}
@article {8281,
	title = {{A multi-ancestry genome-wide study incorporating gene-smoking interactions identifies multiple new loci for pulse pressure and mean arterial pressure},
	journal = {Hum. Mol. Genet.},
	year = {2019},
	month = {Apr},
	abstract = {Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene-smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene-smoking interaction analysis and 38 were newly identified (P < 5 {\~A}{\textemdash} 10-8, false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.},
	author = {Sung, Y. J. and de Las Fuentes, L. and Winkler, T. W. and Chasman, D. I. and Bentley, A. R. and Kraja, A. T. and Ntalla, I. and Warren, H. R. and Guo, X. and Schwander, K. and Manning, A. K. and Brown, M. R. and Aschard, H. and Feitosa, M. F. and Franceschini, N. and Lu, Y. and Cheng, C. Y. and Sim, X. and Vojinovic, D. and Marten, J. and Musani, S. K. and Kilpel?inen, T. O. and Richard, M. A. and Aslibekyan, S. and Bartz, T. M. and Dorajoo, R. and Li, C. and Liu, Y. and Rankinen, T. and Smith, A. V. and Tajuddin, S. M. and Tayo, B. O. and Zhao, W. and Zhou, Y. and Matoba, N. and Sofer, T. and Alver, M. and Amini, M. and Boissel, M. and Chai, J. F. and Chen, X. and Divers, J. and Gandin, I. and Gao, C. and Giulianini, F. and Goel, A. and Harris, S. E. and Hartwig, F. P. and He, M. and Horimoto, A. R. V. R. and Hsu, F. C. and Jackson, A. U. and Kammerer, C. M. and Kasturiratne, A. and Komulainen, P. and K?hnel, B. and Leander, K. and Lee, W. J. and Lin, K. H. and Luan, J. and Lyytik?inen, L. P. and McKenzie, C. A. and Nelson, C. P. and Noordam, R. and Scott, R. A. and Sheu, W. H. H. and Stan??kov?, A. and Takeuchi, F. and van der Most, P. J. and Varga, T. V. and Waken, R. J. and Wang, H. and Wang, Y. and Ware, E. B. and Weiss, S. and Wen, W. and Yanek, L. R. and Zhang, W. and Zhao, J. H. and Afaq, S. and Alfred, T. and Amin, N. and Arking, D. E. and Aung, T. and Barr, R. G. and Bielak, L. F. and Boerwinkle, E. and Bottinger, E. P. and Braund, P. S. and Brody, J. A. and Broeckel, U. and Cade, B. and Campbell, A. and Canouil, M. and Chakravarti, A. and Cocca, M. and Collins, F. S. and Connell, J. M. and de Mutsert, R. and de Silva, H. J. and D?rr, M. and Duan, Q. and Eaton, C. B. and Ehret, G. and Evangelou, E. and Faul, J. D. and Forouhi, N. G. and Franco, O. H. and Friedlander, Y. and Gao, H. and Gigante, B. and Gu, C. C. and Gupta, P. and Hagenaars, S. P. and Harris, T. B. and He, J. and Heikkinen, S. and Heng, C. K. and Hofman, A. and Howard, B. V. and Hunt, S. C. and Irvin, M. R. and Jia, Y. and Katsuya, T. and Kaufman, J. and Kerrison, N. D. and Khor, C. C. and Koh, W. P. and Koistinen, H. A. and Kooperberg, C. B. and Krieger, J. E. and Kubo, M. and Kutalik, Z. and Kuusisto, J. and Lakka, T. A. and Langefeld, C. D. and Langenberg, C. and Launer, L. J. and Lee, J. H. and Lehne, B. and Levy, D. and Lewis, C. E. and Li, Y. and Lim, S. H. and Liu, C. T. and Liu, J. and Liu, J. and Liu, Y. and Loh, M. and Lohman, K. K. and Louie, T. and M?gi, R. and Matsuda, K. and Meitinger, T. and Metspalu, A. and Milani, L. and Momozawa, Y. and Mosley, T. H. and Nalls, M. A. and Nasri, U. and O{\textquoteright}Connell, J. R. and Ogunniyi, A. and Palmas, W. R. and Palmer, N. D. and Pankow, J. S. and Pedersen, N. L. and Peters, A. and Peyser, P. A. and Polasek, O. and Porteous, D. and Raitakari, O. T. and Renstr?m, F. and Rice, T. K. and Ridker, P. M. and Robino, A. and Robinson, J. G. and Rose, L. M. and Rudan, I. and Sabanayagam, C. and Salako, B. L. and Sandow, K. and Schmidt, C. O. and Schreiner, P. J. and Scott, W. R. and Sever, P. and Sims, M. and Sitlani, C. M. and Smith, B. H. and Smith, J. A. and Snieder, H. and Starr, J. M. and Strauch, K. and Tang, H. and Taylor, K. D. and Teo, Y. Y. and Tham, Y. C. and