Benjamin M. Jacobs, Luisa Schalk, Emily Tregaskis-Daniels, Antonio Scalfari, Ashwini Nandoskar, Angie Dunne, Bruno Gran, Charles A. Mein, Charlotte Sellers, Cord E. Spilker, David Rog, Elisa Visentin, Elizabeth Lindsey Bezzina, Emeka Uzochukwu, Emma Tallantyre, Eva Wozniak, Eve Sacre, Ghaniah Hassan‐Smith, Helen L. Ford, Jade Harris, Joan Bradley, Joshua Robert Breedon, Judith Brooke, Karim L. Kreft, Katila George, Maria Martha Papachatzaki, Martin O'Malley, Michelle Peter, Miriam Mattoscio, Laura Azzopardi, Renato Oliveira, Neisha Rhule, Nikos Evangelou, Nimisha Vinod, Outi Quinn, Fhateha Ali, Ramya Shamji, Rashmi Kaimal, Rebecca L. Boulton, Riffat Tanveer, Katherine Tuite-Dalton, Rod Middleton, Roxanne Murray, Ruth Bellfield, Sadid Hoque, Shakeelah Patel, Sonia Raj, Stephanie Gumus, Stephanie Mitchell, Stephen J. Sawcer, Tarunya Arun, Tatiana Pogreban, Terri-Louise Brown, Thamanna Begum, Veronica Antoine, Waqar Rashid, Grace Fawehinmi, Claire Reidy, Shanaz Begum, Shannon A. Bernard Healey, Harriet Cummins, Kelly Westwood, Deborah Spencer, Shegufta Farooq, Katharine Harding, Sarah Williams, G. Radford, Selina White, Nathan Alldred-Douglas, Linford Fernandes, Adil Harroud, Jacob L McCauley, Ashley Beecham, Nicolas Vince, Nayane dos Santos Brito Silva, Huw R. Morris, E. Silber, Gavin Giovannoni, Alastair J. Noyce, Dobson Ruth
BACKGROUND AND OBJECTIVES: The genetic basis of multiple sclerosis (MS) susceptibility has been studied extensively in European (EUR) ancestry populations. The aim of our study was to determine the genetic architecture of MS susceptibility in people of South Asian (SAS) and African (AFR) genetic ancestral backgrounds. METHODS: We recruited and genotyped a cohort of ancestrally diverse people with MS (pwMS) from across the United Kingdom. Cases were combined with controls from the UK Biobank (UKB). After genetic ancestry inference, we performed within-ancestry case-control genetic association studies of MS susceptibility, exploring single nucleotide variants and imputed classical human leukocyte antigen alleles. RESULTS: allele in the SAS cohort, which has not been previously described. DISCUSSION: The genetic architecture of MS susceptibility shows strong concordance across ancestral groups suggesting shared disease mechanisms. Larger studies in diverse populations are likely to enhance our understanding of how genetic variation contributes to MS susceptibility in people of all ancestral backgrounds.