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1. Migraine-Associated Common Genetic Variants Confer Greater Risk of Posterior vs. Anterior Circulation Ischemic Stroke☆

Author: Frid, P., Xu, H., Mitchell, B.D., Drake, M., Wasselius, J., Gaynor, B., Ryan, K., Giese, A.K., Schirmer, M., Donahue, K.L., Irie, R., Bouts, M.J.R.J., McIntosh, E.C., Mocking, S.J.T., Dalca, A.V., Giralt-Steinhauer, E., Holmegaard, L., Jood, K., Roquer, J., Cole, J.W., McArdle, P.F., Broderick, J.P., Jimenez-Conde, J., Jern, C., Kissela, B.M., Kleindorfer, D.O., Lemmens, R., Meschia, J.F., Rosand, J., Rundek, T., Sacco, R.L., Schmidt, R., Sharma, P., Slowik, A., Thijs, V., Woo, D., Worrall, B.B., Kittner, S.J., Petersson, J., Golland, P., Wu, O., Rost, N.S., and Lindgren, A.
Published: 2022
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2. Health Heritage©, a Web-Based Tool for the Collection and Assessment of Family Health History : Initial User Experience and Analytic Validity

Author: Cohn, W.F., Ropka, M.E., Pelletier, S.L., Barrett, J.R., Kinzie, M.B., Harrison, M.B., Liu, Z., Miesfeldt, S., Tucker, A.L., Worrall, B.B., Gibson, J., Mullins, I.M., Elward, K.S., Franko, J., Guterbock, T.M., and Knaus, W.A.
Published: 2010

3. Prestroke physical activity and early functional status after stroke

Author: Stroud, N., Mazwi, T.M.L., Case, L.D., Brown, R.D., Jr., Brott, T.G., Worrall, B.B., and Meschia, J.F.
Subjects: Stroke (Disease) -- Physiological aspects, Stroke (Disease) -- Risk factors, Stroke (Disease) -- Research, Outcome and process assessment (Health Care) -- Research, Exercise -- Physiological aspects, Exercise -- Research, Health, Psychology and mental health
Published: 2009

4. Genome-wide association study of intracranial aneurysms identifies 17 risk loci and genetic overlap with clinical risk factors

Author: Bakker, M.K., Spek, R.A.A. van der, Rheenen, W. van, Morel, S., Bourcier, R., Hostettler, I.C., Alg, V.S., Eijk, Kristel R. van, Koido, M., Akiyama, M., Terao, C., Matsuda, K., Walters, R.G., Lin, K., Li, L, Millwood, I.Y., Chen, Z., Rouleau, G.A., et al., Zhou, S., Rannikmäe, K., Sudlow, C.L., Houlden, H., Berg, L.H. van den, Dina, C., Naggara, O., Gentric, J.C., Shotar, E., Eugène, F., Desal, H., Winsvold, B.S., Børte, S., Johnsen, M.B., Brumpton, B.M., Sandvei, M.S., Willer, C.J., Hveem, K., Zwart, Jacob A., Verschuren, W.M., Friedrich, C.M., Hirsch, S., Schilling, S., Dauvillier, J., Martin, O., Jones, G.T., Bown, M.J., Ko, N.U., Kim, H., Coleman, J.R.I., Breen, G., Zaroff, J.G., Klijn, C.J.M., Malik, R., Dichgans, M., Sargurupremraj, M., Tatlisumak, T., Amouyel, P., Debette, S., Rinkel, G.J., Worrall, B.B., Pera, J., Slowik, A., Gaál-Paavola, E.I., Niemelä, M., Jääskeläinen, J.E., Fraunberg, M. von Und Zu, Lindgren, A., Broderick, J.P., Werring, D.J., Woo, D., Redon, R., Bijlenga, P., Kamatani, Y., Veldink, J.H., Ruigrok, Y.M., Bakker, M.K., Spek, R.A.A. van der, Rheenen, W. van, Morel, S., Bourcier, R., Hostettler, I.C., Alg, V.S., Eijk, Kristel R. van, Koido, M., Akiyama, M., Terao, C., Matsuda, K., Walters, R.G., Lin, K., Li, L, Millwood, I.Y., Chen, Z., Rouleau, G.A., et al., Zhou, S., Rannikmäe, K., Sudlow, C.L., Houlden, H., Berg, L.H. van den, Dina, C., Naggara, O., Gentric, J.C., Shotar, E., Eugène, F., Desal, H., Winsvold, B.S., Børte, S., Johnsen, M.B., Brumpton, B.M., Sandvei, M.S., Willer, C.J., Hveem, K., Zwart, Jacob A., Verschuren, W.M., Friedrich, C.M., Hirsch, S., Schilling, S., Dauvillier, J., Martin, O., Jones, G.T., Bown, M.J., Ko, N.U., Kim, H., Coleman, J.R.I., Breen, G., Zaroff, J.G., Klijn, C.J.M., Malik, R., Dichgans, M., Sargurupremraj, M., Tatlisumak, T., Amouyel, P., Debette, S., Rinkel, G.J., Worrall, B.B., Pera, J., Slowik, A., Gaál-Paavola, E.I., Niemelä, M., Jääskeläinen, J.E., Fraunberg, M. von Und Zu, Lindgren, A., Broderick, J.P., Werring, D.J., Woo, D., Redon, R., Bijlenga, P., Kamatani, Y., Veldink, J.H., and Ruigrok, Y.M.
Abstract: Contains fulltext : 229738.pdf (Publisher’s version ) (Closed access), Rupture of an intracranial aneurysm leads to subarachnoid hemorrhage, a severe type of stroke. To discover new risk loci and the genetic architecture of intracranial aneurysms, we performed a cross-ancestry, genome-wide association study in 10,754 cases and 306,882 controls of European and East Asian ancestry. We discovered 17 risk loci, 11 of which are new. We reveal a polygenic architecture and explain over half of the disease heritability. We show a high genetic correlation between ruptured and unruptured intracranial aneurysms. We also find a suggestive role for endothelial cells by using gene mapping and heritability enrichment. Drug-target enrichment shows pleiotropy between intracranial aneurysms and antiepileptic and sex hormone drugs, providing insights into intracranial aneurysm pathophysiology. Finally, genetic risks for smoking and high blood pressure, the two main clinical risk factors, play important roles in intracranial aneurysm risk, and drive most of the genetic correlation between intracranial aneurysms and other cerebrovascular traits.
Published: 2020

5. Relative effects of LDL-C on ischemic stroke and coronary disease: A Mendelian randomization study

Author: Valdes-Marquez, E., Parish, S., Clarke, R., Stari, T., Worrall, B.B., Hopewell, J.C., and METASTROKE Consortium (Lichtner, P.)
Subjects: Causality, Stroke, Humans, Coronary Disease, Hyperlipidemias, Cholesterol, LDL, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Mendelian Randomization Analysis, Article, Brain Ischemia, Hypolipidemic Agents
Abstract: Objective To examine the causal relevance of lifelong differences in low-density lipoprotein cholesterol (LDL-C) for ischemic stroke (IS) relative to that for coronary heart disease (CHD) using a Mendelian randomization approach. Methods We undertook a 2-sample Mendelian randomization, based on summary data, to estimate the causal relevance of LDL-C for risk of IS and CHD. Information from 62 independent genetic variants with genome-wide significant effects on LDL-C levels was used to estimate the causal effects of LDL-C for IS and IS subtypes (based on 12,389 IS cases from METASTROKE) and for CHD (based on 60,801 cases from CARDIoGRAMplusC4D). We then assessed the effects of LDL-C on IS and CHD for heterogeneity. Results A 1 mmol/L higher genetically determined LDL-C was associated with a 50% higher risk of CHD (odds ratio [OR] 1.49, 95% confidence interval [CI] 1.32−1.68, p = 1.1 × 10−8). By contrast, the causal effect of LDL-C was much weaker for IS (OR 1.12, 95% CI 0.96−1.30, p = 0.14; p for heterogeneity = 2.6 × 10−3) and, in particular, for cardioembolic stroke (OR 1.06, 95% CI 0.84−1.33, p = 0.64; p for heterogeneity = 8.6 × 10−3) when compared with that for CHD. Conclusions In contrast with the consistent effects of LDL-C-lowering therapies on IS and CHD, genetic variants that confer lifelong LDL-C differences show a weaker effect on IS than on CHD. The relevance of etiologically distinct IS subtypes may contribute to the differences observed.
Published: 2019

6. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting

Author: Chauhan, G., Adams, H.H.H., Satizabal, C.L., Bis, J.C., Teumer, A., Sargurupremraj, M., Hofer, E., Trompet, S., Hilal, S., Smith, A.V., Jian, X.Q., Malik, R., Traylor, M., Pulit, S.L., Amouyel, P., Mazoyer, B., Zhu, Y.C., Kaffashian, S., Schilling, S., Beecham, G.W., Montine, T.J., Schellenberg, G.D., Kjartansson, O., Gudnason, V., Knopman, D.S., Griswold, M.E., Windham, B.G., Gottesman, R.F., Mosley, T.H., Schmidt, R., Saba, Y., Schmidt, H., Takeuchi, F., Yamaguchi, S., Nabika, T., Kato, N., Rajan, K.B., Aggarwal, N.T., Jager, P.L. de, Evans, D.A., Psaty, B.M., Rotter, J.I., Rice, K., Lopez, O.L., Liao, J.M., Chen, C., Cheng, C.Y., Wong, T.Y., Ikram, M.K., Lee, S.J. van der, Amin, N., Chouraki, V., DeStefano, A.L., Aparicio, H.J., Romero, J.R., Maillard, P., DeCarli, C., Wardlaw, J.M., Hernandez, M.D.V., Luciano, M., Liewald, D., Deary, I.J., Starr, J.M., Bastin, M.E., Maniega, S.M., Slagboom, P.E., Beekman, M., Deelen, J., Uh, H.W., Lemmens, R., Brodaty, H., Wright, M.J., Ames, D., Boncoraglio, G.B., Hopewell, J.C., Beecham, A.H., Blanton, S.H., Wright, C.B., Sacco, R.L., Wen, W., Thalamuthu, A., Armstrong, N.J., Chong, E., Schofield, P.R., Kwok, J.B., Grond, J. van der, Stott, D.J., Ford, I., Jukema, J.W., Vernooij, M.W., Hofman, A., Uitterlinden, A.G., Lugt, A. van der, Wittfeld, K., Grabe, H.J., Hosten, N., Sarnowski, B. von, Volker, U., Levi, C., Jimenez-Conde, J., Sharma, P., Sudlow, C.L.M., Rosand, J., Woo, D., Cole, J.W., Meschia, J.F., Slowik, A., Thijs, V., Lindgren, A., Melander, O., Grewal, R.P., Rundek, T., Rexrode, K., Rothwell, P.M., Arnett, D.K., Jern, C., Johnson, J.A., Benavente, O.R., Wasssertheil-Smoller, S., Lee, J.M., Wong, Q., Mitchell, B.D., Rich, S.S., McArdle, P.F., Geerlings, M.I., Graaf, Y. van der, Bakker, P.I.W. de, Asselbergs, F.W., Srikanth, V., Thomson, R., McWhirter, R., Moran, C., Callisaya, M., Phan, T., Rutten-Jacobs, L.C.A., Bevan, S., Tzourio, C., Mather, K.A., Sachdev, P.S., Duijn, C.M. van, Worrall, B.B., Dichgans, M., Kittner, S.J., Markus, H.S., Ikram, M.A., Fornage, M., Launer, L.J., Seshadri, S., Longstreth, W.T., Debette, S., Stroke Genetics Network SiGN, ISGC, METASTROKE, ADGC, and CHARGE Consortium
Subjects: Meta-analysis, Mendelian Randomization, Blood Pressure, Polymorphisms, Genome-wide Association, Silent, Insights, Small Vessel Disease, Matter Hyperintensity Volume, Ischemic Stroke, Doenças Cardio e Cérebro-vasculares
Abstract: Collaborators (845): Astrid M. Vicente Free PMC article:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6369905/ Objective: To explore genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts. Methods: We performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely, small subcortical BI (SSBI), in 18 population-based cohorts (n = 20,949) from 5 ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in 7 population-based cohorts (n = 6,862; 1,483 with BI, 630 with SBBI), and we tested associations with related phenotypes including ischemic stroke and pathologically defined BI. Results: The mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, p = 1.77 × 10-8; and LINC00539/ZDHHC20, p = 5.82 × 10-9. Both have been associated with blood pressure (BP)-related phenotypes, but did not replicate in the smaller follow-up sample or show associations with related phenotypes. Age- and sex-adjusted associations with BI and SSBI were observed for BP traits (p value for BI, p [BI] = 9.38 × 10-25; p [SSBI] = 5.23 × 10-14 for hypertension), smoking (p [BI] = 4.4 × 10-10; p [SSBI] = 1.2 × 10-4), diabetes (p [BI] = 1.7 × 10-8; p [SSBI] = 2.8 × 10-3), previous cardiovascular disease (p [BI] = 1.0 × 10-18; p [SSBI] = 2.3 × 10-7), stroke (p [BI] = 3.9 × 10-69; p [SSBI] = 3.2 × 10-24), and MRI-defined white matter hyperintensity burden (p [BI] = 1.43 × 10-157; p [SSBI] = 3.16 × 10-106), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p ≤ 0.0022), without indication of directional pleiotropy. Conclusion: In this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI. info:eu-repo/semantics/publishedVersion
Published: 2019

7. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting.

Author: Aparicio H.J., Del C. Valdes Hernandez M., Luciano M., Liewald D., Deary I.J., Starr J.M., Bastin M.E., Maniega S.M., Slagboom P.E., Beekman M., Deelen J., Uh H.-W., Lemmens R., Brodaty H., Wright M.J., Ames D., Boncoraglio G.B., Hopewell J.C., Beecham A.H., Blanton S.H., Wright C.B., Sacco R.L., Wen W., Thalamuthu A., Armstrong N.J., Chong E., Schofield P.R., Kwok J.B., van der Grond J., Stott D.J., Ford I., Jukema J.W., Vernooij M.W., Hofman A., Uitterlinden A.G., van der Lugt A., Wittfeld K., Grabe H.J., Hosten N., von Sarnowski B., Volker U., Levi C., Jimenez-Conde J., Sharma P., Sudlow C.L.M., Rosand J., Woo D., Cole J.W., Meschia J.F., Slowik A., Thijs V., Lindgren A., Melander O., Grewal R.P., Rundek T., Rexrode K., Rothwell P.M., Arnett D.K., Jern C., Johnson J.A., Benavente O.R., Wasssertheil-Smoller S., Lee J.-M., Wong Q., Mitchell B.D., Rich S.S., McArdle P.F., Geerlings M.I., van der Graaf Y., de Bakker P.I.W., Asselbergs F.W., Srikanth V., Thomson R., McWhirter R., Moran C., Callisaya M., Phan T., Rutten-Jacobs L.C.A., Bevan S., Tzourio C., Mather K.A., Sachdev P.S., van Duijn C.M., Worrall B.B., Dichgans M., Kittner S.J., Markus H.S., Ikram M.A., Fornage M., Launer L.J., Seshadri S., Longstreth W.T., Debette S., Chauhan G., Adams H.H.H., Satizabal C.L., Bis J.C., Teumer A., Sargurupremraj M., Hofer E., Trompet S., Hilal S., Smith A.V., Jian X., Malik R., Traylor M., Pulit S.L., Amouyel P., Mazoyer B., Zhu Y.-C., Kaffashian S., Schilling S., Beecham G.W., Montine T.J., Schellenberg G.D., Kjartansson O., Gudnason V., Knopman D.S., Griswold M.E., Windham B.G., Gottesman R.F., Mosley T.H., Schmidt R., Saba Y., Schmidt H., Takeuchi F., Yamaguchi S., Nabika T., Kato N., Rajan K.B., Aggarwal N.T., De Jager P.L., Evans D.A., Psaty B.M., Rotter J.I., Rice K., Lopez O.L., Liao J., Chen C., Cheng C.-Y., Wong T.Y., Ikram M.K., van der Lee S.J., Amin N., Chouraki V., Destefano A.L., Romero J.R., Maillard P., Decarli C., Wardlaw J.M., Aparicio H.J., Del C. Valdes Hernandez M., Luciano M., Liewald D., Deary I.J., Starr J.M., Bastin M.E., Maniega S.M., Slagboom P.E., Beekman M., Deelen J., Uh H.-W., Lemmens R., Brodaty H., Wright M.J., Ames D., Boncoraglio G.B., Hopewell J.C., Beecham A.H., Blanton S.H., Wright C.B., Sacco R.L., Wen W., Thalamuthu A., Armstrong N.J., Chong E., Schofield P.R., Kwok J.B., van der Grond J., Stott D.J., Ford I., Jukema J.W., Vernooij M.W., Hofman A., Uitterlinden A.G., van der Lugt A., Wittfeld K., Grabe H.J., Hosten N., von Sarnowski B., Volker U., Levi C., Jimenez-Conde J., Sharma P., Sudlow C.L.M., Rosand J., Woo D., Cole J.W., Meschia J.F., Slowik A., Thijs V., Lindgren A., Melander O., Grewal R.P., Rundek T., Rexrode K., Rothwell P.M., Arnett D.K., Jern C., Johnson J.A., Benavente O.R., Wasssertheil-Smoller S., Lee J.-M., Wong Q., Mitchell B.D., Rich S.S., McArdle P.F., Geerlings M.I., van der Graaf Y., de Bakker P.I.W., Asselbergs F.W., Srikanth V., Thomson R., McWhirter R., Moran C., Callisaya M., Phan T., Rutten-Jacobs L.C.A., Bevan S., Tzourio C., Mather K.A., Sachdev P.S., van Duijn C.M., Worrall B.B., Dichgans M., Kittner S.J., Markus H.S., Ikram M.A., Fornage M., Launer L.J., Seshadri S., Longstreth W.T., Debette S., Chauhan G., Adams H.H.H., Satizabal C.L., Bis J.C., Teumer A., Sargurupremraj M., Hofer E., Trompet S., Hilal S., Smith A.V., Jian X., Malik R., Traylor M., Pulit S.L., Amouyel P., Mazoyer B., Zhu Y.-C., Kaffashian S., Schilling S., Beecham G.W., Montine T.J., Schellenberg G.D., Kjartansson O., Gudnason V., Knopman D.S., Griswold M.E., Windham B.G., Gottesman R.F., Mosley T.H., Schmidt R., Saba Y., Schmidt H., Takeuchi F., Yamaguchi S., Nabika T., Kato N., Rajan K.B., Aggarwal N.T., De Jager P.L., Evans D.A., Psaty B.M., Rotter J.I., Rice K., Lopez O.L., Liao J., Chen C., Cheng C.-Y., Wong T.Y., Ikram M.K., van der Lee S.J., Amin N., Chouraki V., Destefano A.L., Romero J.R., Maillard P., Decarli C., and Wardlaw J.M.
Abstract: Objective To explore genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts. Methods We performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely, small subcortical BI (SSBI), in 18 population-based cohorts (n=20,949) from 5 ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in 7 population-based cohorts (n = 6,862; 1,483 with BI, 630 with SBBI), and we tested associations with related phenotypes including ischemic stroke and pathologically defined BI. Results The mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, p = 1.77 x 10-8; and LINC00539/ZDHHC20, p = 5.82 x 10-9. Both have been associated with blood pressure (BP)-related phenotypes, but did not replicate in the smaller follow-up sample or show associations with related phenotypes. Age- and sex-adjusted associations with BI and SSBI were observed for BP traits (p value for BI, p[BI] = 9.38 x 10-25; p [SSBI] = 5.23 x 10-14 for hypertension), smoking (p[BI]= 4.4 x 10-10; p [SSBI] = 1.2 x 10 -4), diabetes (p[BI] = 1.7 x 10 -8; p [SSBI] = 2.8 x 10 -3), previous cardiovascular disease (p [BI] = 1.0 x 10-18; p [SSBI] = 2.3 x 10-7), stroke (p [BI] = 3.9 x 10-69; p [SSBI] = 3.2 x 10 -24), and MRI-defined white matter hyperintensity burden (p [BI]=1.43 x 10-157; p [SSBI] = 3.16 x 10-106), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p <= 0.0022), without indication of directional pleiotropy. Conclusion In this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significa
Published: 2019