Uitterlinden, A. G. and Waldenberger, M. and Wang, L. and Wang, Y. X. and Wei, W. B. and Wilson, G. and Wojczynski, M. K. and Xiang, Y. B. and Yao, J. and Yuan, J. M. and Zonderman, A. B. and Becker, D. M. and Boehnke, M. and Bowden, D. W. and Chambers, J. C. and Chen, Y. I. and Weir, D. R. and de Faire, U. and Deary, I. J. and Esko, T. and Farrall, M. and Forrester, T. and Freedman, B. I. and Froguel, P. and Gasparini, P. and Gieger, C. and Horta, B. L. and Hung, Y. J. and Jonas, J. B. and Kato, N. and Kooner, J. S. and Laakso, M. and Lehtim?ki, T. and Liang, K. W. and Magnusson, P. K. E. and Oldehinkel, A. J. and Pereira, A. C. and Perls, T. and Rauramaa, R. and Redline, S. and Rettig, R. and Samani, N. J. and Scott, J. and Shu, X. O. and van der Harst, P. and Wagenknecht, L. E. and Wareham, N. J. and Watkins, H. and Wickremasinghe, A. R. and Wu, T. and Kamatani, Y. and Laurie, C. C. and Bouchard, C. and Cooper, R. S. and Evans, M. K. and Gudnason, V. and Hixson, J. and Kardia, S. L. R. and Kritchevsky, S. B. and Psaty, B. M. and van Dam, R. M. and Arnett, D. K. and Mook-Kanamori, D. O. and Fornage, M. and Fox, E. R. and Hayward, C. and van Duijn, C. M. and Tai, E. S. and Wong, T. Y. and Loos, R. J. F. and Reiner, A. P. and Rotimi, C. N. and Bierut, L. J. and Zhu, X. and Cupples, L. A. and Province, M. A. and Rotter, J. I. and Franks, P. W. and Rice, K. and Elliott, P. and Caulfield, M. J. and Gauderman, W. J. and Munroe, P. B. and Rao, D. C. and Morrison, A. C.}
}
@article {8917,
	title = {{Rare and low-frequency exonic variants and gene-by-smoking interactions in pulmonary function},
	journal = {Sci Rep},
	volume = {11},
	year = {2021},
	month = {09},
	pages = {19365},
	abstract = {. This study investigates the utility of assessing gene-by-smoking interactions and underscores their effects on potential pulmonary function.},
	author = {Yang, T. and Jackson, V. E. and Smith, A. V. and Chen, H. and Bartz, T. M. and Sitlani, C. M. and Psaty, B. M. and Gharib, S. A. and O{\textquoteright}Connor, G. T. and Dupuis, J. and Xu, J. and Lohman, K. and Liu, Y. and Kritchevsky, S. B. and Cassano, P. A. and Flexeder, C. and Gieger, C. and Karrasch, S. and Peters, A. and Schulz, H. and Harris, S. E. and Starr, J. M. and Deary, I. J. and Manichaikul, A. and Oelsner, E. C. and Barr, R. G. and Taylor, K. D. and Rich, S. S. and Bonten, T. N. and Mook-Kanamori, D. O. and Noordam, R. and Li-Gao, R. and Jarvelin, M. R. and Wielscher, M. and Terzikhan, N. and Lahousse, L. and Brusselle, G. and Weiss, S. and Ewert, R. and Gl{\"a}ser, S. and Homuth, G. and Shrine, N. and Hall, I. P. and Tobin, M. and London, S. J. and Wei, P. and Morrison, A. C.}
}
@article {8999,
	title = {{Genome-wide analysis of mitochondrial DNA copy number reveals loci implicated in nucleotide metabolism, platelet activation, and megakaryocyte proliferation},
	journal = {Hum Genet},
	volume = {141},
	year = {2022},
	month = {Jan},
	pages = {127{\textendash}146},
	abstract = {).},
	author = {Longchamps, R. J. and Yang, S. Y. and Castellani, C. A. and Shi, W. and Lane, J. and Grove, M. L. and Bartz, T. M. and Sarnowski, C. and Liu, C. and Burrows, K. and Guyatt, A. L. and Gaunt, T. R. and Kacprowski, T. and Yang, J. and De Jager, P. L. and Yu, L. and Bergman, A. and Xia, R. and Fornage, M. and Feitosa, M. F. and Wojczynski, M. K. and Kraja, A. T. and Province, M. A. and Amin, N. and Rivadeneira, F. and Tiemeier, H. and Uitterlinden, A. G. and Broer, L. and van Meurs, J. B. J. and van Duijn, C. M. and Raffield, L. M. and Lange, L. and Rich, S. S. and Lemaitre, R. N. and Goodarzi, M. O. and Sitlani, C. M. and Mak, A. C. Y. and Bennett, D. A. and Rodriguez, S. and Murabito, J. M. and Lunetta, K. L. and Sotoodehnia, N. and Atzmon, G. and Ye, K. and Barzilai, N. and Brody, J. A. and Psaty, B. M. and Taylor, K. D. and Rotter, J. I. and Boerwinkle, E. and Pankratz, N. and Arking, D. E.}
