Nimodipine Reduces Dysfunction and Demyelination in Models of Multiple Sclerosis

Author:

Desai Roshni A.1ORCID,Davies Andrew L.1,Del Rossi Natalie1,Tachrount Mohamed23,Dyson Alex4,Gustavson Britta1,Kaynezhad Pardis5,Mackenzie Lewis67,Putten Marieke A.68,McElroy Daniel9,Schiza Dimitra1,Linington Christopher9,Singer Mervyn4,Harvey Andrew R.6,Tachtsidis Ilias5,Golay Xavier2,Smith Kenneth J.1

Affiliation:

1. Department of Neuroinflammation UCL Queen Square Institute of Neurology, University College London London UK

2. Department of Brain Repair and Rehabilitation UCL Queen Square Institute of Neurology, University College London London UK

3. Nuffield Department of Clinical Neurosciences John Radcliffe Hospital Oxford UK

4. Bloomsbury Institute for Intensive Care Medicine, Division of Medicine University College London London UK

5. Biomedical Optics Research Laboratory, Department of Medical Physics and Biomedical Engineering University College London London UK

6. School of Physics & Astronomy, University of Glasgow Glasgow UK

7. Department of Chemistry Durham University Durham UK

8. Northern Centre for Cancer Care, Freeman Hospital Newcastle upon Tyne UK

9. Glasgow Biomedical Research Centre Room B3‐19, 120 University Place, University of Glasgow Glasgow UK

Funder

Fondation Leducq

Multiple Sclerosis Society

National Multiple Sclerosis Society

Rosetrees Trust

Wellcome Trust

Publisher

Wiley

Subject

Clinical Neurology,Neurology

Reference37 articles.

1. Immunomodulators and immunosuppressants for multiple sclerosis: a network meta‐analysis;Filippini G;Cochrane Database Syst Rev,2013

2. Corticosteroids or ACTH for acute exacerbations in multiple sclerosis;Filippini G;Cochrane Database Syst Rev,2000

3. Oral versus intravenous high-dose methylprednisolone for treatment of relapses in patients with multiple sclerosis (COPOUSEP): a randomised, controlled, double-blind, non-inferiority trial

4. The cortical damage, early relapses, and onset of the progressive phase in multiple sclerosis

5. Neurological deficits caused by tissue hypoxia in neuroinflammatory disease

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