8. GWAS and colocalization analyses implicate carotid intima-media thickness and carotid plaque loci in cardiovascular outcomes

Author: Franceschini, N. (Nora), Giambartolomei, C. (Claudia), Vries, P.S. (Paul) de, Finan, C. (Chris), Bis, J.C. (Joshua), Huntley, R.P. (Rachael P.), Lovering, R.C. (Ruth C.), Tajuddin, S.M. (Salman M.), Winkler, T.W. (Thomas W.), Graff, M. (Misa), Kavousi, M. (Maryam), Dale, C. (Caroline), Smith, A.V. (Albert), Hofer, E. (Edith), Leeuwen, E.M. (Elisa) van, Nolte, I.M. (Ilja), Lu, L. (Lingyi), Scholz, M. (Markus), Sargurupremraj, M. (Muralidharan), Pitkanen, N. (Niina), Franzén, O. (Oscar), Joshi, P.K. (Peter), Noordam, R. (Raymond), Marioni, R.E. (Riccardo), Hwang, S.-J. (Shih-Jen), Musani, S.K. (Solomon K.), Schminke, U. (Ulf), Palmas, W. (Walter), Isaacs, A.J. (Aaron), Correa, D.D., Zonderman, A.B., Hofman, A. (Albert), Teumer, A. (Alexander), Cox, A.J. (Amanda J.), Uitterlinden, A.G. (André), Wong, A. (Andrew), Smit, A.J. (Andries), Newman, A.B. (Anne B.), Britton, A.R., Ruusalepp, A. (Arno), Sennblad, B. (Bengt), Hedblad, B. (Bo), Pasaniuc, B. (Bogdan), Penninx, B.W.J.H. (Brenda), Langefeld, C.D. (Carl D.), Wassel, C.L. (Christina), Tzourio, C. (Christophe), Fava, C. (Cristiano), Baldassarre, D. (Damiano), O’Leary, D.H. (Daniel H.), Teupser, D. (Daniel), Kuh, D. (Diana), Tremoli, E. (Elena), Mannarino, E. (Elmo), Grossi, E. (Enzo), Boerwinkle, E.A. (Eric), Schadt, E.E. (Eric E.), Ingelsson, E. (Erik), Veglia, F. (Fabrizio), Rivadeneira Ramirez, F. (Fernando), Beutner, F. (Frank), Chauhan, G. (Ganesh), Heiss, G. (Gerardo), Snieder, H. (Harold), Campbell, H. (Harry), Völzke, H. (Henry), Markus, H.S. (Hugh), Deary, I.J. (Ian), Jukema, J.W. (Jan Wouter), Graaf, J. (Jacqueline) de, Price, J. (Jacqueline), Pott, J. (Janne), Hopewell, J., Liang, J. (Jingjing), Thiery, J.P. (Joachim), Engmann, J. (Jorgen), Gertow, K. (Karl), Rice, K.M. (Kenneth), Taylor, K.D. (Kent), Dhana, K. (Klodian), Kiemeney, L.A.L.M. (Lambertus A. L. M.), Kao, W.H.L. (Wen), Raffield, L.M. (Laura M.), Launer, L.J. (Lenore), Holdt, L.M. (Lesca), Dörr, M. (Marcus), Kubisch, C. (Christian), Traylor, M. (Matthew), Sitzer, M. (Matthias), Kumari, M. (Meena), Kivimaki, M. (Mika), Nalls, M.A. (Michael), Melander, O. (Olle), Raitakari, O. (Olli), Franco, O.H. (Oscar), Rueda-Ochoa, O.L. (Oscar), Roussos, A. (Alexandra), Whincup, P.H. (Peter), Amouyel, P. (Philippe), Giral, P. (Philippe), Anugu, P. (Pramod), Wong, Q. (Quenna), Malik, R. (Rainer), Rauramaa, R. (Rainer), Burkhardt, R. (Ralph), Hardy, R. (Rebecca), Schmidt, R. (Reinhold), Mutsert, R. (Reneé) de, Strawbridge, R.J. (Rona), Wannamethee, S.G. (Goya), Hägg, S. (Sara), Shah, S. (Sonia), McLachlan, S. (Stela), Trompet, S. (Stella), Seshadri, S. (Sudha), Kurl, S. (Sudhir), Heckbert, S.R. (Susan), Ring, S.M. (Susan), Harris, T.B. (Tamara B.), Lehtimäki, T. (Terho), Galesloot, T.E. (Tessel), Shah, T. (Tina), Faire, U. (Ulf) de, Plagnol, V. (Vincent), Rosamond, W.D. (Wayne), Post, W.S. (Wendy S.), Zhu, X. (Xiaofeng), Zhang, X. (Xiaoling), Guo, X. (Xiuqing), Saba, Y. (Yasaman), Okada, Y. (Yukinori), Mishra, A. (Aniket), Rutten-Jacobs, L. (Loes), Giese, A.-K. (Anne-Katrin), van der Laan, S.W. (Sander W.), Gretarsdottir, S. (Solveig), Anderson, C.D. (Christopher D.), Chong, M. (Michael), Adams, H.H.H. (Hieab), Ago, T. (Tetsuro), Almgren, P. (Peter), Ay, H. (Hakan), Bartz, T.M. (Traci M.), Benavente, O.R. (Oscar R.), Bevan, S. (Steve), Boncoraglio, G. (Giorgio Battista), Brown, R.D. (Robert D.), Butterworth, A.S. (Adam S.), Carrera, C. (Caty), Carty, C.L. (Cara L.), Chasman, D.I. (Daniel), Chen, W-M., Cole, J.W. (John W.), Cotlarciuc, I. (Ioana), Cruchaga, C. (Carlos), Danesh, J. (John), Bakker, P.I.W. (Paul) de, DeStefano, A.L. (Anita), Hoed, M. (Marcel) den, Duan, Q. (Qing), Engelter, S.T. (Stefan), Falcone, G.J. (Guido J.), Gottesman, R.F. (Rebecca), Grewal, R.P. (Raji P.), Gustafsson, S. (Stefan), Haessler, J. (Jeff), Harris, T.B. (Tamara), Hassan, A. (Ahamad), Havulinna, A.S. (Aki), Holliday, E.G. (Elizabeth), Howard, G. (George), Hsu, F.-C. (Fang-Chi), Hyacinth, H.I. (Hyacinth I.), Ikram, M.A. (Arfan), Irvin, M.R. (Marguerite R.), Jian, X. (Xueqiu), Jimenez-Conde, J. (Jordi), Johnson, J.A. (Julie A.), Jukema, J.W. (J. Wouter), Kanai, M. (Masahiro), Keene, K.L. (Keith), Kissela, B.M. (Brett M.), Kleindorfer, D.O. (Dawn O.), Kooperberg, C. (Charles), Kubo, M. (Michiaki), Lange, L.A. (Leslie), Langefeld, C.D. (Carl), Langenberg, C. (Claudia), Lee, J.-M. (Jin-Moo), Lemmens, R. (Robin), Leys, D. (Didier), Lewis, C.M. (Cathryn), Lin, W.-Y. (Wei-Yu), Lindgren, A.G. (Arne G.), Lorentzen, E. (Erik), Magnusson, P.K. (Patrik), Maguire, J.M. (Jane), Manichaikul, A. (Ani), McArdle, P.F. (Patrick), Meschia, J.F. (James F.), Mosley, T.H. (Thomas H.), Ninomiya, T. (Toshiharu), O’Donnell, M.J. (Martin J.), Pulit, S.L. (Sara), Rannikmäe, K. (Kristiina), Reiner, A.P. (Alexander P.), Rexrode, K. (Kathryn), Rich, S.S. (Stephen), Ridker, P.M. (Paul), Rost, N.S. (Natalia), Rothwell, P.M. (Peter), Rundek, T. (Tatjana), Muir, K.W. (Keith), Sakaue, S. (Saori), Sale, M.M. (Michele M.), Salomaa, V. (Veikko), Sapkota, B.R. (Bishwa R.), Schmidt, C.O. (Carsten O.), Sharma, P. (Pankaj), Slowik, A. (Agnieszka), Sudlow, C. (Cathie), Tanislav, C. (Christian), Tatlisumak, T. (Turgut), Thijs, V. (Vincent), Thorleifsson, G. (Gudmar), Thorsteinsdottir, U. (Unnur), Tiedt, S. (Steffen), Walters, M. (Matthew), Wareham, N.J. (Nick), Wassertheil-Smoller, S. (Sylvia), Wiggins, K.L. (Kerri), Yang, Q. (Qiong Fang), Yusuf, S. (Salim), Pastinen, T. (Tomi), Schadt, E.E. (Eric), Koplev, S. (Simon), Codoni, V. (Veronica), Civelek, M. (Mete), Smith, N.L. (Nicholas), Tregouet, D.-A. (David-Alexandre), Christophersen, I.E. (Ingrid E.), Roselli, C. (Carolina), Lubitz, S.A. (Steven A.), Ellinor, P.T. (Patrick), Tai, E.S. (E. Shyong), Kooner, J.S. (Jaspal S.), Kato, N. (Norihiro), He, J. (Jiang), Harst, P. (Pim) van der, Elliott, P. (Paul), Chambers, J.C. (John C.), Takeuchi, F. (Fumihiko), Johnson, A.D. (Andrew), Sanghera, D.K. (Dharambir K.), Jern, C. (Christina), Strbian, D. (Daniel), Fernandez-Cadenas, I. (Israel), Longstreth Jr, W.T., Rolfs, A. (Arndt), Hata, J. (Jun), Woo, D. (Daniel), Rosand, J. (Jonathan), Pare, G. (Guillame), Saleheen, D. (Danish), Zwart, J-A. (John-Anker), Worrall, B.B. (Bradford B.), Kittner, T. (Thomas), Howson, J.M.M. (Joanna M. M.), Kamatani, Y. (Yoichiro), Dehghan, A. (Abbas), Seldenrijk, K.A. (Kees), Morrison, A.C. (Alanna), Hamsten, A. (Anders), Psaty, B.M. (Bruce), Duijn, C.M. (Cornelia) van, Lawlor, D.A. (Debbie), Mook-Kanamori, D.O. (Dennis O.), Bowden, D.W. (Donald), Schmidt, H. (Helena), Wilson, J.F. (James F.), Wilson, J.F. (James), Rotter, J.I. (Jerome I.), Wardlaw, J.M. (J.), Deanfield, J. (John), Halcox, J. (Julian), Lyytikäinen, L.-P. (Leo-Pekka), Loeffler, M. (Markus), Evans, M.K. (Michele), Debette, S. (Stéphanie), Humphries, S.E. (Steve), Völker, U. (Uwe), Gudnason, V. (Vilmundur), Hingorani, A. (Aroon), Björkegren, J.L.M. (Johan L.M.), Casas, J.P. (Juan), Ódonnell, C.J. (Christopher), Morris, R.W. (Richard), Franceschini, N. (Nora), Giambartolomei, C. (Claudia), Vries, P.S. (Paul) de, Finan, C. (Chris), Bis, J.C. (Joshua), Huntley, R.P. (Rachael P.), Lovering, R.C. (Ruth C.), Tajuddin, S.M. (Salman M.), Winkler, T.W. (Thomas W.), Graff, M. (Misa), Kavousi, M. (Maryam), Dale, C. (Caroline), Smith, A.V. (Albert), Hofer, E. (Edith), Leeuwen, E.M. (Elisa) van, Nolte, I.M. (Ilja), Lu, L. (Lingyi), Scholz, M. (Markus), Sargurupremraj, M. (Muralidharan), Pitkanen, N. (Niina), Franzén, O. (Oscar), Joshi, P.K. (Peter), Noordam, R. (Raymond), Marioni, R.E. (Riccardo), Hwang, S.-J. (Shih-Jen), Musani, S.K. (Solomon K.), Schminke, U. (Ulf), Palmas, W. (Walter), Isaacs, A.J. (Aaron), Correa, D.D., Zonderman, A.B., Hofman, A. (Albert), Teumer, A. (Alexander), Cox, A.J. (Amanda J.), Uitterlinden, A.G. (André), Wong, A. (Andrew), Smit, A.J. (Andries), Newman, A.B. (Anne B.), Britton, A.R., Ruusalepp, A. (Arno), Sennblad, B. (Bengt), Hedblad, B. (Bo), Pasaniuc, B. (Bogdan), Penninx, B.W.J.H. (Brenda), Langefeld, C.D. (Carl D.), Wassel, C.L. (Christina), Tzourio, C. (Christophe), Fava, C. (Cristiano), Baldassarre, D. (Damiano), O’Leary, D.H. (Daniel H.), Teupser, D. (Daniel), Kuh, D. (Diana), Tremoli, E. (Elena), Mannarino, E. (Elmo), Grossi, E. (Enzo), Boerwinkle, E.A. (Eric), Schadt, E.E. (Eric E.), Ingelsson, E. (Erik), Veglia, F. (Fabrizio), Rivadeneira Ramirez, F. (Fernando), Beutner, F. (Frank), Chauhan, G. (Ganesh), Heiss, G. (Gerardo), Snieder, H. (Harold), Campbell, H. (Harry), Völzke, H. (Henry), Markus, H.S. (Hugh), Deary, I.J. (Ian), Jukema, J.W. (Jan Wouter), Graaf, J. (Jacqueline) de, Price, J. (Jacqueline), Pott, J. (Janne), Hopewell, J., Liang, J. (Jingjing), Thiery, J.P. (Joachim), Engmann, J. (Jorgen), Gertow, K. (Karl), Rice, K.M. (Kenneth), Taylor, K.D. (Kent), Dhana, K. (Klodian), Kiemeney, L.A.L.M. (Lambertus A. L. M.), Kao, W.H.L. (Wen), Raffield, L.M. (Laura M.), Launer, L.J. (Lenore), Holdt, L.M. (Lesca), Dörr, M. (Marcus), Kubisch, C. (Christian), Traylor, M. (Matthew), Sitzer, M. (Matthias), Kumari, M. (Meena), Kivimaki, M. (Mika), Nalls, M.A. (Michael), Melander, O. (Olle), Raitakari, O. (Olli), Franco, O.H. (Oscar), Rueda-Ochoa, O.L. (Oscar), Roussos, A. (Alexandra), Whincup, P.H. (Peter), Amouyel, P. (Philippe), Giral, P. (Philippe), Anugu, P. (Pramod), Wong, Q. (Quenna), Malik, R. (Rainer), Rauramaa, R. (Rainer), Burkhardt, R. (Ralph), Hardy, R. (Rebecca), Schmidt, R. (Reinhold), Mutsert, R. (Reneé) de, Strawbridge, R.J. (Rona), Wannamethee, S.G. (Goya), Hägg, S. (Sara), Shah, S. (Sonia), McLachlan, S. (Stela), Trompet, S. (Stella), Seshadri, S. (Sudha), Kurl, S. (Sudhir), Heckbert, S.R. (Susan), Ring, S.M. (Susan), Harris, T.B. (Tamara B.), Lehtimäki, T. (Terho), Galesloot, T.E. (Tessel), Shah, T. (Tina), Faire, U. (Ulf) de, Plagnol, V. (Vincent), Rosamond, W.D. (Wayne), Post, W.S. (Wendy S.), Zhu, X. (Xiaofeng), Zhang, X. (Xiaoling), Guo, X. (Xiuqing), Saba, Y. (Yasaman), Okada, Y. (Yukinori), Mishra, A. (Aniket), Rutten-Jacobs, L. (Loes), Giese, A.-K. (Anne-Katrin), van der Laan, S.W. (Sander W.), Gretarsdottir, S. (Solveig), Anderson, C.D. (Christopher D.), Chong, M. (Michael), Adams, H.H.H. (Hieab), Ago, T. (Tetsuro), Almgren, P. (Peter), Ay, H. (Hakan), Bartz, T.M. (Traci M.), Benavente, O.R. (Oscar R.), Bevan, S. (Steve), Boncoraglio, G. (Giorgio Battista), Brown, R.D. (Robert D.), Butterworth, A.S. (Adam S.), Carrera, C. (Caty), Carty, C.L. (Cara L.), Chasman, D.I. (Daniel), Chen, W-M., Cole, J.W. (John W.), Cotlarciuc, I. (Ioana), Cruchaga, C. (Carlos), Danesh, J. (John), Bakker, P.I.W. (Paul) de, DeStefano, A.L. (Anita), Hoed, M. (Marcel) den, Duan, Q. (Qing), Engelter, S.T. (Stefan), Falcone, G.J. (Guido J.), Gottesman, R.F. (Rebecca), Grewal, R.P. (Raji P.), Gustafsson, S. (Stefan), Haessler, J. (Jeff), Harris, T.B. (Tamara), Hassan, A. (Ahamad), Havulinna, A.S. (Aki), Holliday, E.G. (Elizabeth), Howard, G. (George), Hsu, F.-C. (Fang-Chi), Hyacinth, H.I. (Hyacinth I.), Ikram, M.A. (Arfan), Irvin, M.R. (Marguerite R.), Jian, X. (Xueqiu), Jimenez-Conde, J. (Jordi), Johnson, J.A. (Julie A.), Jukema, J.W. (J. Wouter), Kanai, M. (Masahiro), Keene, K.L. (Keith), Kissela, B.M. (Brett M.), Kleindorfer, D.O. (Dawn O.), Kooperberg, C. (Charles), Kubo, M. (Michiaki), Lange, L.A. (Leslie), Langefeld, C.D. (Carl), Langenberg, C. (Claudia), Lee, J.-M. (Jin-Moo), Lemmens, R. (Robin), Leys, D. (Didier), Lewis, C.M. (Cathryn), Lin, W.-Y. (Wei-Yu), Lindgren, A.G. (Arne G.), Lorentzen, E. (Erik), Magnusson, P.K. (Patrik), Maguire, J.M. (Jane), Manichaikul, A. (Ani), McArdle, P.F. (Patrick), Meschia, J.F. (James F.), Mosley, T.H. (Thomas H.), Ninomiya, T. (Toshiharu), O’Donnell, M.J. (Martin J.), Pulit, S.L. (Sara), Rannikmäe, K. (Kristiina), Reiner, A.P. (Alexander P.), Rexrode, K. (Kathryn), Rich, S.S. (Stephen), Ridker, P.M. (Paul), Rost, N.S. (Natalia), Rothwell, P.M. (Peter), Rundek, T. (Tatjana), Muir, K.W. (Keith), Sakaue, S. (Saori), Sale, M.M. (Michele M.), Salomaa, V. (Veikko), Sapkota, B.R. (Bishwa R.), Schmidt, C.O. (Carsten O.), Sharma, P. (Pankaj), Slowik, A. (Agnieszka), Sudlow, C. (Cathie), Tanislav, C. (Christian), Tatlisumak, T. (Turgut), Thijs, V. (Vincent), Thorleifsson, G. (Gudmar), Thorsteinsdottir, U. (Unnur), Tiedt, S. (Steffen), Walters, M. (Matthew), Wareham, N.J. (Nick), Wassertheil-Smoller, S. (Sylvia), Wiggins, K.L. (Kerri), Yang, Q. (Qiong Fang), Yusuf, S. (Salim), Pastinen, T. (Tomi), Schadt, E.E. (Eric), Koplev, S. (Simon), Codoni, V. (Veronica), Civelek, M. (Mete), Smith, N.L. (Nicholas), Tregouet, D.-A. (David-Alexandre), Christophersen, I.E. (Ingrid E.), Roselli, C. (Carolina), Lubitz, S.A. (Steven A.), Ellinor, P.T. (Patrick), Tai, E.S. (E. Shyong), Kooner, J.S. (Jaspal S.), Kato, N. (Norihiro), He, J. (Jiang), Harst, P. (Pim) van der, Elliott, P. (Paul), Chambers, J.C. (John C.), Takeuchi, F. (Fumihiko), Johnson, A.D. (Andrew), Sanghera, D.K. (Dharambir K.), Jern, C. (Christina), Strbian, D. (Daniel), Fernandez-Cadenas, I. (Israel), Longstreth Jr, W.T., Rolfs, A. (Arndt), Hata, J. (Jun), Woo, D. (Daniel), Rosand, J. (Jonathan), Pare, G. (Guillame), Saleheen, D. (Danish), Zwart, J-A. (John-Anker), Worrall, B.B. (Bradford B.), Kittner, T. (Thomas), Howson, J.M.M. (Joanna M. M.), Kamatani, Y. (Yoichiro), Dehghan, A. (Abbas), Seldenrijk, K.A. (Kees), Morrison, A.C. (Alanna), Hamsten, A. (Anders), Psaty, B.M. (Bruce), Duijn, C.M. (Cornelia) van, Lawlor, D.A. (Debbie), Mook-Kanamori, D.O. (Dennis O.), Bowden, D.W. (Donald), Schmidt, H. (Helena), Wilson, J.F. (James F.), Wilson, J.F. (James), Rotter, J.I. (Jerome I.), Wardlaw, J.M. (J.), Deanfield, J. (John), Halcox, J. (Julian), Lyytikäinen, L.-P. (Leo-Pekka), Loeffler, M. (Markus), Evans, M.K. (Michele), Debette, S. (Stéphanie), Humphries, S.E. (Steve), Völker, U. (Uwe), Gudnason, V. (Vilmundur), Hingorani, A. (Aroon), Björkegren, J.L.M. (Johan L.M.), Casas, J.P. (Juan), Ódonnell, C.J. (Christopher), and Morris, R.W. (Richard)
Abstract: Carotid artery intima media thickness (cIMT) and carotid plaque are measures of subclinical atherosclerosis associated with ischemic stroke and coronary heart disease (CHD). Here, we undertake meta-analyses of genome-wide association studies (GWAS) in 71,128 individuals for cIMT, and 48,434 individuals for carotid plaque traits. We identify eight novel susceptibility loci for cIMT, one independent association at the previously-identified PINX1 locus, and one novel locus for carotid plaque. Colocalization analysis with nearby vascular expression quantitative loci (cis-eQTLs) derived from arterial wall and metabolic tissues obtained from patients with CHD identifies candidate genes at two potentially additional loci, ADAMTS9 and LOXL4. LD score regression reveals significant genetic correlations between cIMT and plaque traits, and both cIMT and plaque with CHD, any stroke subtype and ischemic stroke. Our study provides insights into genes and tissue-specific regulatory mechanisms linking atherosclerosis both to its functional genomic origins and its clinical consequences in humans.
Published: 2018
Full Text: View/download PDF

9. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study

Author: Haycock, P.C., Burgess, S., Nounu, A., Zheng, J., Okoli, G.N., Bowden, J., Wade, K.H., Timpson, N.J., Evans, D.M., Willeit, P., Aviv, A., Gaunt, T.R., Hemani, G., Mangino, M., Ellis, H.P., Kurian, K.M., Pooley, K.A., Eeles, R.A., Lee, J.E., Fang, S., Chen, W.V., Law, M.H., Bowdler, L.M., Iles, M.M., Yang, Q., Worrall, B.B., Markus, H.S., Hung, R.J., Amos, C.I., Spurdle, A.B., Thompson, D.J., O'Mara, T.A., Wolpin, B., Amundadottir, L., Stolzenberg-Solomon, R., Trichopoulou, A., Onland-Moret, N.C., Lund, E., Duell, E.J., Canzian, F., Severi, G., Overvad, K., Gunter, M.J., Tumino, R., Svenson, U., Rij, A. van, Baas, A.F., Bown, M.J., Samani, N.J., t'Hof, F.N.G. van, Tromp, G., Jones, G.T., Kuivaniemi, H., Elmore, J.R., Johansson, M., McKay, J., Scelo, G., Carreras-Torres, R., Gaborieau, V., Brennan, P., Bracci, P.M., Neale, R.E., Olson, S.H., Gallinger, S., Li, D., Petersen, G.M., Risch, H.A., Klein, A.P., Han, J., Abnet, C.C., Freedman, N.D., Taylor, P.R., Maris, J.M., Aben, K.K.H., Kiemeney, L.A., Vermeulen, S.H., Wiencke, J.K., Walsh, K.M., Wrensch, M., Rice, T., Turnbull, C., Litchfield, K., Paternoster, L., Standl, M., Abecasis, G.R., SanGiovanni, J.P., Li, Y., Mijatovic, V., Sapkota, Y., Low, S.K., Zondervan, K.T., Montgomery, G.W., Nyholt, D.R., Heel, D.A. van, Hunt, K., Arking, D.E., Ashar, F.N., Sotoodehnia, N., Woo, D., et al., Haycock, P.C., Burgess, S., Nounu, A., Zheng, J., Okoli, G.N., Bowden, J., Wade, K.H., Timpson, N.J., Evans, D.M., Willeit, P., Aviv, A., Gaunt, T.R., Hemani, G., Mangino, M., Ellis, H.P., Kurian, K.M., Pooley, K.A., Eeles, R.A., Lee, J.E., Fang, S., Chen, W.V., Law, M.H., Bowdler, L.M., Iles, M.M., Yang, Q., Worrall, B.B., Markus, H.S., Hung, R.J., Amos, C.I., Spurdle, A.B., Thompson, D.J., O'Mara, T.A., Wolpin, B., Amundadottir, L., Stolzenberg-Solomon, R., Trichopoulou, A., Onland-Moret, N.C., Lund, E., Duell, E.J., Canzian, F., Severi, G., Overvad, K., Gunter, M.J., Tumino, R., Svenson, U., Rij, A. van, Baas, A.F., Bown, M.J., Samani, N.J., t'Hof, F.N.G. van, Tromp, G., Jones, G.T., Kuivaniemi, H., Elmore, J.R., Johansson, M., McKay, J., Scelo, G., Carreras-Torres, R., Gaborieau, V., Brennan, P., Bracci, P.M., Neale, R.E., Olson, S.H., Gallinger, S., Li, D., Petersen, G.M., Risch, H.A., Klein, A.P., Han, J., Abnet, C.C., Freedman, N.D., Taylor, P.R., Maris, J.M., Aben, K.K.H., Kiemeney, L.A., Vermeulen, S.H., Wiencke, J.K., Walsh, K.M., Wrensch, M., Rice, T., Turnbull, C., Litchfield, K., Paternoster, L., Standl, M., Abecasis, G.R., SanGiovanni, J.P., Li, Y., Mijatovic, V., Sapkota, Y., Low, S.K., Zondervan, K.T., Montgomery, G.W., Nyholt, D.R., Heel, D.A. van, Hunt, K., Arking, D.E., Ashar, F.N., Sotoodehnia, N., Woo, D., and et al.
Abstract: Contains fulltext : 174181.pdf (publisher's version ) (Closed access), Importance: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. Objective: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. Data Sources: Genomewide association studies (GWAS) published up to January 15, 2015. Study Selection: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. Data Extraction and Synthesis: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. Main Outcomes and Measures: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. Results: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420081 cases (median cases, 2526 per disease) and 1093105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cance
Published: 2017

