Gao, Yixin and Wang, Ting and Yu, Xinghao and Zhao, Huashuo and Zeng, Ping and Ferrari, Raffaele and Hernandez, Dena G. and Nails, Michael A. and Rohrers, Jonathan D. and Ramasamys, Adaikalavan and Kwok, John B. J. and Dobson-Stone, Carol and Brooks, William S. and Schofield, Peter R. and Halliday, Glenda M. and Hodges, John R. and Piguet, Olivier and Bartley, Lauren and Thompson, Elizabeth and Haan, Eric and Hernandez, Isabel and Ruiz, Agustin and Boada, Merce and Borronils, Barbara and Padovani, Alessandro and Cruchaga, Carlos and Cairns, Nigel J. and Benussi, Luisa and Binetti, Giuliano and Ghidoni, Roberta and Forloni, Gianluigi and Albani, Diego and Galimberti, Daniela and Fenoglio, Chiara and Serpente, Maria and Scarpini, Elio and Clarim, Jordi and Lie, Alberto and Blesa, Rafael and Waldo, Maria Landqvist and Nilsson, Karin and Nilsson, Christer and Mackenzie, Ian R. A. and Hsiung, Ging-Yuek R. and Mann, David M. A. and Grafman, Jordan and Morris, Christopher M. and Attems, Johannes and Griffiths, Timothy D. and McKeith, Ian G. and Thomas, Alan J. and Pietrini, Pietro and Huey, Edward D. and Wassermann, Eric M. and Baborie, Atik and Jaros, Evelyn and Tierney, Michael C. and Pastor, Pau and Razquin, Cristina and Ortega-Cubero, Sara and Alonso, Elena and Perneczky, Robert and Diehl-Schmid, Janine and Alexopoulos, Panagiotis and Kurz, Alexander and Rainero, Innocenzo and Rubino, Elisa and Pinessi, Lorenzo and Rogaeva, Ekaterina and St George-Hyslop, Peter and Rossi, Giacomina and Tagliavini, Fabrizio and Giacconen, Giorgio and Rowe, James B. and Schlachetzki, Johannes C. M. and Uphill, James and Collinge, John and Mead, Simon and Danek, Adrian and Van Deerlin, Vivienne M. and Grossman, Murray and Trojanowski, John Q. and van der Zee, Julie and Cruts, Marc and Van Broeckhoven, Christine and Cappa, Stefano F. and Leber, Isabelle and Hannequin, Didier and Golfier, Veronique and Vercelletto, Martine and Brice, Alexis and Nacmias, Benedetta and Sorbi, Sandro and Bagnoli, Silvia and Piaceri, Irene and Nielsen, Jorgen E. and Hjermind, Lena E. and Riemenschneider, Matthias and Mayhaus, Manuel and Ibach, Bernd and Gasparoni, Gilles and Pichler, Sabrina and Gu, Wei and Rossor, Martin N. and Fox, Nick C. and Warren, Jason D. and Spillantini, Maria Grazia and Morris, Huw R. and Rizzu, Patrizia and Heutink, Peter and Snowden, Julie S. and Rollinson, Sara and Richardson, Anna and Gerhard, Alexander and Bruni, Amalie C. and Maletta, Raffaele and Frangipane, Francesca and Cupidi, Chiara and Bernardi, Livia and Anfossi, Maria and Gallo, Maura and Conidi, Maria Elena and Smirne, Nicoletta and Rademakers, Rosa and Baker, Matt and Dickson, Dennis W. and Graff-Radford, Neill R. and Petersen, Ronald C. and Knopman, David and Josephs, Keith A. and Boeve, Bradley F. and Parisi, Joseph E. and Seeley, William W. and Miller, Bruce L. and Karydas, Anna M. and Rosen, Howard and van Swieten, John C. and Dopper, Elise G. P. and Seelaar, Harro and Pijnenburg, Yolande A. L. and Scheltens, Philip and Logroscino, Giancarlo and Capozzo, Rosa and Novelli, Valeria and Puca, Annibale A. and Franceschi, Massimo and Postiglione, Alfredo and Milan, Graziella and Sorrentino, Paolo and Kristiansen, Mark and Huei-Hsin, G. and Graff, Chian Caroline and Pasquier, Florence and Rollin, Adeline and Deramecourt, Vincent and Lebouvier, Thibaud and Ferrucci, Luigi and Pickering-Brown, Stuart and Singleton, Andrew B. and Hardy, John and Momeni, Parastoo (2020) Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis. SCIENTIFIC REPORTS, 10 (1): 12184. ISSN 2045-2322,
Full text not available from this repository. (Request a copy)Abstract
We employed Mendelian randomization (MR) to evaluate the causal relationship between leukocyte telomere length (LTL) and amyotrophic lateral sclerosis (ALS) with summary statistics from genome-wide association studies (n=similar to 38,000 for LTL and similar to 81,000 for ALS in the European population; n=similar to 23,000 for LTL and similar to 4,100 for ALS in the Asian population). We further evaluated mediation roles of lipids in the pathway from LTL to ALS. The odds ratio per standard deviation decrease of LTL on ALS was 1.10 (95% CI 0.93-1.31, p=0.274) in the European population and 0.75 (95% CI 0.53-1.07, p=0.116) in the Asian population. This null association was also detected between LTL and frontotemporal dementia in the European population. However, we found that an indirect effect of LTL on ALS might be mediated by low density lipoprotein (LDL) or total cholesterol (TC) in the European population. These results were robust against extensive sensitivity analyses. Overall, our MR study did not support the direct causal association between LTL and the ALS risk in neither population, but provided suggestive evidence for the mediation role of LDL or TC on the influence of LTL and ALS in the European population.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | PARKINSONS-DISEASE; FRONTOTEMPORAL DEMENTIA; GENETIC-VARIANTS; MEDIATION ANALYSIS; WEAK INSTRUMENTS; ALS; RISK; EPIDEMIOLOGY; PROGRESSION; ONSET; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Psychiatrie und Psychotherapie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 18 Mar 2021 07:59 |
| Last Modified: | 18 Mar 2021 07:59 |
| URI: | https://pred.uni-regensburg.de/id/eprint/44179 |
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