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1. A genome-wide association study in multiple system atrophy

Author

Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., Houlden, H., Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., and Houlden, H.

Abstract

Contains fulltext : 167706.pdf (publisher's version ) (Open Access), OBJECTIVE: To identify genetic variants that play a role in the pathogenesis of multiple system atrophy (MSA), we undertook a genome-wide association study (GWAS). METHODS: We performed a GWAS with >5 million genotyped and imputed single nucleotide polymorphisms (SNPs) in 918 patients with MSA of European ancestry and 3,864 controls. MSA cases were collected from North American and European centers, one third of which were neuropathologically confirmed. RESULTS: We found no significant loci after stringent multiple testing correction. A number of regions emerged as potentially interesting for follow-up at p < 1 x 10-6, including SNPs in the genes FBXO47, ELOVL7, EDN1, and MAPT. Contrary to previous reports, we found no association of the genes SNCA and COQ2 with MSA. CONCLUSIONS: We present a GWAS in MSA. We have identified several potentially interesting gene loci, including the MAPT locus, whose significance will have to be evaluated in a larger sample set. Common genetic variation in SNCA and COQ2 does not seem to be associated with MSA. In the future, additional samples of well-characterized patients with MSA will need to be collected to perform a larger MSA GWAS, but this initial study forms the basis for these next steps.

Published
2016

2. DNA methylation-based measures of biological age: Meta-analysis predicting time to death

Author

Chen, B.H. (Brian), Marioni, R.E. (Riccardo), Colicino, E. (Elena), Peters, M.J. (Marjolein), Ward-Caviness, C.K. (Cavin K.), Tsai, P.-C. (Pei-Chien), Roetker, N.S. (Nicholas S.), Just, A.C. (Allan C.), Demerath, E.W. (Ellen), Guan, W. (Weihua), Bressler, J. (Jan), Fornage, M. (Myriam), Studenski, S. (Stephanie), Vandiver, A.R. (Amy R.), Moore, A.Z. (Ann Zenobia), Tanaka, T. (Toshiko), Kiel, D.P. (Douglas P.), Liang, L. (Liming), Vokonas, P. (Pantel), Schwartz, J. (Joel), Lunetta, K.L. (Kathryn), Murabito, J. (Joanne), Bandinelli, S. (Stefania), Hernandez, D.G. (Dena), Melzer, D. (David), Nalls, M.A. (Michael), Pilling, L.C. (Luke), Price, T.R. (Timothy R.), Singleton, A. (Andrew), Gieger, C. (Christian), Holle, R. (Rolf), Kretschmer, A. (Anja), Kronenberg, F. (Florian), Kunze, S. (Sonja), Linseisen, J. (Jakob), Meisinger, C. (Christine), Rathmann, W. (Wolfgang), Waldenberger, M. (Melanie), Visscher, P.M. (Peter), Shah, S. (Sonia), Wray, N.R. (Naomi), McRae, A.F. (Allan F.), Franco, O.H. (Oscar), Hofman, A. (Albert), Uitterlinden, A.G. (André), Absher, D. (Devin), Assimes, T.L. (Themistocles), Levine, M.E. (Morgan E.), Lu, A.T. (Ake T.), Tsao, P.S. (Philip S.), Hou, L. (Lifang), Manson, J.E. (Joann), Carty, C. (Cara), LaCroix, A.Z. (Andrea Z.), Reiner, A. (Alexander), Spector, T.D. (Timothy), Feinberg, A.P. (Andrew P.), Levy, D. (Daniel), Baccarelli, A.A. (Andrea), Meurs, J. (Joyce van), Bell, J.T. (Jordana), Peters, A. (Annette), Deary, I.J. (Ian), Pankow, J.S. (James), Ferrucci, L. (Luigi), Horvath, S. (Steve), Chen, B.H. (Brian), Marioni, R.E. (Riccardo), Colicino, E. (Elena), Peters, M.J. (Marjolein), Ward-Caviness, C.K. (Cavin K.), Tsai, P.-C. (Pei-Chien), Roetker, N.S. (Nicholas S.), Just, A.C. (Allan C.), Demerath, E.W. (Ellen), Guan, W. (Weihua), Bressler, J. (Jan), Fornage, M. (Myriam), Studenski, S. (Stephanie), Vandiver, A.R. (Amy R.), Moore, A.Z. (Ann Zenobia), Tanaka, T. (Toshiko), Kiel, D.P. (Douglas P.), Liang, L. (Liming), Vokonas, P. (Pantel), Schwartz, J. (Joel), Lunetta, K.L. (Kathryn), Murabito, J. (Joanne), Bandinelli, S. (Stefania), Hernandez, D.G. (Dena), Melzer, D. (David), Nalls, M.A. (Michael), Pilling, L.C. (Luke), Price, T.R. (Timothy R.), Singleton, A. (Andrew), Gieger, C. (Christian), Holle, R. (Rolf), Kretschmer, A. (Anja), Kronenberg, F. (Florian), Kunze, S. (Sonja), Linseisen, J. (Jakob), Meisinger, C. (Christine), Rathmann, W. (Wolfgang), Waldenberger, M. (Melanie), Visscher, P.M. (Peter), Shah, S. (Sonia), Wray, N.R. (Naomi), McRae, A.F. (Allan F.), Franco, O.H. (Oscar), Hofman, A. (Albert), Uitterlinden, A.G. (André), Absher, D. (Devin), Assimes, T.L. (Themistocles), Levine, M.E. (Morgan E.), Lu, A.T. (Ake T.), Tsao, P.S. (Philip S.), Hou, L. (Lifang), Manson, J.E. (Joann), Carty, C. (Cara), LaCroix, A.Z. (Andrea Z.), Reiner, A. (Alexander), Spector, T.D. (Timothy), Feinberg, A.P. (Andrew P.), Levy, D. (Daniel), Baccarelli, A.A. (Andrea), Meurs, J. (Joyce van), Bell, J.T. (Jordana), Peters, A. (Annette), Deary, I.J. (Ian), Pankow, J.S. (James), Ferrucci, L. (Luigi), and Horvath, S. (Steve)