10. Association between telomere length and risk of cancer and non-neoplastic diseases a mendelian randomization study

Author: Haycock, P. (Philip), Burgess, S. (Stephen), Nounu, A. (Aayah), Zheng, J. (Jie), Okoli, G.N. (George N.), Bowden, J., Wade, K.H. (Kaitlin Hazel), Timpson, N.J. (Nicholas J.), Evans, D.M. (David M.), Willeit, P. (Peter), Aviv, A. (Abraham), Gaunt, T.R. (Tom), Hemani, G., Mangino, M. (Massimo), Ellis, H.P. (Hayley Patricia), Kurian, K.M. (Kathreena M.), Pooley, K.A. (Karen A.), Eeles, R. (Rosalind), Lee, J.E. (Jeffrey E.), Fang, S. (Shenying), Chen, W.V. (Wei V.), Law, M.H. (Matthew H.), Bowdler, L.M. (Lisa M.), Iles, M.M. (Mark M.), Yang, Q. (Qiong Fang), Worrall, B.B. (Bradford B.), Markus, H.S. (Hugh), Hung, R.J. (Rayjean J.), Amos, W., Spurdle, A.B. (Amanda), Thompson, D. (Deborah), O'Mara, T.A. (Tracy A.), Wolpin, B. (Brian), Amundadottir, L. (Laufey), Stolzenberg-Solomon, R. (Rachael), Trichopoulou, A. (Antonia), Onland-Moret, N.C. (Charlotte), Lund, E. (Eiliv), Duell, E.J. (Eric), Canzian, F. (Federico), Severi, G. (Gianluca), Overvad, K. (Kim), Gunter, M.J. (Marc J.), Tumino, R. (Rosario), Svenson, U. (Ulrika), Rij, A.M. (Andre) van, Baas, A.F. (Annette), Bown, N., Samani, N.J. (Nilesh), Van t'Hof, F.N.G. (Femke N.G.), Tromp, G. (Gerard), Jones, G.T. (Gregory T.), Kuivaniemi, H. (Helena), Elmore, J.R. (James R.), Johansson, M. (Mattias), Mckay, J. (James), Scelo, G. (Ghislaine), Carreras-Torres, R. (Robert), Gaborieau, V. (Valerie), Brennan, P. (Paul), Bracci, P.M. (Paige M.), Neale, R.E. (Rachel E.), Olson, S.H. (Sara H.), Gallinger, S. (Steve), Li, D. (Donghui), Olson, S.H. (Sara), Risch, H. (Harvey), Klein, A.P. (Alison P.), Han, J., Abnet, C.C. (Christian C.), Freedman, N.D. (Neal D.), Taylor, P.R. (Phil R.), Maris, J.M. (John), Aben, K.K.H. (Katja), Kiemeney, L.A.L.M. (Bart), Vermeulen, S.H.H.M. (Sita), Wiencke, J.K. (John K.), Walsh, K.M. (Kyle M.), Wrensch, M. (Margaret), Rice, T. (Terri), Turnbull, C. (Clare), Litchfield, K. (Kevin), Paternoster, L. (Lavinia), Standl, M. (Marie), Abecasis, G.R. (Gonçalo), SanGiovanni, J.P. (John Paul), Li, Y. (Yong), Mijatovic, V. (Vladan), Sapkota, Y. (Yadav), Low, S.-K. (Siew-Kee), Zondervan, K.T. (Krina), Montgomery, G.W. (Grant W.), Nyholt, D.R. (Dale), Heel, D.A. (David) van, Hunt, K. (Karen), Arking, D.E. (Dan), Ashar, F.N. (Foram N.), Sotoodehnia, N. (Nona), Woo, D. (Daniel), Rosand, J. (Jonathan), Comeau, M.E. (Mary E.), Brown, W.M. (W. Mark), Silverman, E. (Edwin), Hokanson, J.E. (John E.), Cho, M.H. (Michael), Hui, J. (Jennie), Ferreira, M.A. (Manuel A.), Thompson, P.J. (Philip J.), Morrison, A.C. (Alanna), Felix, J.F. (Janine F.), Smith, N.L. (Nicholas L.), Christiano, A.M. (Angela), Petukhova, L. (Lynn), Betz, R.C. (Regina), Fan, X. (Xing), Zhang, X. (Xuejun), Zhu, C. (Caihong), Langefeld, C.D. (Carl), Thompson, S.D. (Susan D.), Wang, F. (Feijie), Lin, X. (Xu), Schwartz, D.A. (David A.), Fingerlin, T.E. (Tasha E.), Rotter, J.I. (Jerome I.), Cotch, M.F. (Mary Frances), Jensen, R.A. (Richard A.), Munz, M. (Matthias), Dommisch, H. (Henrik), Schaefer, A. (Antje), Han, F. (Fang), Ollila, H.M., Hillary, R.P. (Ryan P.), Albagha, O.M.E. (Omar M.), Ralston, S.H. (Stuart), Zeng, C. (Chenjie), Zheng, W. (Wei), Shu, X.-O. (Xiao-Ou), Reis, A. (André), Uebe, S. (Steffen), Hüffmeier, U. (Ulrike), Kawamura, Y. (Yoshiya), Otowa, T. (Takeshi), Sasaki, T. (Tsukasa), Hibberd, M.L. (Martin), Davila, S. (Sonia), Xie, G. (Gang), Siminovitch, K.A. (Katherine), Bei, J.-X. (Jin-Xin), Zeng, Y.X., Försti, A. (Asta), Chen, B. (Bowang), Landi, S. (Stefano), Franke, A. (Andre), Fischer, A. (Annegret), Ellinghaus, D. (David), Flores, C. (Carlos), Noth, I. (Imre), Ma, S.-F. (Shwu-Fan), Foo, J.-N. (Jia-Nee), Liu, J. (Jianjun), Kim, J.-W. (Jong-Won), Cox, D.G. (David), Delattre, O. (Olivier), Mirabeau, O. (Olivier), Skibola, C.F. (Christine F.), Tang, C.S. (Clara S.), Garcia-Barcelo, M., Chang, K.-P. (Kai-Ping), Su, W.-H. (Wen-Hui), Chang, Y.-S. (Yu-Sun), Martin, N.G. (Nicholas G.), Gordon, S.D. (Scott D.), Wade, T.D. (Tracey D.), Lee, C. (Chaeyoung), Kubo, M. (Michiaki), Cha, P.-C. (Pei-Chieng), Nakamura, Y. (Yusuke), Levy, D. (Daniel), Kimura, M. (Masayuki), Hwang, S.-J. (Shih-Jen), Hunt, S.C. (Steven), Spector, T.D. (Timothy), Soranzo, N. (Nicole), Manichaikul, A.W. (Ani W.), Barr, R.G. (Graham), Kahali, B. (Bratati), Speliotes, E.K. (Elizabeth), Yerges-Armstrong, L.M. (Laura), Cheng, C-Y. (Ching-Yu), Jonas, J.B. (Jost B.), Wong, T.Y. (Tien Yin), Fogh, I. (Isabella), Lin, K. (Kuang), Powell, J. (John), Rice, K. (Kenneth), Relton, C.L. (Caroline), Martin, R.M. (Richard M.), Smith, A.V. (Davey), Haycock, P. (Philip), Burgess, S. (Stephen), Nounu, A. (Aayah), Zheng, J. (Jie), Okoli, G.N. (George N.), Bowden, J., Wade, K.H. (Kaitlin Hazel), Timpson, N.J. (Nicholas J.), Evans, D.M. (David M.), Willeit, P. (Peter), Aviv, A. (Abraham), Gaunt, T.R. (Tom), Hemani, G., Mangino, M. (Massimo), Ellis, H.P. (Hayley Patricia), Kurian, K.M. (Kathreena M.), Pooley, K.A. (Karen A.), Eeles, R. (Rosalind), Lee, J.E. (Jeffrey E.), Fang, S. (Shenying), Chen, W.V. (Wei V.), Law, M.H. (Matthew H.), Bowdler, L.M. (Lisa M.), Iles, M.M. (Mark M.), Yang, Q. (Qiong Fang), Worrall, B.B. (Bradford B.), Markus, H.S. (Hugh), Hung, R.J. (Rayjean J.), Amos, W., Spurdle, A.B. (Amanda), Thompson, D. (Deborah), O'Mara, T.A. (Tracy A.), Wolpin, B. (Brian), Amundadottir, L. (Laufey), Stolzenberg-Solomon, R. (Rachael), Trichopoulou, A. (Antonia), Onland-Moret, N.C. (Charlotte), Lund, E. (Eiliv), Duell, E.J. (Eric), Canzian, F. (Federico), Severi, G. (Gianluca), Overvad, K. (Kim), Gunter, M.J. (Marc J.), Tumino, R. (Rosario), Svenson, U. (Ulrika), Rij, A.M. (Andre) van, Baas, A.F. (Annette), Bown, N., Samani, N.J. (Nilesh), Van t'Hof, F.N.G. (Femke N.G.), Tromp, G. (Gerard), Jones, G.T. (Gregory T.), Kuivaniemi, H. (Helena), Elmore, J.R. (James R.), Johansson, M. (Mattias), Mckay, J. (James), Scelo, G. (Ghislaine), Carreras-Torres, R. (Robert), Gaborieau, V. (Valerie), Brennan, P. (Paul), Bracci, P.M. (Paige M.), Neale, R.E. (Rachel E.), Olson, S.H. (Sara H.), Gallinger, S. (Steve), Li, D. (Donghui), Olson, S.H. (Sara), Risch, H. (Harvey), Klein, A.P. (Alison P.), Han, J., Abnet, C.C. (Christian C.), Freedman, N.D. (Neal D.), Taylor, P.R. (Phil R.), Maris, J.M. (John), Aben, K.K.H. (Katja), Kiemeney, L.A.L.M. (Bart), Vermeulen, S.H.H.M. (Sita), Wiencke, J.K. (John K.), Walsh, K.M. (Kyle M.), Wrensch, M. (Margaret), Rice, T. (Terri), Turnbull, C. (Clare), Litchfield, K. (Kevin), Paternoster, L. (Lavinia), Standl, M. (Marie), Abecasis, G.R. (Gonçalo), SanGiovanni, J.P. (John Paul), Li, Y. (Yong), Mijatovic, V. (Vladan), Sapkota, Y. (Yadav), Low, S.-K. (Siew-Kee), Zondervan, K.T. (Krina), Montgomery, G.W. (Grant W.), Nyholt, D.R. (Dale), Heel, D.A. (David) van, Hunt, K. (Karen), Arking, D.E. (Dan), Ashar, F.N. (Foram N.), Sotoodehnia, N. (Nona), Woo, D. (Daniel), Rosand, J. (Jonathan), Comeau, M.E. (Mary E.), Brown, W.M. (W. Mark), Silverman, E. (Edwin), Hokanson, J.E. (John E.), Cho, M.H. (Michael), Hui, J. (Jennie), Ferreira, M.A. (Manuel A.), Thompson, P.J. (Philip J.), Morrison, A.C. (Alanna), Felix, J.F. (Janine F.), Smith, N.L. (Nicholas L.), Christiano, A.M. (Angela), Petukhova, L. (Lynn), Betz, R.C. (Regina), Fan, X. (Xing), Zhang, X. (Xuejun), Zhu, C. (Caihong), Langefeld, C.D. (Carl), Thompson, S.D. (Susan D.), Wang, F. (Feijie), Lin, X. (Xu), Schwartz, D.A. (David A.), Fingerlin, T.E. (Tasha E.), Rotter, J.I. (Jerome I.), Cotch, M.F. (Mary Frances), Jensen, R.A. (Richard A.), Munz, M. (Matthias), Dommisch, H. (Henrik), Schaefer, A. (Antje), Han, F. (Fang), Ollila, H.M., Hillary, R.P. (Ryan P.), Albagha, O.M.E. (Omar M.), Ralston, S.H. (Stuart), Zeng, C. (Chenjie), Zheng, W. (Wei), Shu, X.-O. (Xiao-Ou), Reis, A. (André), Uebe, S. (Steffen), Hüffmeier, U. (Ulrike), Kawamura, Y. (Yoshiya), Otowa, T. (Takeshi), Sasaki, T. (Tsukasa), Hibberd, M.L. (Martin), Davila, S. (Sonia), Xie, G. (Gang), Siminovitch, K.A. (Katherine), Bei, J.-X. (Jin-Xin), Zeng, Y.X., Försti, A. (Asta), Chen, B. (Bowang), Landi, S. (Stefano), Franke, A. (Andre), Fischer, A. (Annegret), Ellinghaus, D. (David), Flores, C. (Carlos), Noth, I. (Imre), Ma, S.-F. (Shwu-Fan), Foo, J.-N. (Jia-Nee), Liu, J. (Jianjun), Kim, J.-W. (Jong-Won), Cox, D.G. (David), Delattre, O. (Olivier), Mirabeau, O. (Olivier), Skibola, C.F. (Christine F.), Tang, C.S. (Clara S.), Garcia-Barcelo, M., Chang, K.-P. (Kai-Ping), Su, W.-H. (Wen-Hui), Chang, Y.-S. (Yu-Sun), Martin, N.G. (Nicholas G.), Gordon, S.D. (Scott D.), Wade, T.D. (Tracey D.), Lee, C. (Chaeyoung), Kubo, M. (Michiaki), Cha, P.-C. (Pei-Chieng), Nakamura, Y. (Yusuke), Levy, D. (Daniel), Kimura, M. (Masayuki), Hwang, S.-J. (Shih-Jen), Hunt, S.C. (Steven), Spector, T.D. (Timothy), Soranzo, N. (Nicole), Manichaikul, A.W. (Ani W.), Barr, R.G. (Graham), Kahali, B. (Bratati), Speliotes, E.K. (Elizabeth), Yerges-Armstrong, L.M. (Laura), Cheng, C-Y. (Ching-Yu), Jonas, J.B. (Jost B.), Wong, T.Y. (Tien Yin), Fogh, I. (Isabella), Lin, K. (Kuang), Powell, J. (John), Rice, K. (Kenneth), Relton, C.L. (Caroline), Martin, R.M. (Richard M.), and Smith, A.V. (Davey)
Abstract: IMPORTANCE: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. OBJECTIVE: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. DATA SOURCES: Genomewide association studies (GWAS) published up to January 15, 2015. STUDY SELECTION: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. DATA EXTRACTION AND SYNTHESIS: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. MAIN OUTCOMES AND MEASURES: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. RESULTS: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer ca
Published: 2017
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11. Genetic variation at 16q24.2 is associated with small vessel stroke

Author: Traylor, M. (Matthew), Malik, R. (Rainer), Nalls, M.A. (Michael), Cotlarciuc, I. (Ioana), Radmanesh, F. (Farid), Thorleifsson, G. (Gudmar), Hanscombe, K.B. (Ken B.), Langefeld, C.D. (Carl), Saleheen, D. (Danish), Rost, N.S. (Natalia), Yet, I. (Idil), Spector, T.D. (Timothy), Bell, J.T. (Jordana), Hannon, E. (Eilis), Mill, J. (Jonathan), Chauhan, G. (Ganesh), Debette, S. (Stéphanie), Bis, J.C. (Joshua), Longstreth Jr, W.T., Ikram, M.K. (Kamran), Launer, L.J. (Lenore), Seshadri, S. (Sudha), Hamilton-Bruce, M.A. (Monica Anne), Jimenez-Conde, J. (Jordi), Cole, J.W. (John W.), Schmidt, R. (Reinhold), Slowik, A. (Agnieszka), Lemmens, R. (Robin), Lindgren, A.G. (Arne G.), Melander, O. (Olle), Grewal, R.P. (Raji P.), Sacco, R.L. (Ralph), Rundek, T. (Tatjana), Rexrode, K. (Kathryn), Arnett, D.K. (Donna), Johnson, J.A. (Julie A.), Benavente, O.R. (Oscar R.), Wasssertheil-Smoller, S. (Sylvia), Lee, J.-M. (Jin-Moo), Pulit, S.L. (Sara), Wong, Q. (Quenna), Rich, S.S. (Stephen), Bakker, P.I.W. (Paul) de, McArdle, P.F. (Patrick), Woo, D. (Daniel), Anderson, C.D. (Christopher D.), Xu, H. (Huichun), Heitsch, L. (Laura), Fornage, M. (Myriam), Jern, C. (Christina), Zwart, J-A. (John-Anker), Thorsteinsdottir, U. (Unnur), Gretarsdottir, S. (Solveig), Lewis, C.M. (Cathryn), Sharma, P. (Pankaj), Sudlow, C. (Cathie), Rothwell, P.M. (Peter), Boncoraglio, G. (Giorgio Battista), Thijs, V. (Vincent), Levi, C. (Christopher), Meschia, J.F. (James F.), Rosand, J. (Jonathan), Kittner, T. (Thomas), Mitchell, B.D. (Braxton), Kubisch, C. (Christian), Worrall, B.B. (Bradford B.), Markus, H.S. (Hugh), Traylor, M. (Matthew), Malik, R. (Rainer), Nalls, M.A. (Michael), Cotlarciuc, I. (Ioana), Radmanesh, F. (Farid), Thorleifsson, G. (Gudmar), Hanscombe, K.B. (Ken B.), Langefeld, C.D. (Carl), Saleheen, D. (Danish), Rost, N.S. (Natalia), Yet, I. (Idil), Spector, T.D. (Timothy), Bell, J.T. (Jordana), Hannon, E. (Eilis), Mill, J. (Jonathan), Chauhan, G. (Ganesh), Debette, S. (Stéphanie), Bis, J.C. (Joshua), Longstreth Jr, W.T., Ikram, M.K. (Kamran), Launer, L.J. (Lenore), Seshadri, S. (Sudha), Hamilton-Bruce, M.A. (Monica Anne), Jimenez-Conde, J. (Jordi), Cole, J.W. (John W.), Schmidt, R. (Reinhold), Slowik, A. (Agnieszka), Lemmens, R. (Robin), Lindgren, A.G. (Arne G.), Melander, O. (Olle), Grewal, R.P. (Raji P.), Sacco, R.L. (Ralph), Rundek, T. (Tatjana), Rexrode, K. (Kathryn), Arnett, D.K. (Donna), Johnson, J.A. (Julie A.), Benavente, O.R. (Oscar R.), Wasssertheil-Smoller, S. (Sylvia), Lee, J.-M. (Jin-Moo), Pulit, S.L. (Sara), Wong, Q. (Quenna), Rich, S.S. (Stephen), Bakker, P.I.W. (Paul) de, McArdle, P.F. (Patrick), Woo, D. (Daniel), Anderson, C.D. (Christopher D.), Xu, H. (Huichun), Heitsch, L. (Laura), Fornage, M. (Myriam), Jern, C. (Christina), Zwart, J-A. (John-Anker), Thorsteinsdottir, U. (Unnur), Gretarsdottir, S. (Solveig), Lewis, C.M. (Cathryn), Sharma, P. (Pankaj), Sudlow, C. (Cathie), Rothwell, P.M. (Peter), Boncoraglio, G. (Giorgio Battista), Thijs, V. (Vincent), Levi, C. (Christopher), Meschia, J.F. (James F.), Rosand, J. (Jonathan), Kittner, T. (Thomas), Mitchell, B.D. (Braxton), Kubisch, C. (Christian), Worrall, B.B. (Bradford B.), and Markus, H.S. (Hugh)
Abstract: Objective: Genome-wide association studies (GWAS) have been successful at identifying associations with stroke and stroke subtypes, but have not yet identified any associations solely with small vessel stroke (SVS). SVS comprises one quarter of all ischemic stroke and is a major manifestation of cerebral small vessel disease, the primary cause of vascular cognitive impairment. Studies across neurological traits have shown that younger-onset cases have an increased genetic burden. We leveraged this increased genetic burden by performing an age-at-onset informed GWAS meta-analysis, including a large younger-onset SVS population, to identify novel associations with stroke. Methods: We used a three-stage age-at-onset informed GWAS to identify novel genetic variants associated with stroke. On identifying a novel locus associated with SVS, we assessed its influence on other small vessel disease phenotypes, as well as on messenger RNA (mRNA) expression of nearby genes, and on DNA methylation of nearby CpG sites in whole blood and in the fetal brain. Results: We identified an association with SVS in 4,203 cases and 50,728 controls on chromosome 16q24.2 (odds ratio [OR; 95% confidence interval {CI}] = 1.16 [1.10–1.22]; p = 3.2 × 10−9). The lead single-nucleotide polymorphism (rs12445022) was also associated with cerebral white matter hyperintensities (OR [95% CI] = 1.10 [1.05–1.16]; p = 5.3 × 10−5; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84–1.12]; p = 0.71; 1,545 cases, 1,481 controls). rs12445022 is associated with mRNA expression of ZCCHC14 in arterial tissues (p = 9.4 × 10−7) and DNA methylation at probe cg16596957
Published: 2017
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12. Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N = 112 151) and 24 GWAS consortia

Author: Hagenaars, S.P., Harris, S.E., Davies, G., Hill, W.D., Liewald, D.C.M., Ritchie, S. J., Marioni, R.E., Fawns-Ritchie, C., Cullen, B., Malik, R., Worrall, B.B., Sudlow, C.L.M., Wardlaw, J.M., Gallacher, J., Pell, J., McIntosh, A.M., Smith, D.J., Gale, C.R., and Deary, I.J.
Abstract: The causes of the known associations between poorer cognitive function and many adverse neuropsychiatric outcomes, poorer physical health, and earlier death remain unknown. We used linkage disequilibrium regression and polygenic profile scoring to test for shared genetic aetiology between cognitive functions and neuropsychiatric disorders and physical health. Using information provided by many published genome-wide association study consortia, we created polygenic profile scores for 24 vascular-metabolic, neuropsychiatric, physiological-anthropometric, and cognitive traits in the participants of UK Biobank, a very large population-based sample (N = 112 151). Pleiotropy between cognitive and health traits was quantified by deriving genetic correlations using summary genome-wide association study statistics applied to the method of linkage disequilibrium regression. Substantial and significant genetic correlations were observed between cognitive test scores in the UK Biobank sample and many of the mental and physical health-related traits and disorders assessed here. In addition, highly significant associations were observed between the cognitive test scores in the UK Biobank sample and many polygenic profile scores, including coronary artery disease, stroke, Alzheimer's disease, schizophrenia, autism, major depressive disorder, BMI, intracranial volume, infant head circumference, and childhood cognitive ability. Where disease diagnosis was available for UK Biobank participants we were able to show that these results were not confounded by those who had the relevant disease. These findings indicate that a substantial level of pleiotropy exists between cognitive abilities and many human mental and physical health disorders and traits and that it can be used to predict phenotypic variance across samples.
Published: 2016

