Rowe, J.B. (James B.)

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    Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis
    (2020) Boeve, B.F. (Bradley F.); Blesa, R. (Rafael); Petersen, R.C. (Ronald C.); Schlachetzki, J.C.M. (Johannes C. M.); Thompson, E. (Elizabeth); Scarpini, E. (Elio); Graf-Radford, N.R. (Neill R.); Benussi, L. (Luisa); Ortega-Cubero, S. (Sara); Riemenschneider, M. (Matthias); Baker, M. (Matt); Giaccone, G. (Giorgio); Tagliavini, F. (Fabrizio); Spillantini, M.G. (Maria Grazia); Piguet, O. (Olivier); Ibach, B. (Bernd); Dickson, D.W. (Dennis W.); Hjermind, L.E. (Lena E.); Forloni, G. (Gianluigi); Nilsson, C. (Christer); Pijnenburg, Y.A.L. (Yolande A. L.); Serpente, M. (Maria); Grifths, T.D. (Timothy D.); Morris, C.M. (Christopher M.); Pickering-Brown, S. (Stuart); Seelaar, H. (Harro); Landqvist-Waldö, M. (Maria); Binetti, G. (Giuliano); Rosen, H. (Howard); Albani, D. (Diego); Perneczky, R. (Robert); Heutink, P. (Peter); Brice, A. (Alexis); Mann, D.M.A. (David M.A.); Trojanowski, J.Q. (John Q.); Ferrari, R. (Rafaele); Ferrucci, L. (Luigi); Padovani, A. (Alessandro); Danek, A. (Adrian); Rossor, M.N. (Martin N.); Leber, I. (Isabelle); Grafman, J. (Jordan); Sorrentino, P. (Paolo); Graf, C. (Caroline); Novelli, V. (Valeria); Dobson-Stone, C. (Carol); Gu, W. (Wei); Cruchaga, C. (Carlos); Hernandez, D.G. (Dena G.); Fenoglio, C. (Chiara); Deramecourt, V. (Vincent); Anfossi, M. (Maria); Zhao, H. (Huashuo); Franceschi, M. (Massimo); Borroni, B. (Barbara); Grossman, M. (Murray); Kapogiannis, D. (Dimitrios); Van-der-Zee, J. (Julie); Bernardi, L. (Livia); Vercelletto, M. (Martine); Rogaeva, E. (Ekaterina); Hodges, J.R. (John R.); Richardson, A. (Anna); Ghidoni, R. (Roberta); Mayhaus, M. (Manuel); Scheltens, P. (Philip); McKeith, I.G. (Ian G.); Rollin, A. (Adeline); Frangipane, F. (Francesca); Pastor, P. (Pau); Wassermann, E.M. (Eric M.); Rainero, I. (Innocenzo); Nalls, M.A. (Michael A.); Rohrer, J.D. (Jonathan D.); Van-Swieten, J.C. (John C.); Josephs, K.A. (Keith A.); Diehl-Schmid, J. (Janine); Momeni, P. (Parastoo); Fox, N.C. (Nick C.); Jaros, E. (Evelyn); Uphill, J. (James); Rossi, G. (Giacomina); Piaceri, I. (Irene); Lebouvier, T. (Thibaud); Halliday, G.M. (Glenda M.); Bagnoli, S. (Silvia); Schofeld, P.R. (Peter R.); Lleó, A. (Alberto); Cruts, M. (Marc); Nacmias, B. (Benedetta); Puca, A.A. (Annibale A.); Ramasamy, A. (Adaikalavan); Singleton, A.B. (Andrew B.); Mead, S. (Simon); Alexopoulos, P. (Panagiotis); Baborie, A. (Atik); Haan, E. (Eric); Miller, B.L. (Bruce L.); Pasquier, F. (Florence); Wang, T. (Ting); Rowe, J.B. (James B.); Razquin, C. (Cristina); Van-Deerlin, V.M. (Vivianna M.); Milan, G. (Graziella ); Bartley, L. (Lauren); Collinge, J. (John); Pinessi, L. (Lorenzo); Hernández, I. (Isabel); Rademakers, R. (Rosa); Sorbi, S. (Sandro); Attems, J. (Johannes); Capozzo, R. (Rosa); Morris, H.R. (Huw R.); Hardy, J. (John); Nielsen, J.E. (Jørgen E.); Kristiansen, M. (Mark); Smirne, N. (Nicoletta); Galimberti, D. (Daniela); Maletta, R. (Rafaele); Zeng, P. (Ping); Knopman, D. (David); Ruiz, A. (Agustín); Karydas, A.M. (Anna M.); Pichler, S. (Sabrina); Brooks, W.S. (William S.); Nilsson, K. (Karin); Dopper, E.G.P. (Elise G. P.); Rubino, E. (Elisa); Clarimon, J. (Jordi); Hannequin, D. (Didier); Huey, E.D. (Edward D.); Alonso, E. (Elena); Pietrini, P. (Pietro); Cappa, S.F. (Stefano F.); Van-Broeckhoven, C. (Christine); Gerhard, A. (Alexander); Rollinson, S. (Sara); Thomas, A.J. (Alan J.); Conidi, M.E. (Maria Elena); Tierney, M.C. (Michael C.); Bruni, A.C. (Amalia C.); Rizzu, P. (Patrizia); Gallo, M. (Maura); Cairns, N.J. (Nigel J.); Chiang, H.H. (Huei Hsin); Kurz, A. (Alexander); Kwok, J.B.J. (John B. J.); Gao, Y. (Yixin); Parisi, J.E. (Joseph E.); Seely, W.W. (William W.); Yu, X. (Xinghao); St-George Hyslop, P. (Peter); Boada, M. (Mercè); Snowden, J.S. (Julie S.); Gasparoni, G. (Gilles); Warren, J.D. (Jason D.); Postiglione, A. (Alfredo); Logroscino, G. (Giancarlo); Mackenzie, I.R.A. (Ian R.A.); Cupidi, C. (Chiara); Golfer, V. (Véronique)
