At a glance
Affiliates
Sara Bandres-Ciga1,2, Alastair J. Noyce3,4, Gibran Hemani5, Aude Nicolas6, Andrea Calvo7, Gabriele Mora8, The ITALSGEN Consortium, The International ALS Genomics Consortium, Pentti J. Tienari9, David J. Stone10, Mike A. Nalls1,11, Andrew B. Singleton1, Adriano Chiò7,12,13, & Bryan J. Traynor6,14
- Molecular Genetics Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health
- Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA)
- Preventive Neurology Unit, Wolfson Institute of Preventive Medicine, Queen Mary University of London
- Department of Clinical and Movement Neurosciences, University College London, Institute of Neurology
- MRC Integrative Epidemiology Unit, University of Bristol
- Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health
- 'Rita Levi Montalcini' Department of Neuroscience, University of Turin
- ALS Center, Istituti Clinici Scientifici Maugeri, IRCCS
- Department of Neurology, Helsinki University Hospital and Molecular Neurology Programme, Biomedicum, University of Helsinki
- Genetics and Pharmacogenomics, Merck Research Laboratories, Merck & Co., Inc.
- Institute of Cognitive Sciences and Technologies, C.N.R
- Azienda Ospedaliero Universitaria Città della Salute e della Scienza
- Department of Neurology, Johns Hopkins University
Summary
This study identifies shared polygenic risk and causal associations in ALS; moreover, a public resource for the ALS community was generated to understand these risks and causal associations (https://lng-nia.shinyapps.io/mrshiny). Shared polygenic risk exists between ALS and educational attainment, physical activity, smoking, and tenseness/restlessness. Additionally, elevated low-density lipoprotein cholesterol was identified as a causal risk factor for ALS.