13. Low-frequency and common genetic variation in ischemic stroke : the METASTROKE collaboration

Author: Malik, R., Traylor, M., Pulit, S.L., Bevan, S., Hopewell, J.C., Holliday, E.G., Zhao, W., Abrantes, P., Amouyel, P., Attia, J.R., Battey, T.W., Berger, K., Boncoraglio, G.B., Chauhan, G., Cheng, Y.C., Chen, W.M., Clarke, R., Cotlarciuc, I., Debette, S., Falcone, G.J., Ferro, J.M., Gamble, D.M., Ilinca, A., Kittner, S.J., Kourkoulis, C.E., Lemmens, R., Levi, C.R., Lichtner, P., Lindgren, A., Liu, J., Meschia, J.F., Mitchell, B.D., Oliveira, S.A., Pera, J., Reiner, A.P., Rothwell, P.M., Sharma, P., Slowik, A., Sudlow, C.L., Tatlisumak, T., Thijs, V., Vicente, A.M., Woo, D., Seshadri, S., Saleheen, D., Rosand, J., Markus, H.S., Worrall, B.B., Dichgans, M., ISGC Analysis Group, METASTROKE collaboration, Wellcome Trust Case Control Consortium 2 (WTCCC2), and NINDS Stroke Genetics Network (SiGN)
Subjects: 0301 basic medicine, medicine.medical_specialty, Genome-wide association study, Polymorphism, Single Nucleotide, Gastroenterology, Article, Brain Ischemia, Doenças Cardio e Cérebro-vasculares, 03 medical and health sciences, 0302 clinical medicine, Missing heritability problem, Internal medicine, ABO blood group system, Genetic variation, Humans, Medicine, Cooperative Behavior, 1000 Genomes Project, Allele frequency, Stroke, Ischemic Stroke, Genetic association, Genetics, business.industry, Genetic Variation, Correction, medicine.disease, 030104 developmental biology, Case-Control Studies, Ischemic stroke, Cardiology, Neurology (clinical), business, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: Erratum in: Low-frequency and common genetic variation in ischemic stroke: The METASTROKE collaboration. [Neurology. 2016] Objective: To investigate the influence of common and low-frequency genetic variants on the risk of ischemic stroke (all IS) and etiologic stroke subtypes. Methods: We meta-analyzed 12 individual genome-wide association studies comprising 10,307 cases and 19,326 controls imputed to the 1000 Genomes (1 KG) phase I reference panel. We selected variants showing the highest degree of association (p , 1E-5) in the discovery phase for replication in Caucasian (13,435 cases and 29,269 controls) and South Asian (2,385 cases and 5,193 controls) samples followed by a transethnic meta-analysis. We further investigated the p value distribution for different bins of allele frequencies for all IS and stroke subtypes. Results: We showed genome-wide significance for 4 loci: ABO for all IS, HDAC9 for large vessel disease (LVD), and both PITX2 and ZFHX3 for cardioembolic stroke (CE). We further refined the association peaks for ABO and PITX2. Analyzing different allele frequency bins, we showed significant enrichment in low-frequency variants (allele frequency ,5%) for both LVD and small vessel disease, and an enrichment of higher frequency variants (allele frequency 10% and 30%) for CE (all p , 1E-5). Conclusions: Our findings suggest that the missing heritability in IS subtypes can in part be attributed to low-frequency and rare variants. Larger sample sizes are needed to identify the variants associated with all IS and stroke subtypes.
Published: 2016

14. Genome-wide meta-analysis of cerebral white matter hyperintensities in patients with stroke

Author: Traylor, M., Zhang, C.R., Adib-Samii, P., Devan, W.J., Parsons, O.E., Lanfranconi, S., Gregory, S., Cloonan, L., Falcone, G.J., Radmanesh, F., Fitzpatrick, K., Kanakis, A., Barrick, T.R., Moynihan, B., Lewis, C.M., Boncoraglio, G.B., Lemmens, R., Thijs, V., Sudlow, C., Wardlaw, J., Rothwell, P.M., Meschia, J.F., Worrall, B.B., Levi, C., Bevan, S., Furie, K.L., Dichgans, M., Rosand, J., Markus, H.S., Rost, N., and Klijn, C.J.M.
Subjects: Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]
Abstract: Contains fulltext : 169551.pdf (Publisher’s version ) (Open Access) OBJECTIVE: For 3,670 stroke patients from the United Kingdom, United States, Australia, Belgium, and Italy, we performed a genome-wide meta-analysis of white matter hyperintensity volumes (WMHV) on data imputed to the 1000 Genomes reference dataset to provide insights into disease mechanisms. METHODS: We first sought to identify genetic associations with white matter hyperintensities in a stroke population, and then examined whether genetic loci previously linked to WMHV in community populations are also associated in stroke patients. Having established that genetic associations are shared between the 2 populations, we performed a meta-analysis testing which associations with WMHV in stroke-free populations are associated overall when combined with stroke populations. RESULTS: There were no associations at genome-wide significance with WMHV in stroke patients. All previously reported genome-wide significant associations with WMHV in community populations shared direction of effect in stroke patients. In a meta-analysis of the genome-wide significant and suggestive loci (p < 5 x 10(-6)) from community populations (15 single nucleotide polymorphisms in total) and from stroke patients, 6 independent loci were associated with WMHV in both populations. Four of these are novel associations at the genome-wide level (rs72934505 [NBEAL1], p = 2.2 x 10(-8); rs941898 [EVL], p = 4.0 x 10(-8); rs962888 [C1QL1], p = 1.1 x 10(-8); rs9515201 [COL4A2], p = 6.9 x 10(-9)). CONCLUSIONS: Genetic associations with WMHV are shared in otherwise healthy individuals and patients with stroke, indicating common genetic susceptibility in cerebral small vessel disease.
Published: 2016

15. Genetic variants in CETP increase risk of intracerebral hemorrhage

Author: Anderson, C.D., Falcone, G.J., Phuah, C.L., Radmanesh, F., Brouwers, H.B., Battey, T.W., Biffi, A., Peloso, G.M., Liu, D.J., Ayres, A.M., Goldstein, J.N., Viswanathan, A., Greenberg, S.M., Selim, M., Meschia, J.F., Brown, D.L., Worrall, B.B., Silliman, S.L., Tirschwell, D.L., Flaherty, M.L., Kraft, P., Jagiella, J.M., Schmidt, H., Hansen, B.M., Jimenez-Conde, J., Giralt-Steinhauer, E., Elosua, R., Cuadrado-Godia, E., Soriano, C., Nieuwenhuizen, K.M. van, Klijn, C.J.M., Rannikmae, K., Samarasekera, N., Salman, R.A., Sudlow, C.L., Deary, I.J., Morotti, A., Pezzini, A., Pera, J., Urbanik, A., Pichler, A., Enzinger, C., Norrving, B., Montaner, J., Fernandez-Cadenas, I., Delgado, P., Roquer, J., Lindgren, A., Slowik, A., Schmidt, R., Kidwell, C.S., Kittner, S.J., Waddy, S.P., Langefeld, C.D., Abecasis, G., Willer, C.J., Kathiresan, S., Woo, D., Rosand, J., Anderson, C.D., Falcone, G.J., Phuah, C.L., Radmanesh, F., Brouwers, H.B., Battey, T.W., Biffi, A., Peloso, G.M., Liu, D.J., Ayres, A.M., Goldstein, J.N., Viswanathan, A., Greenberg, S.M., Selim, M., Meschia, J.F., Brown, D.L., Worrall, B.B., Silliman, S.L., Tirschwell, D.L., Flaherty, M.L., Kraft, P., Jagiella, J.M., Schmidt, H., Hansen, B.M., Jimenez-Conde, J., Giralt-Steinhauer, E., Elosua, R., Cuadrado-Godia, E., Soriano, C., Nieuwenhuizen, K.M. van, Klijn, C.J.M., Rannikmae, K., Samarasekera, N., Salman, R.A., Sudlow, C.L., Deary, I.J., Morotti, A., Pezzini, A., Pera, J., Urbanik, A., Pichler, A., Enzinger, C., Norrving, B., Montaner, J., Fernandez-Cadenas, I., Delgado, P., Roquer, J., Lindgren, A., Slowik, A., Schmidt, R., Kidwell, C.S., Kittner, S.J., Waddy, S.P., Langefeld, C.D., Abecasis, G., Willer, C.J., Kathiresan, S., Woo, D., and Rosand, J.
Abstract: Contains fulltext : 167830.pdf (Publisher’s version ) (Open Access), OBJECTIVE: In observational epidemiologic studies, higher plasma high-density lipoprotein cholesterol (HDL-C) has been associated with increased risk of intracerebral hemorrhage (ICH). DNA sequence variants that decrease cholesteryl ester transfer protein (CETP) gene activity increase plasma HDL-C; as such, medicines that inhibit CETP and raise HDL-C are in clinical development. Here, we test the hypothesis that CETP DNA sequence variants associated with higher HDL-C also increase risk for ICH. METHODS: We performed 2 candidate-gene analyses of CETP. First, we tested individual CETP variants in a discovery cohort of 1,149 ICH cases and 1,238 controls from 3 studies, followed by replication in 1,625 cases and 1,845 controls from 5 studies. Second, we constructed a genetic risk score comprised of 7 independent variants at the CETP locus and tested this score for association with HDL-C as well as ICH risk. RESULTS: Twelve variants within CETP demonstrated nominal association with ICH, with the strongest association at the rs173539 locus (odds ratio [OR] = 1.25, standard error [SE] = 0.06, p = 6.0 x 10-4 ) with no heterogeneity across studies (I2 = 0%). This association was replicated in patients of European ancestry (p = 0.03). A genetic score of CETP variants found to increase HDL-C by approximately 2.85mg/dl in the Global Lipids Genetics Consortium was strongly associated with ICH risk (OR = 1.86, SE = 0.13, p = 1.39 x 10-6 ). INTERPRETATION: Genetic variants in CETP associated with increased HDL-C raise the risk of ICH. Given ongoing therapeutic development in CETP inhibition and other HDL-raising strategies, further exploration of potential adverse cerebrovascular outcomes may be warranted. Ann Neurol 2016;80:730-740.
Published: 2016

16. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study

Author: Laan, S.W. van der, Fall, T., Soumare, A., Teumer, A., Sedaghat, S., Baumert, J., Zabaneh, D., Setten, J. van, Isgum, I., Galesloot, T.E., Arpegard, J., Amouyel, P., Trompet, S., Waldenberger, M., Dorr, M., Magnusson, P.K., Giedraitis, V., Larsson, A., Morris, A.P., Felix, J.F., Morrison, A.C., Franceschini, N., Bis, J.C., Kavousi, M., O'Donnell, C., Drenos, F., Tragante, V., Munroe, P.B., Malik, R., Dichgans, M., Worrall, B.B., Erdmann, J., Nelson, C.P., Samani, N.J., Schunkert, H., Marchini, J., Patel, R.S., Hingorani, A.D., Lind, L., Pedersen, N.L., Graaf, J. de, Kiemeney, L.A.L.M., Baumeister, S.E., Franco, O.H., Hofman, A., Uitterlinden, A.G., Koenig, W., Meisinger, C., Peters, A., Thorand, B., Jukema, J.W., Eriksen, B.O., Toft, I., Wilsgaard, T., Onland-Moret, N.C., Schouw, Y.T. van der, Debette, S., Kumari, M., Svensson, P., Harst, P. van der, Kivimäki, M., Keating, B.J., Sattar, N., Dehghan, A., Reiner, A.P., Ingelsson, E., Ruijter, H.M. Den, Bakker, P.I. de, Pasterkamp, G., Arnlov, J., Holmes, M.V., Asselbergs, F.W., Laan, S.W. van der, Fall, T., Soumare, A., Teumer, A., Sedaghat, S., Baumert, J., Zabaneh, D., Setten, J. van, Isgum, I., Galesloot, T.E., Arpegard, J., Amouyel, P., Trompet, S., Waldenberger, M., Dorr, M., Magnusson, P.K., Giedraitis, V., Larsson, A., Morris, A.P., Felix, J.F., Morrison, A.C., Franceschini, N., Bis, J.C., Kavousi, M., O'Donnell, C., Drenos, F., Tragante, V., Munroe, P.B., Malik, R., Dichgans, M., Worrall, B.B., Erdmann, J., Nelson, C.P., Samani, N.J., Schunkert, H., Marchini, J., Patel, R.S., Hingorani, A.D., Lind, L., Pedersen, N.L., Graaf, J. de, Kiemeney, L.A.L.M., Baumeister, S.E., Franco, O.H., Hofman, A., Uitterlinden, A.G., Koenig, W., Meisinger, C., Peters, A., Thorand, B., Jukema, J.W., Eriksen, B.O., Toft, I., Wilsgaard, T., Onland-Moret, N.C., Schouw, Y.T. van der, Debette, S., Kumari, M., Svensson, P., Harst, P. van der, Kivimäki, M., Keating, B.J., Sattar, N., Dehghan, A., Reiner, A.P., Ingelsson, E., Ruijter, H.M. Den, Bakker, P.I. de, Pasterkamp, G., Arnlov, J., Holmes, M.V., and Asselbergs, F.W.
Abstract: Contains fulltext : 172252.pdf (Publisher’s version ) (Open Access), BACKGROUND: Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. OBJECTIVES: The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. METHODS: We incorporated participant data from 16 prospective cohorts (n = 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n = 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. RESULTS: Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p = 2.12 x 10(-14)). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p = 5.95 x 10(-211)), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p = 0.994), which was statistically different from the observational estimate (p = 1.6 x 10(-5)). A causal effect of cystatin C was not detected for any individual component of CVD. CONCLUSIONS: Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD.
Published: 2016

17. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study

Author: Van Der Laan, S.W. (Sander W.), Fall, M. (Magnus), Soumaré, A. (Aicha), Teumer, A. (Alexander), Sedaghat, S. (Sanaz), Baumert, J. (Jens), Zabaneh, D. (Delilah), Setten, J. (Jessica) van, Isgum, I. (Ivana), Galesloot, T.E. (Tessel), Arpegård, J. (Johannes), Amouyel, P. (Philippe), Trompet, S. (Stella), Waldenberger, M. (Melanie), Dörr, M. (Marcus), Magnusson, P.K. (Patrik), Giedraitis, V. (Vilmantas), Larsson, A. (Anders), Morris, A.P. (Andrew), Felix, J.F. (Janine), Morrison, A.C. (Alanna C.), Franceschini, N. (Nora), Bis, J.C. (Joshua), Kavousi, M. (Maryam), O'Donnell, C.J. (Christopher), Drenos, F. (Fotios), Tragante, V. (Vinicius), Munroe, P. (Patricia), Malik, R. (Rainer), Kubisch, C. (Christian), Worrall, B.B. (Bradford B.), Erdmann, J. (Jeanette), Nelson, C.P. (Christopher P.), Samani, N.J. (Nilesh), Schunkert, H. (Heribert), Marchini, J. (Jonathan), Patel, R.S. (Riyaz), Hingorani, A. (Aroon), Kao, W.H.L. (Wen), Pedersen, N.L. (Nancy), Graaf, J. (Jacqueline) de, Kiemeney, L.A.L.M. (Bart), Baumeister, S.E. (Sebastian), Franco, O.H. (Oscar), Hofman, A. (Albert), Uitterlinden, A.G. (André), Koenig, W. (Wolfgang), Meisinger, C. (Christa), Peters, A. (Annette), Thorand, B. (Barbara), Jukema, J.W. (Jan Wouter), Eriksen, B.O. (Bjørn Odvar), Toft, I. (Ingrid), Wilsgaard, T. (Tom), Onland-Moret, N.C. (N. Charlotte), Schouw, Y.T. (Yvonne) van der, Debette, S. (Stéphanie), Kumari, M. (Meena), Svensson, P. (Per), van der Harst, P. (Pim), Kivimaki, M. (Mika), Keating, J. (John), Sattar, N. (Naveed), Dehghan, A. (Abbas), Reiner, A. (Alexander), Ingelsson, E. (Erik), Ruijter, H.M. (Hester ) den, Bakker, P.I.W. (Paul) de, Pasterkamp, G. (Gerard), Ärnlöv, J. (Johan), Holmes, M.V. (Michael), Asselbergs, F.W. (Folkert), Van Der Laan, S.W. (Sander W.), Fall, M. (Magnus), Soumaré, A. (Aicha), Teumer, A. (Alexander), Sedaghat, S. (Sanaz), Baumert, J. (Jens), Zabaneh, D. (Delilah), Setten, J. (Jessica) van, Isgum, I. (Ivana), Galesloot, T.E. (Tessel), Arpegård, J. (Johannes), Amouyel, P. (Philippe), Trompet, S. (Stella), Waldenberger, M. (Melanie), Dörr, M. (Marcus), Magnusson, P.K. (Patrik), Giedraitis, V. (Vilmantas), Larsson, A. (Anders), Morris, A.P. (Andrew), Felix, J.F. (Janine), Morrison, A.C. (Alanna C.), Franceschini, N. (Nora), Bis, J.C. (Joshua), Kavousi, M. (Maryam), O'Donnell, C.J. (Christopher), Drenos, F. (Fotios), Tragante, V. (Vinicius), Munroe, P. (Patricia), Malik, R. (Rainer), Kubisch, C. (Christian), Worrall, B.B. (Bradford B.), Erdmann, J. (Jeanette), Nelson, C.P. (Christopher P.), Samani, N.J. (Nilesh), Schunkert, H. (Heribert), Marchini, J. (Jonathan), Patel, R.S. (Riyaz), Hingorani, A. (Aroon), Kao, W.H.L. (Wen), Pedersen, N.L. (Nancy), Graaf, J. (Jacqueline) de, Kiemeney, L.A.L.M. (Bart), Baumeister, S.E. (Sebastian), Franco, O.H. (Oscar), Hofman, A. (Albert), Uitterlinden, A.G. (André), Koenig, W. (Wolfgang), Meisinger, C. (Christa), Peters, A. (Annette), Thorand, B. (Barbara), Jukema, J.W. (Jan Wouter), Eriksen, B.O. (Bjørn Odvar), Toft, I. (Ingrid), Wilsgaard, T. (Tom), Onland-Moret, N.C. (N. Charlotte), Schouw, Y.T. (Yvonne) van der, Debette, S. (Stéphanie), Kumari, M. (Meena), Svensson, P. (Per), van der Harst, P. (Pim), Kivimaki, M. (Mika), Keating, J. (John), Sattar, N. (Naveed), Dehghan, A. (Abbas), Reiner, A. (Alexander), Ingelsson, E. (Erik), Ruijter, H.M. (Hester ) den, Bakker, P.I.W. (Paul) de, Pasterkamp, G. (Gerard), Ärnlöv, J. (Johan), Holmes, M.V. (Michael), and Asselbergs, F.W. (Folkert)
Abstract: __Background__ Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. __Objectives__ The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. __Methods__ We incorporated participant data from 16 prospective cohorts (n = 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n = 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. __Results__ Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p = 2.12 × 10−14). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p = 5.95 × 10−211), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p = 0.994), which was statistically different from the observational estimate (p = 1.6 × 10−5). A causal effect of cystatin C was not detected for any individual component of CVD. __Conclusions__ Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD.
Published: 2016
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18. Genome-Wide Association Analysis of Young-Onset Stroke Identifies a Locus on Chromosome 10q25 Near HABP2