    We employed Mendelian randomization (MR) to evaluate the causal relationship between leukocyte telomere length (LTL) and amyotrophic lateral sclerosis (ALS) with summary statistics from genomewide association studies (n= ~ 38,000 for LTL and ~ 81,000 for ALS in the European population; n= ~ 23,000 for LTL and ~ 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 efect 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 infuence of LTL and ALS in the European population.
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    Neuroimaging biomarkers for clinical trials in atypical parkinsonian disorders: Proposal for a Neuroimaging Biomarker Utility System
    (Wiley, 2019) Berg, D. (Daniela); Pavese, N. (Nicola); Eimeren, T. (Thilo) van; Ondrus, M. (Matej); Piccini, P. (Paola); Höglinger, G.U. (Günter U.); Drzezga, A. (Alexander); Rektorova, I. (Irena); Siebner, H.R. (Hartwig R.); Nestor, P. (Peter); Lewis, S. (Simon); Tessitore, A. (Alessandro); Peralta, M.C. (María Cecilia); Monchi, O. (Oury); Rowe, J.B. (James B.); Higuchi, M. (Makoto); Rominger, A. (Axel); Thobois, S. (Stephane); Seppi, K. (Klaus); Bohnen, N. (Nico); Lehericy, S. (Stephane); Rodriguez-Oroz, M.C. (María Cruz); Pineda-Pardo, J.A. (José Ángel); Strafella, A.P. (Antonio P.); Kaasinen, V. (Valtteri); Wenning, G. (Gregor); Antonini, A. (Angelo); Ceravolo, R. (Roberto); Stoessl, A.J. (A. Jon)
    Introduction: Therapeutic strategies targeting protein aggregations are ready for clinical trials in atypical parkinsonian disorders. Therefore, there is an urgent need for neuroimaging biomarkers to help with the early detection of neurodegenerative processes, the early differentiation of the underlying pathology, and the objective assessment of disease progression. However, there currently is not yet a consensus in the field on how to describe utility of biomarkers for clinical trials in atypical parkinsonian disorders. Methods: To promote standardized use of neuroimaging biomarkers for clinical trials, we aimed to develop a conceptual framework to characterize in more detail the kind of neuroimaging biomarkers needed in atypical parkinsonian disorders, identify the current challenges in ascribing utility of these biomarkers, and propose criteria for a system that may guide future studies. Results: As a consensus outcome, we describe the main challenges in ascribing utility of neuroimaging biomarkers in atypical parkinsonian disorders, and we propose a conceptual framework that includes a graded system for the description of utility of a specific neuroimaging measure. We included separate categories for the ability to accurately identify an intention-to-treat patient population early in the disease (Early), to accurately detect a specific underlying pathology (Specific), and the ability to monitor disease progression (Progression). Discussion: We suggest that the advancement of standardized neuroimaging in the field of atypical parkinsonian disorders will be furthered by a well-defined reference frame for the utility of biomarkers. The proposed utility system allows a detailed and graded description of the respective strengths of neuroimaging biomarkers in the currently most relevant areas of application in clinical trials.