Abstract

Estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. We previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, we expanded our original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, we examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality (p ≤ 8.2 x 10-9), independent of chronological age, even after adjusting for additional risk factors (p < 5.4 x 10-4), and within the racial/ethnic groups that we examined (non-Hispanic whites, Hispanics, African Americans). Epigenetic age estimates that incorporated information on blood cell composition led to the smallest p-values for time to death (p≤ 7.5 x 10-43). Overall, this study a) strengthens the evidence that epigenetic age predicts all-cause mortality above and beyond chronological age and traditional risk factors, and b) demonstrates that epigenetic age estimates that incorporate information on blood cell counts lead to highly significant associations with all-cause mortality.

Published
2016
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3. A genome-wide association study in multiple system atrophy

Author

Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., Houlden, H., Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., and Houlden, H.

Abstract

Contains fulltext : 167706.pdf (publisher's version ) (Open Access), OBJECTIVE: To identify genetic variants that play a role in the pathogenesis of multiple system atrophy (MSA), we undertook a genome-wide association study (GWAS). METHODS: We performed a GWAS with >5 million genotyped and imputed single nucleotide polymorphisms (SNPs) in 918 patients with MSA of European ancestry and 3,864 controls. MSA cases were collected from North American and European centers, one third of which were neuropathologically confirmed. RESULTS: We found no significant loci after stringent multiple testing correction. A number of regions emerged as potentially interesting for follow-up at p < 1 x 10-6, including SNPs in the genes FBXO47, ELOVL7, EDN1, and MAPT. Contrary to previous reports, we found no association of the genes SNCA and COQ2 with MSA. CONCLUSIONS: We present a GWAS in MSA. We have identified several potentially interesting gene loci, including the MAPT locus, whose significance will have to be evaluated in a larger sample set. Common genetic variation in SNCA and COQ2 does not seem to be associated with MSA. In the future, additional samples of well-characterized patients with MSA will need to be collected to perform a larger MSA GWAS, but this initial study forms the basis for these next steps.

Published
2016

4. A genome-wide association study in multiple system atrophy

Author

Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., Houlden, H., Sailer, A., Scholz, S.W., Nalls, M.A., Schulte, C., Federoff, M., Price, T.R., Lees, A., Ross, O.A., Dickson, D.W., Mok, K., Mencacci, N.E., Schottlaender, L., Chelban, V., Ling, H., O'Sullivan, S.S, Wood, N.W., Traynor, B.J., Ferrucci, L., Federoff, H.J., Mhyre, T.R., Morris, H.R., Deuschl, G., Quinn, N., Widner, H., Albanese, A., Infante, J., Bhatia, K.P., Poewe, W., Oertel, W., Hoglinger, G.U., Wullner, U., Goldwurm, S., Pellecchia, M.T., Ferreira, J., Tolosa, E., Bloem, B.R., Rascol, O., Meissner, W.G., Hardy, J.A., Revesz, T., Holton, J.L., Gasser, T., Wenning, G.K., Singleton, A.B., and Houlden, H.

Abstract

Contains fulltext : 167706.pdf (publisher's version ) (Open Access), OBJECTIVE: To identify genetic variants that play a role in the pathogenesis of multiple system atrophy (MSA), we undertook a genome-wide association study (GWAS). METHODS: We performed a GWAS with >5 million genotyped and imputed single nucleotide polymorphisms (SNPs) in 918 patients with MSA of European ancestry and 3,864 controls. MSA cases were collected from North American and European centers, one third of which were neuropathologically confirmed. RESULTS: We found no significant loci after stringent multiple testing correction. A number of regions emerged as potentially interesting for follow-up at p < 1 x 10-6, including SNPs in the genes FBXO47, ELOVL7, EDN1, and MAPT. Contrary to previous reports, we found no association of the genes SNCA and COQ2 with MSA. CONCLUSIONS: We present a GWAS in MSA. We have identified several potentially interesting gene loci, including the MAPT locus, whose significance will have to be evaluated in a larger sample set. Common genetic variation in SNCA and COQ2 does not seem to be associated with MSA. In the future, additional samples of well-characterized patients with MSA will need to be collected to perform a larger MSA GWAS, but this initial study forms the basis for these next steps.

Published
2016

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