Author: Cheng, Y.-C. (Yu-Ching), Stanne, T.M. (Tara M.), Giese, A.-K. (Anne-Katrin), Ho, W.K. (Weang K.), Traylor, M. (Matthew), Amouyel, P. (Philippe), Holliday, E.G. (Elizabeth), Malik, R. (Rainer), Xu, H. (Huichun), Kittner, T. (Thomas), Cole, J.W. (John W.), O´Connell, J.R., Danesh, J. (John), Rasheed, A. (Asif), Zhao, W. (Wei), Engelter, S.T. (Stefan), Grond-Ginsbach, C. (Caspar), Kamatani, Y. (Yoichiro), Lathrop, M. (Mark), Leys, D. (Didier), Thijs, V. (Vincent), Metso, T.M. (Tiina M.), Tatlisumak, T. (Turgut), Pezzini, A. (Alessandro), Parati, E.A. (Eugenio A.), Norrving, B. (Bo), Bevan, S. (Steve), Rothwell, P.M. (Peter), Sudlow, C. (Cathie), Slowik, A. (Agnieszka), Lindgren, A.G. (Arne G.), Walters, M. (Matthew), Jannes, J. (Jim), Shen, J. (Jess), Crosslin, D.R. (David), Doheny, K.F. (Kimberly), Laurie, C.C. (Cathy), Kanse, S.M. (Sandip ), Bis, J.C. (Joshua), Fornage, M. (Myriam), Mosley, T.H. (Thomas H.), Hopewell, J., Strauch, K. (Konstantin), Müller-Nurasyid, M. (Martina), Gieger, C. (Christian), Waldenberger, M. (Melanie), Peters, A. (Annette), Meisinger, C. (Christine), Ikram, M.A. (Arfan), Longstreth Jr, W.T., Meschia, J.F. (James F.), Seshadri, S. (Sudha), Sharma, P. (Pankaj), Worrall, B.B. (Bradford B.), Jern, C. (Christina), Levi, C. (Christopher), Kubisch, C. (Christian), Boncoraglio, G. (Giorgio Battista), Markus, H.S. (Hugh), Debette, S. (Stéphanie), Rolfs, A. (Arndt), Saleheen, D., Mitchell, B.D. (Braxton), Cheng, Y.-C. (Yu-Ching), Stanne, T.M. (Tara M.), Giese, A.-K. (Anne-Katrin), Ho, W.K. (Weang K.), Traylor, M. (Matthew), Amouyel, P. (Philippe), Holliday, E.G. (Elizabeth), Malik, R. (Rainer), Xu, H. (Huichun), Kittner, T. (Thomas), Cole, J.W. (John W.), O´Connell, J.R., Danesh, J. (John), Rasheed, A. (Asif), Zhao, W. (Wei), Engelter, S.T. (Stefan), Grond-Ginsbach, C. (Caspar), Kamatani, Y. (Yoichiro), Lathrop, M. (Mark), Leys, D. (Didier), Thijs, V. (Vincent), Metso, T.M. (Tiina M.), Tatlisumak, T. (Turgut), Pezzini, A. (Alessandro), Parati, E.A. (Eugenio A.), Norrving, B. (Bo), Bevan, S. (Steve), Rothwell, P.M. (Peter), Sudlow, C. (Cathie), Slowik, A. (Agnieszka), Lindgren, A.G. (Arne G.), Walters, M. (Matthew), Jannes, J. (Jim), Shen, J. (Jess), Crosslin, D.R. (David), Doheny, K.F. (Kimberly), Laurie, C.C. (Cathy), Kanse, S.M. (Sandip ), Bis, J.C. (Joshua), Fornage, M. (Myriam), Mosley, T.H. (Thomas H.), Hopewell, J., Strauch, K. (Konstantin), Müller-Nurasyid, M. (Martina), Gieger, C. (Christian), Waldenberger, M. (Melanie), Peters, A. (Annette), Meisinger, C. (Christine), Ikram, M.A. (Arfan), Longstreth Jr, W.T., Meschia, J.F. (James F.), Seshadri, S. (Sudha), Sharma, P. (Pankaj), Worrall, B.B. (Bradford B.), Jern, C. (Christina), Levi, C. (Christopher), Kubisch, C. (Christian), Boncoraglio, G. (Giorgio Battista), Markus, H.S. (Hugh), Debette, S. (Stéphanie), Rolfs, A. (Arndt), Saleheen, D., and Mitchell, B.D. (Braxton)
Abstract: Background and Purpose - Although a genetic contribution to ischemic stroke is well recognized, only a handful of stroke loci have been identified by large-scale genetic association studies to date. Hypothesizing that genetic effects might be stronger for early-versus late-onset str
Published: 2016
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19. The development of algorithms to assess family health history in a web based application - HealthHeritage

Author: Pelletier, S.L., Worrall, B.B., Harrison, M.B., Miesfeldt, S. Tucker, A.L., Kelly, T.E., Schnatterly, P., Einbinder, J., Reitmeyer, M., Cohn, W.F., and Knaus, W.A.
Subjects: Genetic research -- Analysis, Human genetics -- Research, Family -- Health aspects, Biological sciences
Published: 2000

20. Common variation in PHACTR1 is associated with susceptibility to cervical artery dissection

Author: Debette, S., Kamatani, Y., Metso, T.M., Kloss, M., Chauhan, G., Engelter, S.T., Pezzini, S, Thijs, V., Markus, H.S., Dichgans, M., Wolf, C., Dittrich, R., Touze, E., Southerland, A.M., Samson, Y., Abboud, S., Bejot, Y., Caso, V., Bersano, A., Gschwendtner, A., Sessa, M., Cole, J., Lamy, C., Medeiros, E., Beretta, S., Bonati, L.H., Grau, A.J., Michel, P., Majersik, J.J., Sharma, P., Kalashnikova, L., Nazarova, M., Dobrynina, L., Bartels, E., Guillon, B., Herik, E.G. van den, Fernandez-Cadenas, I., Jood, K., Nalls, M.A., Leeuw, H.F. de, Jern, C., Cheng, Y.C., Werner, I., Metso, A.J., Lichy, C., Lyrer, P.A., Brandt, T., Boncoraglio, G.B., Wichmann, H.E., Gieger, C., Johnson, A.D., Bottcher, T., Castellano, M., Arveiler, D., Ikram, M.A., Breteler, M.M., Padovani, A., Meschia, J.F., Kuhlenbaumer, G., Rolfs, A., Worrall, B.B., Ringelstein, E.B., Zelenika, D., Tatlisumak, T., Lathrop, M., Leys, D., Amouyel, P., Dallongeville, J., Debette, S., Kamatani, Y., Metso, T.M., Kloss, M., Chauhan, G., Engelter, S.T., Pezzini, S, Thijs, V., Markus, H.S., Dichgans, M., Wolf, C., Dittrich, R., Touze, E., Southerland, A.M., Samson, Y., Abboud, S., Bejot, Y., Caso, V., Bersano, A., Gschwendtner, A., Sessa, M., Cole, J., Lamy, C., Medeiros, E., Beretta, S., Bonati, L.H., Grau, A.J., Michel, P., Majersik, J.J., Sharma, P., Kalashnikova, L., Nazarova, M., Dobrynina, L., Bartels, E., Guillon, B., Herik, E.G. van den, Fernandez-Cadenas, I., Jood, K., Nalls, M.A., Leeuw, H.F. de, Jern, C., Cheng, Y.C., Werner, I., Metso, A.J., Lichy, C., Lyrer, P.A., Brandt, T., Boncoraglio, G.B., Wichmann, H.E., Gieger, C., Johnson, A.D., Bottcher, T., Castellano, M., Arveiler, D., Ikram, M.A., Breteler, M.M., Padovani, A., Meschia, J.F., Kuhlenbaumer, G., Rolfs, A., Worrall, B.B., Ringelstein, E.B., Zelenika, D., Tatlisumak, T., Lathrop, M., Leys, D., Amouyel, P., and Dallongeville, J.
Abstract: Item does not contain fulltext, Cervical artery dissection (CeAD), a mural hematoma in a carotid or vertebral artery, is a major cause of ischemic stroke in young adults although relatively uncommon in the general population (incidence of 2.6/100,000 per year). Minor cervical traumas, infection, migraine and hypertension are putative risk factors, and inverse associations with obesity and hypercholesterolemia are described. No confirmed genetic susceptibility factors have been identified using candidate gene approaches. We performed genome-wide association studies (GWAS) in 1,393 CeAD cases and 14,416 controls. The rs9349379[G] allele (PHACTR1) was associated with lower CeAD risk (odds ratio (OR) = 0.75, 95% confidence interval (CI) = 0.69-0.82; P = 4.46 x 10(-10)), with confirmation in independent follow-up samples (659 CeAD cases and 2,648 controls; P = 3.91 x 10(-3); combined P = 1.00 x 10(-11)). The rs9349379[G] allele was previously shown to be associated with lower risk of migraine and increased risk of myocardial infarction. Deciphering the mechanisms underlying this pleiotropy might provide important information on the biological underpinnings of these disabling conditions.
Published: 2015

21. No additional prognostic value of genetic information in the prediction of vascular events after cerebral ischemia of arterial origin

Author: Achterberg, S. (Sefanja), Kappelle, L.J. (Jaap), Bakker, P.I.W. (Paul) de, Traylor, M. (Matthew), Algra, A. (Ale), Graaf, Y. (Yolanda) van der, Grobbee, D.E. (Diederick), Rutten, G.E.H.M. (Guy), Visseren, F.L.J. (Frank), Moll, F.L. (Frans), Mali, W.P. (Willem), Doevendans, P.A. (Pieter), Martin, F. (Farrall), Holliday, E.G. (Elizabeth), Sudlow, C. (Cathie), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Fornage, M. (Myriam), Ikram, M.K. (Kamran), Malik, R. (Rainer), Bevan, S. (Steve), Thorsteinsdottir, U. (Unnur), DeStefano, A.L. (Anita), Worrall, B.B. (Bradford B.), Reiner, A. (Alexander), Mitchell, B.D. (Braxton), Clarke, R. (Robert), Levi, C. (Christopher), Seshadri, S. (Sudha), Boncoraglio, G. (Giorgio Battista), Sharma, P. (Pankaj), Bis, J.C. (Joshua), Gretarsdottir, S. (Solveig), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Rosand, J. (Jonathan), Meschia, J.F. (James F.), Stefansson, K. (Kari), Kubisch, C. (Christian), Markus, H.S. (Hugh), Achterberg, S. (Sefanja), Kappelle, L.J. (Jaap), Bakker, P.I.W. (Paul) de, Traylor, M. (Matthew), Algra, A. (Ale), Graaf, Y. (Yolanda) van der, Grobbee, D.E. (Diederick), Rutten, G.E.H.M. (Guy), Visseren, F.L.J. (Frank), Moll, F.L. (Frans), Mali, W.P. (Willem), Doevendans, P.A. (Pieter), Martin, F. (Farrall), Holliday, E.G. (Elizabeth), Sudlow, C. (Cathie), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Fornage, M. (Myriam), Ikram, M.K. (Kamran), Malik, R. (Rainer), Bevan, S. (Steve), Thorsteinsdottir, U. (Unnur), DeStefano, A.L. (Anita), Worrall, B.B. (Bradford B.), Reiner, A. (Alexander), Mitchell, B.D. (Braxton), Clarke, R. (Robert), Levi, C. (Christopher), Seshadri, S. (Sudha), Boncoraglio, G. (Giorgio Battista), Sharma, P. (Pankaj), Bis, J.C. (Joshua), Gretarsdottir, S. (Solveig), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Rosand, J. (Jonathan), Meschia, J.F. (James F.), Stefansson, K. (Kari), Kubisch, C. (Christian), and Markus, H.S. (Hugh)
Abstract: Background: Patients who have suffered from cerebral ischemia have a high risk of recurrent vascular events. Predictive models based on classical risk factors typically have limited prognostic value. Given that cerebral ischemia has a heritable component, genetic information might improve performance of these risk models. Our aim was to develop and compare two models: one containing traditional vascular risk factors, the other also including genetic information. Methods and Results: We studied 1020 patients with cerebral ischemia and genotyped them with the Illumina Immunochip. Median follow-up time was 6.5 years; the annual incidence of new ischemic events (primary outcome, n=198) was 3.0%. The prognostic model based on classical vascular risk factors had an area under the receiver operating characteristics curve (AUC-ROC) of 0.65 (95% confidence interval 0.61-0.69). When we added a genetic risk score based on prioritized SNPs from a genome-wide association study of ischemic stroke (using summary statistics from the METASTROKE study which included 12389 cases and 62004 controls), the AUC-ROC remained the same. Similar results were found for the secondary outcome ischemic stroke. Conclusions: We found no additional value of genetic information in a prognostic model for the risk of ischemic events in patients with cerebral ischemia of arterial origin. This is consistent with a complex, polygenic architecture, where many genes of weak effect likely act in concert to influence the heritable risk of an individual to develop (recurrent) vascular events. At present, genetic information cannot help clinicians to distinguish patients at high risk for recurrent vascular events.
Published: 2015
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22. Genetic overlap between diagnostic subtypes of ischemic stroke

Author: Holliday, E.G. (Elizabeth), Traylor, M. (Matthew), Malik, R. (Rainer), Bevan, S. (Steve), Falcone, G.J. (Guido J.), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Cotlarciuc, I. (Ioana), Bis, J.C. (Joshua), Boerwinkle, E.A. (Eric), Boncoraglio, G. (Giorgio Battista), Clarke, R. (Robert), Cole, J.W. (John W.), Fornage, M. (Myriam), Furie, K.L. (Karen), Ikram, M.A. (Arfan), Jannes, J. (Jim), Kittner, T. (Thomas), Lincz, L.F. (Lisa), Maguire, J.M. (Jane), Meschia, J.F. (James F.), Mosley, T.H. (Thomas H.), Nalls, M.A. (Michael), Oldmeadow, C. (Christopher), Parati, E.A. (Eugenio A.), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Seshadri, S. (Sudha), Scott, R.J. (Rodney J.), Sharma, P. (Pankaj), Sudlow, C. (Cathie), Wiggins, K.L. (Kerri), Worrall, B.B. (Bradford B.), Rosand, J. (Jonathan), Mitchell, B.D. (Braxton), Kubisch, C. (Christian), Markus, H.S. (Hugh), Levi, C. (Christopher), Attia, J. (John), Wray, N.R. (Naomi), Holliday, E.G. (Elizabeth), Traylor, M. (Matthew), Malik, R. (Rainer), Bevan, S. (Steve), Falcone, G.J. (Guido J.), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Cotlarciuc, I. (Ioana), Bis, J.C. (Joshua), Boerwinkle, E.A. (Eric), Boncoraglio, G. (Giorgio Battista), Clarke, R. (Robert), Cole, J.W. (John W.), Fornage, M. (Myriam), Furie, K.L. (Karen), Ikram, M.A. (Arfan), Jannes, J. (Jim), Kittner, T. (Thomas), Lincz, L.F. (Lisa), Maguire, J.M. (Jane), Meschia, J.F. (James F.), Mosley, T.H. (Thomas H.), Nalls, M.A. (Michael), Oldmeadow, C. (Christopher), Parati, E.A. (Eugenio A.), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Seshadri, S. (Sudha), Scott, R.J. (Rodney J.), Sharma, P. (Pankaj), Sudlow, C. (Cathie), Wiggins, K.L. (Kerri), Worrall, B.B. (Bradford B.), Rosand, J. (Jonathan), Mitchell, B.D. (Braxton), Kubisch, C. (Christian), Markus, H.S. (Hugh), Levi, C. (Christopher), Attia, J. (John), and Wray, N.R. (Naomi)
Abstract: Background and Purpose: Despite moderate heritability, the phenotypic heterogeneity of ischemic stroke has hampered gene discovery, motivating analyses of diagnostic subtypes with reduced sample sizes. We assessed evidence for a shared genetic basis among the 3 major subtypes: large artery atherosclerosis (LAA), cardioembolism, and small vessel disease (SVD), to inform potential cross-subtype analyses. Methods: Analyses used genome-wide summary data for 12 389 ischemic stroke cases (including 2167 LAA, 2405 cardioembolism, and 1854 SVD) and 62 004 controls from the Metastroke consortium. For 4561 cases and 7094 controls, individual-level genotype data were also available. Genetic correlations between subtypes were estimated using linear mixed models and polygenic profile scores. Meta-analysis of a combined LAA-SVD phenotype (4021 cases and 51 976 controls) was performed to identify shared risk alleles. Results: High genetic correlation was identified between LAA and SVD using linear mixed models (rg=0.96, SE=0.47, P=9×10-4) and profile scores (rg=0.72; 95% confide
Published: 2015
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23. Genome-wide association study of intracranial aneurysm identifies a new association on chromosome 7