}
@article {8982,
	title = {{Obesity Partially Mediates the Diabetogenic Effect of Lowering LDL Cholesterol},
	journal = {Diabetes Care},
	volume = {45},
	year = {2022},
	month = {Jan},
	pages = {232{\textendash}240},
	abstract = {LDL cholesterol (LDLc)-lowering drugs modestly increase body weight and type 2 diabetes risk, but the extent to which the diabetogenic effect of lowering LDLc is mediated through increased BMI is unknown.\ We conducted summary-level univariable and multivariable Mendelian randomization (MR) analyses in 921,908 participants to investigate the effect of lowering LDLc on type 2 diabetes risk and the proportion of this effect mediated through BMI. We used data from 92,532 participants from 14 observational studies to replicate findings in individual-level MR analyses.\ A 1-SD decrease in genetically predicted LDLc was associated with increased type 2 diabetes odds (odds ratio [OR] 1.12 [95\% CI 1.01, 1.24]) and BMI (β = 0.07 SD units [95\% CI 0.02, 0.12]) in univariable MR analyses. The multivariable MR analysis showed evidence of an indirect effect of lowering LDLc on type 2 diabetes through BMI (OR 1.04 [95\% CI 1.01, 1.08]) with a proportion mediated of 38\% of the total effect (P = 0.03). Total and indirect effect estimates were similar across a number of sensitivity analyses. Individual-level MR analyses confirmed the indirect effect of lowering LDLc on type 2 diabetes through BMI with an estimated proportion mediated of 8\% (P = 0.04).\ These findings suggest that the diabetogenic effect attributed to lowering LDLc is partially mediated through increased BMI. Our results could help advance understanding of adipose tissue and lipids in type 2 diabetes pathophysiology and inform strategies to reduce diabetes risk among individuals taking LDLc-lowering medications.},
	author = {Wu, P. and Moon, J. Y. and Daghlas, I. and Franco, G. and Porneala, B. C. and Ahmadizar, F. and Richardson, T. G. and Isaksen, J. L. and Hindy, G. and Yao, J. and Sitlani, C. M. and Raffield, L. M. and Yanek, L. R. and Feitosa, M. F. and Cuadrat, R. R. C. and Qi, Q. and Arfan Ikram, M. and Ellervik, C. and Ericson, U. and Goodarzi, M. O. and Brody, J. A. and Lange, L. and Mercader, J. M. and Vaidya, D. and An, P. and Schulze, M. B. and Masana, L. and Ghanbari, M. and Olesen, M. S. and Cai, J. and Guo, X. and Floyd, J. S. and J{\"a}ger, S. and Province, M. A. and Kalyani, R. R. and Psaty, B. M. and Orho-Melander, M. and Ridker, P. M. and Kanters, J. K. and Uitterlinden, A. and Davey Smith, G. and Gill, D. and Kaplan, R. C. and Kavousi, M. and Raghavan, S. and Chasman, D. I. and Rotter, J. I. and Meigs, J. B. and Florez, J. C. and Dupuis, J. and Liu, C. T. and Merino, J.}
}
@article {9263,
	title = {{A saturated map of common genetic variants associated with human height},
	journal = {Nature},
	volume = {610},
	year = {2022},
	month = {Oct},
	pages = {704{\textendash}712},
	abstract = {) account for 40\% (45\%) of phenotypic variance in populations of European ancestry but only around 10-20\% (14-24\%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries.},
	author = {Yengo, L. and Vedantam, S. and Marouli, E. and Sidorenko, J. and Bartell, E. and Sakaue, S. and Graff, M. and Eliasen, A. U. and Jiang, Y. and Raghavan, S. and Miao, J. and Arias, J. D. and Graham, S. E. and Mukamel, R. E. and Spracklen, C. N. and Yin, X. and Chen, S. H. and Ferreira, T. and Highland, H. H. and Ji, Y. and Karaderi, T. and Lin, K. and ll, K. and Malden, D. E. and Medina-Gomez, C. and Machado, M. and Moore, A. and eger, S. and Sim, X. and Vrieze, S. and Ahluwalia, T. S. and Akiyama, M. and Allison, M. A. and Alvarez, M. and Andersen, M. K. and Ani, A. and Appadurai, V. and