Author: Foroud, T., Lai, D., Koller, D., Hof, F. Van't, Kurki, M.I., Anderson, C.S., Brown, R.D., Jr., Connolly, E.S., Jr., Eriksson, J.G., Flaherty, M., Fornage, M., Fraunberg, M. von Und Zu, Gaal, E.I., Laakso, A., Hernesniemi, J., Huston, J., Jaaskelainen, J.E., Kiemeney, L.A.L.M., Kivisaari, R., Kleindorfer, D., Ko, N., Lehto, H., Mackey, J., Meissner, I., Moomaw, C.J., Mosley, T.H., Moskala, M., Niemela, M., Palotie, A., Pera, J., Rinkel, G., Ripke, S., Rouleau, G., Ruigrok, Y., Sauerbeck, L., Slowik, A., Vermeulen, S., Woo, D., Worrall, B.B., Broderick, J., et al., Foroud, T., Lai, D., Koller, D., Hof, F. Van't, Kurki, M.I., Anderson, C.S., Brown, R.D., Jr., Connolly, E.S., Jr., Eriksson, J.G., Flaherty, M., Fornage, M., Fraunberg, M. von Und Zu, Gaal, E.I., Laakso, A., Hernesniemi, J., Huston, J., Jaaskelainen, J.E., Kiemeney, L.A.L.M., Kivisaari, R., Kleindorfer, D., Ko, N., Lehto, H., Mackey, J., Meissner, I., Moomaw, C.J., Mosley, T.H., Moskala, M., Niemela, M., Palotie, A., Pera, J., Rinkel, G., Ripke, S., Rouleau, G., Ruigrok, Y., Sauerbeck, L., Slowik, A., Vermeulen, S., Woo, D., Worrall, B.B., Broderick, J., and et al.
Abstract: Item does not contain fulltext, BACKGROUND AND PURPOSE: Common variants have been identified using genome-wide association studies which contribute to intracranial aneurysms (IA) susceptibility. However, it is clear that the variants identified to date do not account for the estimated genetic contribution to disease risk. METHODS: Initial analysis was performed in a discovery sample of 2617 IA cases and 2548 controls of white ancestry. Novel chromosomal regions meeting genome-wide significance were further tested for association in 2 independent replication samples: Dutch (717 cases; 3004 controls) and Finnish (799 cases; 2317 controls). A meta-analysis was performed to combine the results from the 3 studies for key chromosomal regions of interest. RESULTS: Genome-wide evidence of association was detected in the discovery sample on chromosome 9 (CDKN2BAS; rs10733376: P<1.0x10(-11)), in a gene previously associated with IA. A novel region on chromosome 7, near HDAC9, was associated with IA (rs10230207; P=4.14x10(-8)). This association replicated in the Dutch sample (P=0.01) but failed to show association in the Finnish sample (P=0.25). Meta-analysis results of the 3 cohorts reached statistical significant (P=9.91x10(-10)). CONCLUSIONS: We detected a novel region associated with IA susceptibility that was replicated in an independent Dutch sample. This region on chromosome 7 has been previously associated with ischemic stroke and the large vessel stroke occlusive subtype (including HDAC9), suggesting a possible genetic link between this stroke subtype and IA.
Published: 2014

24. Effect of genetic variants associated with plasma homocysteine levels on stroke risk

Author: Cotlarciuc, I. (Ioana), Malik, R. (Rainer), Holliday, E.G. (Elizabeth), Ahmadi, K.R. (Kourosh), Paré, G. (Guillaume), Psaty, B.M. (Bruce), Fornage, M. (Myriam), Hasan, N. (Nazeeha), Rinne, P.E. (Paul), Ikram, M.A. (Arfan), Markus, H.S. (Hugh), Rosand, J. (Jonathan), Mitchell, B.D. (Braxton), Kittner, T. (Thomas), Meschia, J.F. (James F.), Meurs, J.B.J. (Joyce) van, Uitterlinden, A.G. (André), Worrall, B.B. (Bradford B.), Kubisch, C. (Christian), Sharma, P. (Pankaj), Cotlarciuc, I. (Ioana), Malik, R. (Rainer), Holliday, E.G. (Elizabeth), Ahmadi, K.R. (Kourosh), Paré, G. (Guillaume), Psaty, B.M. (Bruce), Fornage, M. (Myriam), Hasan, N. (Nazeeha), Rinne, P.E. (Paul), Ikram, M.A. (Arfan), Markus, H.S. (Hugh), Rosand, J. (Jonathan), Mitchell, B.D. (Braxton), Kittner, T. (Thomas), Meschia, J.F. (James F.), Meurs, J.B.J. (Joyce) van, Uitterlinden, A.G. (André), Worrall, B.B. (Bradford B.), Kubisch, C. (Christian), and Sharma, P. (Pankaj)
Abstract: BACKGROUND AND PURPOSE - : Elevated total plasma homocysteine (tHcy) levels are known to be associated with increased risk of ischemic stroke (IS). Given that both tHcy and IS are heritable traits, we investigated a potential genetic relationship between homocysteine levels and stroke risk by assessing 18 polymorphisms previously associated with tHcy levels for their association with IS and its subtypes. METHODS - : Previous meta-analysis results from an international stroke collaborative network, METASTROKE, were used to assess association of the 18 tHcy-associated single-nucleotide polymorphisms (SNPs) in 12 389 IS cases and 62 004 controls. We also investigated the associations in regions located within 50 kb from the 18 tHcy-related SNPs and the association of a genetic risk score, including the 18 SNPs. RESULTS - : One SNP located in the RASIP1 gene and a cluster of 3 SNPs located at and near SLC17A3 were significantly associated with IS (P<0.0003) after correcting for multiple testing. For stroke subtypes, the sentinel SNP located upstream of MUT was significantly associated with small-vessel disease (P=0.0022), whereas 1 SNP located in MTHFR was significantly associated with large-vessel dis
Published: 2014
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25. International collaboration to assess the risk of Guillain Barré Syndrome following Influenza A (H1N1) 2009 monovalent vaccines

Author: Dodd, C.N. (Caitlin), Romio, S.A. (Silvana), Black, S. (Steve), Vellozzi, C. (Claudia), Andrews, N.J. (Nick), Sturkenboom, M.C.J.M. (Miriam), Zuber, P. (Patrick), Hua, W. (Wei), Bonhoeffer, J. (Jan), Buttery, J. (Jim), Crawford, N. (Nigel), Deceuninck, G. (Genevieve), Vries, C.S. (Corinne) de, Wals, P. (Philippe) de, Gimeno, D. (David), Heijbel, H. (Harald), Hughes, H. (Hayley), Hur, K. (Kwan), Hviid, A. (Anders), Kelman, J. (Jeffrey), Kilpi, T. (Tehri), Chuang, S.K. (S.), Macartney, T. (Thomas), Rett, M. (Melisa), Lopez-Callada, V.R. (Vesta Richardson), Salmon, D. (Daniel), Sanchez, F.G. (Francisco Gimenez), Sanz, N. (Nuria), Silverman, B. (Bernard), Storsaeter, J. (Jann), Thirugnanam, U. (Umapathi), Maas, N.A.T. (Nicoline) van der, Yih, K. (Katherine), Zhang, T. (Teng Fei), Izurieta, H.S. (Hector), Addis, B.J., Akhtar, A. (Aysha), Cope, J. (Judith), Davis, R.L. (Robert), Gargiullo, P. (Paul), Kurz, X. (Xavier), Law, B. (Barbara), Sahinovic, I. (Isabelle), Tokars, J. (Jerry), Serrano, P. (Pedro), Cheng, A. (Aixin), Charles, P. (Pat), Clothier, H. (Hazel), Day, B. (Bruce), Day, T. (Timothy), Gates, P. (Peter), MacDonnell, R. (Richard), Roberts, L. (Les), Rodriguez-Casero, V. (Vic-toria), Wijeratne, T. (Tissa), Kiers, H.A.L. (Henk), Blyth, C. (Christopher), Booy, R. (Robert), Elliott, E. (Elizabeth), Gold, M.R. (Michael), Marshall, H., McIntyre, P. (Peter), Richmond, P. (Peter), Royle, J. (Jenny), Wood, N.W. (Nicholas), Zurynski, Y. (Yvonne), Calvo, G. (Gonzalo), Campins, M. (Magda), Corominas, N. (Nuria), Torres, F. (Ferran), Valls, V., Vilella, A. (Ángels), Dutra, A. (Amalia), Eick-Cost, A. (Angelia), Jackson, H.M. (Henry), Garman, K. (Katherine), Hu, Z. (Zheng), Rigo, J., Badoo, J. (Judith), Cho, D (David), Polakowski, L.L. (Laura), Sandhu, S.K. (Sukhminder), Sun, G. (Guoying), Chan, H.-S.S. (Hoi-Shan Sophelia), Chan, K.-Y. (Kwok-Yin), Cheung, R. (Raymond), Cheung, Y-F. (Yuk-Fai), Cherk, S. (Sharon), Chuang, S.K (S.), Fok, D. (Dennis), Fung, B.-H. (Bun-Hey), Ko, K.-F. (Kwai-Fu), Lau, K.W. (Ka Wing), Lau, K.-K. (Kwok-Kwong), Li, P. (Pulin), Liu, H.-T. (Hui-Tung), Liu, S.-H. (Shao-Haei), Mok, K. (Kin), So, J. (Joanna), Wong, W. (Winnie), Wu, S.-P. (Shun-Ping), Ball, R. (Robert), Burwen, D. (Dale), Franks, R.L. (Riley), Gibbs, J.M. (Jonathan), Kliman, R.E. (Rebecca), Kropp, S. (Silke), MaCurdy, T.E. (Thomas), Martin, D.B. (David), Sandhu, S.-D.K. (Sukhmin-Der), Worrall, B.B. (Bradford B.), Fuentes, D.E.F. (Dra. Elvira Fuentes), González, P.C.O. (Paola Carolina Ojeda), Reyna, V.F. (Valerie ), Kulldorff, M. (Martin), Lee, G. (Grace), Lieu, T.A. (Tracy), Platt, S., Serres, G.D. (Gaston De), Jabin, K. (Kamilah), Soh, B.L.S. (Bee Leng Sally), Arnheim-Dahlström, L. (Lisen), Castot, A. (Anne), Melker, H.E. (Hester) de, Dieleman, J.P. (Jeanne), Hallgren, J. (Jonal), Jacobs, B.C. (Bart), Johansen, K. (Kari), Kramarz, P (Piotr), Lapeyre, M. (Maryse), Leino, T. (Tuija), Mølgaard-Nielsen, D. (Ditte), Mosseveld, M. (Mees), Olberg, H.K. (Henning K), Sammon, C.-M. (Cor-Mac), Saussier, C. (Christel), Schuemie, M.J. (Martijn), Sommet, A. (Agnès), Sparen, P. (Pär), Svanström, H. (Henrik), Vanrolleghem, A.M. (Ann M.), Weibel, D.M. (Daniel), Domingo, J.D. (Javier Diez), Esparza, J.L. (José LuísMicó), Lucas, R.M.O. (Rafael M. Ortí), Maseres, J.B.M. (Juan B. Mollar), Sánchez, J.L.A. (José Luís Alfonso), Sánchez, M.G. (Mercedes Garcés), Viguer, V.Z. (Vicente Zanón), Cunningham, F. (Francesca), Avagyan, A. (Armen), Thakkar, B. (Bharat), Zhang, R. (Rongping), Dodd, C.N. (Caitlin), Romio, S.A. (Silvana), Black, S. (Steve), Vellozzi, C. (Claudia), Andrews, N.J. (Nick), Sturkenboom, M.C.J.M. (Miriam), Zuber, P. (Patrick), Hua, W. (Wei), Bonhoeffer, J. (Jan), Buttery, J. (Jim), Crawford, N. (Nigel), Deceuninck, G. (Genevieve), Vries, C.S. (Corinne) de, Wals, P. (Philippe) de, Gimeno, D. (David), Heijbel, H. (Harald), Hughes, H. (Hayley), Hur, K. (Kwan), Hviid, A. (Anders), Kelman, J. (Jeffrey), Kilpi, T. (Tehri), Chuang, S.K. (S.), Macartney, T. (Thomas), Rett, M. (Melisa), Lopez-Callada, V.R. (Vesta Richardson), Salmon, D. (Daniel), Sanchez, F.G. (Francisco Gimenez), Sanz, N. (Nuria), Silverman, B. (Bernard), Storsaeter, J. (Jann), Thirugnanam, U. (Umapathi), Maas, N.A.T. (Nicoline) van der, Yih, K. (Katherine), Zhang, T. (Teng Fei), Izurieta, H.S. (Hector), Addis, B.J., Akhtar, A. (Aysha), Cope, J. (Judith), Davis, R.L. (Robert), Gargiullo, P. (Paul), Kurz, X. (Xavier), Law, B. (Barbara), Sahinovic, I. (Isabelle), Tokars, J. (Jerry), Serrano, P. (Pedro), Cheng, A. (Aixin), Charles, P. (Pat), Clothier, H. (Hazel), Day, B. (Bruce), Day, T. (Timothy), Gates, P. (Peter), MacDonnell, R. (Richard), Roberts, L. (Les), Rodriguez-Casero, V. (Vic-toria), Wijeratne, T. (Tissa), Kiers, H.A.L. (Henk), Blyth, C. (Christopher), Booy, R. (Robert), Elliott, E. (Elizabeth), Gold, M.R. (Michael), Marshall, H., McIntyre, P. (Peter), Richmond, P. (Peter), Royle, J. (Jenny), Wood, N.W. (Nicholas), Zurynski, Y. (Yvonne), Calvo, G. (Gonzalo), Campins, M. (Magda), Corominas, N. (Nuria), Torres, F. (Ferran), Valls, V., Vilella, A. (Ángels), Dutra, A. (Amalia), Eick-Cost, A. (Angelia), Jackson, H.M. (Henry), Garman, K. (Katherine), Hu, Z. (Zheng), Rigo, J., Badoo, J. (Judith), Cho, D (David), Polakowski, L.L. (Laura), Sandhu, S.K. (Sukhminder), Sun, G. (Guoying), Chan, H.-S.S. (Hoi-Shan Sophelia), Chan, K.-Y. (Kwok-Yin), Cheung, R. (Raymond), Cheung, Y-F. (Yuk-Fai), Cherk, S. (Sharon), Chuang, S.K (S.), Fok, D. (Dennis), Fung, B.-H. (Bun-Hey), Ko, K.-F. (Kwai-Fu), Lau, K.W. (Ka Wing), Lau, K.-K. (Kwok-Kwong), Li, P. (Pulin), Liu, H.-T. (Hui-Tung), Liu, S.-H. (Shao-Haei), Mok, K. (Kin), So, J. (Joanna), Wong, W. (Winnie), Wu, S.-P. (Shun-Ping), Ball, R. (Robert), Burwen, D. (Dale), Franks, R.L. (Riley), Gibbs, J.M. (Jonathan), Kliman, R.E. (Rebecca), Kropp, S. (Silke), MaCurdy, T.E. (Thomas), Martin, D.B. (David), Sandhu, S.-D.K. (Sukhmin-Der), Worrall, B.B. (Bradford B.), Fuentes, D.E.F. (Dra. Elvira Fuentes), González, P.C.O. (Paola Carolina Ojeda), Reyna, V.F. (Valerie ), Kulldorff, M. (Martin), Lee, G. (Grace), Lieu, T.A. (Tracy), Platt, S., Serres, G.D. (Gaston De), Jabin, K. (Kamilah), Soh, B.L.S. (Bee Leng Sally), Arnheim-Dahlström, L. (Lisen), Castot, A. (Anne), Melker, H.E. (Hester) de, Dieleman, J.P. (Jeanne), Hallgren, J. (Jonal), Jacobs, B.C. (Bart), Johansen, K. (Kari), Kramarz, P (Piotr), Lapeyre, M. (Maryse), Leino, T. (Tuija), Mølgaard-Nielsen, D. (Ditte), Mosseveld, M. (Mees), Olberg, H.K. (Henning K), Sammon, C.-M. (Cor-Mac), Saussier, C. (Christel), Schuemie, M.J. (Martijn), Sommet, A. (Agnès), Sparen, P. (Pär), Svanström, H. (Henrik), Vanrolleghem, A.M. (Ann M.), Weibel, D.M. (Daniel), Domingo, J.D. (Javier Diez), Esparza, J.L. (José LuísMicó), Lucas, R.M.O. (Rafael M. Ortí), Maseres, J.B.M. (Juan B. Mollar), Sánchez, J.L.A. (José Luís Alfonso), Sánchez, M.G. (Mercedes Garcés), Viguer, V.Z. (Vicente Zanón), Cunningham, F. (Francesca), Avagyan, A. (Armen), Thakkar, B. (Bharat), and Zhang, R. (Rongping)
Abstract: Background: The global spread of the 2009 novel pandemic influenza A (H1N1) virus led to the accelerated production and distribution of monovalent 2009 Influenza A (H1N1) vaccines (pH1N1). This pandemic provided the opportunity to evaluate the risk of Guillain-Barré syndrome (GBS), which has been an influenza vaccine safety concern since the swine flu pandemic of 1976, using a common protocol among high and middle-income countries. The primary objective of this project was to demonstrate the feasibility and utility of global collaboration in the assessment of vaccine safety, including countries both with and without an established infrastructure for vaccine active safety surveillance. A second objective, included a priori, was to assess the risk of GBS following pH1N1 vaccination. Methods: The primary analysis used the self-controlled case series (SCCS) design to estimate the relative incidence (RI) of GBS in the 42 days following vaccination with pH1N1 vaccine in a pooled analysis across databases and in analysis using a meta-analytic approach. Results: We found a relative incidence of GBS of 2.42 (95% CI 1.58-3.72) in the 42 days following exposure to pH1N1 vaccine in analysis of pooled data and 2.09 (95% CI 1
Published: 2013
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26. Genetic risk factors for ischaemic stroke and its subtypes (the METASTROKE Collaboration): A meta-analysis of genome-wide association studies