Arbeeva, L. and Bhaskar, S. and Bielak, L. F. and Bollepalli, S. and Bonnycastle, L. L. and Bork-Jensen, J. and Bradfield, J. P. and Bradford, Y. and Braund, P. S. and Brody, J. A. and Burgdorf, K. S. and Cade, B. E. and Cai, H. and Cai, Q. and Campbell, A. and adas-Garre, M. and Catamo, E. and Chai, J. F. and Chai, X. and Chang, L. C. and Chang, Y. C. and Chen, C. H. and Chesi, A. and Choi, S. H. and Chung, R. H. and Cocca, M. and Concas, M. P. and Couture, C. and Cuellar-Partida, G. and Danning, R. and Daw, E. W. and Degenhard, F. and Delgado, G. E. and Delitala, A. and Demirkan, A. and Deng, X. and Devineni, P. and Dietl, A. and Dimitriou, M. and Dimitrov, L. and Dorajoo, R. and Ekici, A. B. and Engmann, J. E. and Fairhurst-Hunter, Z. and Farmaki, A. E. and Faul, J. D. and Fernandez-Lopez, J. C. and Forer, L. and Francescatto, M. and Freitag-Wolf, S. and Fuchsberger, C. and Galesloot, T. E. and Gao, Y. and Gao, Z. and Geller, F. and Giannakopoulou, O. and Giulianini, F. and Gjesing, A. P. and Goel, A. and Gordon, S. D. and Gorski, M. and Grove, J. and Guo, X. and Gustafsson, S. and Haessler, J. and Hansen, T. F. and Havulinna, A. S. and Haworth, S. J. and He, J. and Heard-Costa, N. and Hebbar, P. and Hindy, G. and Ho, Y. A. and Hofer, E. and Holliday, E. and Horn, K. and Hornsby, W. E. and Hottenga, J. J. and Huang, H. and Huang, J. and Huerta-Chagoya, A. and Huffman, J. E. and Hung, Y. J. and Huo, S. and Hwang, M. Y. and Iha, H. and Ikeda, D. D. and Isono, M. and Jackson, A. U. and ger, S. and Jansen, I. E. and Johansson, I. and Jonas, J. B. and Jonsson, A. and rgensen, T. and Kalafati, I. P. and Kanai, M. and Kanoni, S. and rhus, L. L. and Kasturiratne, A. and Katsuya, T. and Kawaguchi, T. and Kember, R. L. and Kentistou, K. A. and Kim, H. N. and Kim, Y. J. and Kleber, M. E. and Knol, M. J. and Kurbasic, A. and Lauzon, M. and Le, P. and Lea, R. and Lee, J. Y. and Leonard, H. L. and Li, S. A. and Li, X. and Li, X. and Liang, J. and Lin, H. and Lin, S. Y. and Liu, J. and Liu, X. and Lo, K. S. and Long, J. and Lor{\'e}s-Motta, L. and Luan, J. and Lyssenko, V. and inen, L. P. and Mahajan, A. and Mamakou, V. and Mangino, M. and Manichaikul, A. and Marten, J. and Mattheisen, M. and Mavarani, L. and McDaid, A. F. and Meidtner, K. and Melendez, T. L. and Mercader, J. 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}
@article {9546,
	title = {{Identification of circulating proteins associated with general cognitive function among middle-aged and older adults},
	journal = {Commun Biol},
	volume = {6},
	year = {2023},
	month = {Nov},
	pages = {1117},
	abstract = {2.0E-4). Proteins implicated as causes or consequences of AD susceptibility may provide new insight into the potential relationship between immunity and AD susceptibility as well as potential therapeutic targets.},
	author = {Tin, A. and Fohner, A. E. and Yang, Q. and Brody, J. A. and Davies, G. and Yao, J. and Liu, D. and Caro, I. and Lindbohm, J. V. and Duggan, M. R. and Meirelles, O. and Harris, S. E. and Gudmundsdottir, V. and Taylor, A. M. and Henry, A. and Beiser, A. S. and Shojaie, A. and Coors, A. and Fitzpatrick, A. L. and Langenberg, C. and Satizabal, C. L. and Sitlani, C. M. and Wheeler, E. and Tucker-Drob, E. M. and Bressler, J. and Coresh, J. and Bis, J. C. and Candia, J. and Jennings, L. L. and Pietzner, M. and Lathrop, M. and Lopez, O. L. and Redmond, P. and Gerszten, R. E. and Rich, S. S. and Heckbert, S. R. and Austin, T. R. and Hughes, T. M. and Tanaka, T. and Emilsson, V. and Vasan, R. S. and Guo, X. and Zhu, Y. and Tzourio, C. and Rotter, J. I. and Walker, K. A. and Ferrucci, L. and ki, M. and Breteler, M. M. B. and Cox, S. R. and Debette, S. and Mosley, T. H. and Gudnason, V. G. and Launer, L. J. and Psaty, B. M. and Seshadri, S. and Fornage, M.}
}