Author: Traylor, M. (Matthew), Farrall, M. (Martin), Holliday, E.G. (Elizabeth), Sudlow, C. (Cathie), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Fornage, M. (Myriam), Ikram, M.A. (Arfan), Malik, R. (Rainer), Bevan, S. (Steve), Thorsteinsdottir, U. (Unnur), Nalls, M.A. (Michael), Longstreth Jr, W.T., Wiggins, K.L. (Kerri), Yadav, S. (Sunaina), Parati, E.A. (Eugenio), DeStefano, A.L. (Anita), Worrall, B.B. (Bradford B.), Kittner, T. (Thomas), Khan, M.I. (Muhammad), Reiner, A. (Alexander), Helgadottir, H.T. (Hafdis), Achterberg, S. (Sefanja), Fernandez-Cadenas, I. (Israel), Abboud, S. (Shimon), Schmidt, R. (Reinhold), Walters, M.R. (Matthew), Chen, W-M., Ringelstein, E.B. (E. Bernd), O'Donnell, M. (Martin), Ho, W.K. (Weang Kee), Pera, M.F. (Martin ), Lemmens, R. (Robin), Norrving, B. (Bo), Higgins, P. (Peter), Benn, M. (Marianne), Sale, P. (Patrizio), Kuhlenbäumer, G. (Gregor), Doney, A.S.F. (Alex), Vicente, A.M. (Astrid M), Delavaran, H. (Hossein), Algra, A. (Ale), Davies, G. (Gail), Oliveira, S.A. (Sofia), Palmer, C.N.A. (Colin), Deary, I.J. (Ian), Pandolfo, M. (Massimo), Montaner, J. (Joan), Carty, C. (Cara), Bakker, P.I.W. (Paul) de, Kostulas, K. (Konstantinos), Ferro, M.T. (María), Zuydam, N.R. (Natalie) van, Valdimarsson, E. (Einar), Nordestgaard, B.G. (Børge), Lindgren, A. (Arne), Thijs, V. (Vincent), Slowik, A. (Agnieszka), Saleheen, D., Paré, G. (Guillaume), Berger, K. (Klaus), Thorleifsson, G. (Gudmar), Hofman, A. (Albert), Mosley, T.H. (Thomas), Mitchell, B.D. (Braxton), Furie, K.L. (Karen), Clarke, R. (Robert), Levi, C. (Christopher), Seshadri, S. (Sudha), Gschwendtner, A. (Andreas), Boncoraglio, G. (Giorgio Battista), Sharma, P. (Pankaj), Bis, J.C. (Joshua), Gretarsdottir, S. (Solveig), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Rosand, J. (Jonathan), Meschia, J.F. (James F.), Zwart, J-A. (John-Anker), Kubisch, C. (Christian), Markus, H.S. (Hugh), Traylor, M. (Matthew), Farrall, M. (Martin), Holliday, E.G. (Elizabeth), Sudlow, C. (Cathie), Hopewell, J., Cheng, Y.-C. (Yu-Ching), Fornage, M. (Myriam), Ikram, M.A. (Arfan), Malik, R. (Rainer), Bevan, S. (Steve), Thorsteinsdottir, U. (Unnur), Nalls, M.A. (Michael), Longstreth Jr, W.T., Wiggins, K.L. (Kerri), Yadav, S. (Sunaina), Parati, E.A. (Eugenio), DeStefano, A.L. (Anita), Worrall, B.B. (Bradford B.), Kittner, T. (Thomas), Khan, M.I. (Muhammad), Reiner, A. (Alexander), Helgadottir, H.T. (Hafdis), Achterberg, S. (Sefanja), Fernandez-Cadenas, I. (Israel), Abboud, S. (Shimon), Schmidt, R. (Reinhold), Walters, M.R. (Matthew), Chen, W-M., Ringelstein, E.B. (E. Bernd), O'Donnell, M. (Martin), Ho, W.K. (Weang Kee), Pera, M.F. (Martin ), Lemmens, R. (Robin), Norrving, B. (Bo), Higgins, P. (Peter), Benn, M. (Marianne), Sale, P. (Patrizio), Kuhlenbäumer, G. (Gregor), Doney, A.S.F. (Alex), Vicente, A.M. (Astrid M), Delavaran, H. (Hossein), Algra, A. (Ale), Davies, G. (Gail), Oliveira, S.A. (Sofia), Palmer, C.N.A. (Colin), Deary, I.J. (Ian), Pandolfo, M. (Massimo), Montaner, J. (Joan), Carty, C. (Cara), Bakker, P.I.W. (Paul) de, Kostulas, K. (Konstantinos), Ferro, M.T. (María), Zuydam, N.R. (Natalie) van, Valdimarsson, E. (Einar), Nordestgaard, B.G. (Børge), Lindgren, A. (Arne), Thijs, V. (Vincent), Slowik, A. (Agnieszka), Saleheen, D., Paré, G. (Guillaume), Berger, K. (Klaus), Thorleifsson, G. (Gudmar), Hofman, A. (Albert), Mosley, T.H. (Thomas), Mitchell, B.D. (Braxton), Furie, K.L. (Karen), Clarke, R. (Robert), Levi, C. (Christopher), Seshadri, S. (Sudha), Gschwendtner, A. (Andreas), Boncoraglio, G. (Giorgio Battista), Sharma, P. (Pankaj), Bis, J.C. (Joshua), Gretarsdottir, S. (Solveig), Psaty, B.M. (Bruce), Rothwell, P.M. (Peter), Rosand, J. (Jonathan), Meschia, J.F. (James F.), Zwart, J-A. (John-Anker), Kubisch, C. (Christian), and Markus, H.S. (Hugh)
Abstract: Background: Various genome-wide association studies (GWAS) have been done in ischaemic stroke, identifying a few loci associated with the disease, but sample sizes have been 3500 cases or less. We established the METASTROKE collaboration with the aim of validating associations from previous GWAS and identifying novel genetic associations through meta-analysis of GWAS datasets for ischaemic stroke and its subtypes. Methods: We meta-analysed data from 15 ischaemic stroke cohorts with a total of 12 389 individuals with ischaemic stroke and 62 004 controls, all of European ancestry. For the associations reaching genome-wide significance in METASTROKE, we did a further analysis, conditioning on the lead single nucleotide polymorphism in every associated region. Replication of novel suggestive signals was done in 13 347 cases and 29 083 controls. Findings: We verified previous associations for cardioembolic stroke near PITX2 (p=2·8×10-16) and ZFHX3 (p=2·28×10-8), and for large-vessel stroke at a 9p21 locus (p=3·32×10-5) and HDAC9 (p=2·03×10-12). Additionally, we verified that all associations were subtype specific. Conditional analysis in the three regions for which the associations reached genome-wide significance (PITX2, ZFHX3, and HDAC9) indicated that all the signal in each region could be attributed to one risk haplotype. We also identified 12 potentially novel loci at p<5×10-6. However, we were unable to replicate any of these novel associations in the replication cohort. Interpretation: Our results show that, although genetic variants can be detected in patients with ischaemic stroke when compared with controls, all associations we were able to confirm are specific to a stroke subtype. This finding has two implications. First, to maximise success of genetic studies in ischaemic stroke, detailed stroke subtyping is required. Second, different genetic pathophysiological mechanisms seem to be associated with different stroke subtypes. Funding: Wellcome Trust, UK Medic
Published: 2012
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27. Common variants at 6p21.1 are associated with large artery atherosclerotic stroke

Author: Holliday, E.G., Maguire, J.M., Evans, T-J, Koblar, S.A., Jannes, J., Sturm, J.W., Hankey, G.J., Baker, R., Golledge, J., Parsons, M.W., Malik, R., McEvoy, M., Biros, E., Lewis, M.D., Lincz, L.F., Peel, R., Oldmeadow, C., Smith, W., Moscato, P., Barlera, S., Bevan, S., Bis, J.C., Boerwinkle, E., Boncoraglio, G.B., Brott, T.G., Brown, R.D., Cheng, Y-C, Cole, J.W., Cotlarciuc, I., Devan, W.J., Fornage, M., Furie, K.L., Grétarsdóttir, S., Gschwendtner, A., Ikram, M.A., Longstreth, W.T., Meschia, J.F., Mitchell, B.D., Mosley, T.H., Nalls, M.A., Parati, E.A., Psaty, B.M., Sharma, P., Stefansson, K., Thorleifsson, G., Thorsteinsdottir, U., Traylor, M., Verhaaren, B.F.J., Wiggins, K.L., Worrall, B.B., Sudlow, C., Rothwell, P.M., Farrall, M., Dichgans, M., Rosand, J., Markus, H.S., Scott, R.J., Levi, C., Attia, J., Holliday, E.G., Maguire, J.M., Evans, T-J, Koblar, S.A., Jannes, J., Sturm, J.W., Hankey, G.J., Baker, R., Golledge, J., Parsons, M.W., Malik, R., McEvoy, M., Biros, E., Lewis, M.D., Lincz, L.F., Peel, R., Oldmeadow, C., Smith, W., Moscato, P., Barlera, S., Bevan, S., Bis, J.C., Boerwinkle, E., Boncoraglio, G.B., Brott, T.G., Brown, R.D., Cheng, Y-C, Cole, J.W., Cotlarciuc, I., Devan, W.J., Fornage, M., Furie, K.L., Grétarsdóttir, S., Gschwendtner, A., Ikram, M.A., Longstreth, W.T., Meschia, J.F., Mitchell, B.D., Mosley, T.H., Nalls, M.A., Parati, E.A., Psaty, B.M., Sharma, P., Stefansson, K., Thorleifsson, G., Thorsteinsdottir, U., Traylor, M., Verhaaren, B.F.J., Wiggins, K.L., Worrall, B.B., Sudlow, C., Rothwell, P.M., Farrall, M., Dichgans, M., Rosand, J., Markus, H.S., Scott, R.J., Levi, C., and Attia, J.
Abstract: Genome-wide association studies (GWAS) have not consistently detected replicable genetic risk factors for ischemic stroke, potentially due to etiological heterogeneity of this trait. We performed GWAS of ischemic stroke and a major ischemic stroke subtype (large artery atherosclerosis, LAA) using 1,162 ischemic stroke cases (including 421 LAA cases) and 1,244 population controls from Australia. Evidence for a genetic influence on ischemic stroke risk was detected, but this influence was higher and more significant for the LAA subtype. We identified a new LAA susceptibility locus on chromosome 6p21.1 (rs556621: odds ratio (OR) = 1.62, P = 3.9 × 10 -8) and replicated this association in 1,715 LAA cases and 52,695 population controls from 10 independent population cohorts (meta-analysis replication OR = 1.15, P = 3.9 × 10 -4; discovery and replication combined OR = 1.21, P = 4.7 × 10 -8). This study identifies a genetic risk locus for LAA and shows how analyzing etiological subtypes may better identify genetic risk alleles for ischemic stroke.
Published: 2012

28. The Causative Classification of Stroke system

Author: Arsava, E.M., primary, Ballabio, E., additional, Benner, T., additional, Cole, J.W., additional, Delgado-Martinez, M.P., additional, Dichgans, M., additional, Fazekas, F., additional, Furie, K.L., additional, Illoh, K., additional, Jood, K., additional, Kittner, S., additional, Lindgren, A.G., additional, Majersik, J.J., additional, Macleod, M.J., additional, Meurer, W.J., additional, Montaner, J., additional, Olugbodi, A.A., additional, Pasdar, A., additional, Redfors, P., additional, Schmidt, R., additional, Sharma, P., additional, Singhal, A.B., additional, Sorensen, A.G., additional, Sudlow, C., additional, Thijs, V., additional, Worrall, B.B., additional, Rosand, J., additional, and Ay, H., additional
Published: 2010
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29. Genetic variation at CR1increases risk of cerebral amyloid angiopathy

Author: Biffi, A., Shulman, J.M., Jagiella, J.M., Cortellini, L., Ayres, A.M., Schwab, K., Brown, D.L., Silliman, S.L., Selim, M., Worrall, B.B., Meschia, J.F., Slowik, A., De Jager, P.L., Greenberg, S.M., Schneider, J.A., Bennett, D.A., and Rosand, J.
Abstract: Accumulated evidence suggests that a variant within the CR1gene (single nucleotide polymorphism rs6656401), known to increase risk for Alzheimer disease (AD), influences -amyloid (A) deposition in brain tissue. Given the biologic overlap between AD and cerebral amyloid angiopathy (CAA), a leading cause of intracerebral hemorrhage (ICH) in elderly individuals, we investigated whether rs6656401 increases the risk of CAA-related ICH and influences vascular A deposition.
Published: 2012
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30. Transcobalamin 2 variant associated with poststroke homocysteine modifies recurrent stroke risk

Author: Hsu, F.-C., Sides, E.G., Mychaleckyj, J.C., Worrall, B.B., Elias, G.A., Liu, Y., Chen, W.-M., Coull, B.M., Toole, J.F., Rich, S.S., Furie, K.L., and Sale, M.M.
Abstract: The Vitamin Intervention for Stroke Prevention trial found an association between baseline poststroke homocysteine (Hcy) and recurrent stroke. We investigated genes for enzymes and cofactors in the Hcy metabolic pathway for association with Hcy and determined whether associated single nucleotide polymorphisms (SNPs) influenced recurrent stroke risk.
Published: 2011
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31. White matter hyperintensity volume is increased in small vessel stroke subtypes

Author: Rost, N.S., Rahman, R.M., Biffi, A., Smith, E.E., Kanakis, A., Fitzpatrick, K., Lima, F., Worrall, B.B., Meschia, J.F., Brown, R.D., Brott, T.G., Sorensen, A.G., Greenberg, S.M., Furie, K.L., and Rosand, J.
Abstract: White matter hyperintensity (WMH) may be a marker of an underlying cerebral microangiopathy. Therefore, we hypothesized that WMH would be most severe in patients with lacunar stroke and intracerebral hemorrhage (ICH), 2 types of stroke in which cerebral small vessel (SV) changes are pathophysiologically relevant.
Published: 2010
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32. Advancing Stroke Therapeutics Through Genetic Understanding

Author: Ross, O.A., Worrall, B.B., and Meschia, J.F.
Abstract: Stroke is a complex neurological disorder that most likely results from an intricate interplay between lifestyle, environment and genetics. Genes can influence susceptibility to stroke, alter responses to pharmacotherapy, and affect disease outcome. Recently, common variations within the PDE4D and ALOX5AP genes have been identified that increase population-attributable risk of stroke in Iceland. These genes are yet to be unequivocally confirmed and the functional variants identified. Characterizing the genetic profile of individuals at highest risk of stroke will permit more targeted pharmacological approaches to early primary and secondary stroke prevention. Pharmacogenomics is likely to be particularly important for stroke prevention because of the narrow therapeutic index for treatments like warfarin that prevents thrombosis but also promotes hemorrhage. Identifying possible genetic determinants of outcome will also open new avenues of research into stroke therapeutics beyond thrombolysis.
Published: 2007

33. The genetics of cerebrovascular atherosclerosis

Author: Worrall, B.B. and Degraba, T.J.
Abstract: Ischemic stroke attributable to atherosclerosis remains a major public health problem. Genetic factors are increasingly recognized as influencing risk for atherosclerosis directly and indirectly. Genetic makeup may influence the development of major vascular risk factors or alter susceptibility of the cerebral vasculature to these risk factors. More recently, newly identified risk factors for atherosclerosis, such as plasma homocysteine and infection, have also been reported to be influenced by important genetic determinants. This article reviews the current literature on genetics of cerebral and precerebral atherosclerosis and seeks to identify areas of promise for future clinical application.
Published: 2002
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34. Economics and Urban Problems (Book Review).

Author: Worrall, B.B.
Subjects: URBAN policy, NONFICTION
Abstract: Reviews the book 'Economics and Urban Problems,' by D. Netzer.
Published: 1971

35. Technology, Investment and Growth (Book Review).

Author: Worrall, B.B.
Subjects: ECONOMIC development, NONFICTION
Abstract: Reviews the book 'Technology, Investment and Growth,' by B.R. Williams.
Published: 1968

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1. Migraine-Associated Common Genetic Variants Confer Greater Risk of Posterior vs. Anterior Circulation Ischemic Stroke☆

2. Health Heritage©, a Web-Based Tool for the Collection and Assessment of Family Health History : Initial User Experience and Analytic Validity

3. Prestroke physical activity and early functional status after stroke

4. Genome-wide association study of intracranial aneurysms identifies 17 risk loci and genetic overlap with clinical risk factors

5. Relative effects of LDL-C on ischemic stroke and coronary disease: A Mendelian randomization study

6. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting

7. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting.

8. GWAS and colocalization analyses implicate carotid intima-media thickness and carotid plaque loci in cardiovascular outcomes

9. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study

10. Association between telomere length and risk of cancer and non-neoplastic diseases a mendelian randomization study

11. Genetic variation at 16q24.2 is associated with small vessel stroke

12. Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N = 112 151) and 24 GWAS consortia

13. Low-frequency and common genetic variation in ischemic stroke : the METASTROKE collaboration

14. Genome-wide meta-analysis of cerebral white matter hyperintensities in patients with stroke

15. Genetic variants in CETP increase risk of intracerebral hemorrhage

16. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study

17. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study

18. Genome-Wide Association Analysis of Young-Onset Stroke Identifies a Locus on Chromosome 10q25 Near HABP2

19. The development of algorithms to assess family health history in a web based application - HealthHeritage

20. Common variation in PHACTR1 is associated with susceptibility to cervical artery dissection

21. No additional prognostic value of genetic information in the prediction of vascular events after cerebral ischemia of arterial origin

22. Genetic overlap between diagnostic subtypes of ischemic stroke

23. Genome-wide association study of intracranial aneurysm identifies a new association on chromosome 7

24. Effect of genetic variants associated with plasma homocysteine levels on stroke risk

25. International collaboration to assess the risk of Guillain Barré Syndrome following Influenza A (H1N1) 2009 monovalent vaccines

26. Genetic risk factors for ischaemic stroke and its subtypes (the METASTROKE Collaboration): A meta-analysis of genome-wide association studies

27. Common variants at 6p21.1 are associated with large artery atherosclerotic stroke

28. The Causative Classification of Stroke system

29. Genetic variation at CR1increases risk of cerebral amyloid angiopathy

30. Transcobalamin 2 variant associated with poststroke homocysteine modifies recurrent stroke risk

31. White matter hyperintensity volume is increased in small vessel stroke subtypes

32. Advancing Stroke Therapeutics Through Genetic Understanding

33. The genetics of cerebrovascular atherosclerosis

34. Economics and Urban Problems (Book Review).

35. Technology, Investment and Growth (Book Review).

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35 results on '"Worrall B.B."'

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