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Ageing and multiple sclerosis - 13/12/22

Doi : 10.1016/S1474-4422(22)00184-3 
Jennifer S Graves, MD PhD a, b, c, , Kristen M Krysko, MD d, Le H Hua, MD e, Martina Absinta, MD PhD f, g, Robin J M Franklin, ProfPhD h, Benjamin M Segal, ProfMD i
a Department of Neurosciences, University of California, San Diego, CA, USA 
b Pediatric Multiple Sclerosis Center, Rady Children’s Hospital, San Diego, CA, USA 
c Department of Neurology, San Diego VA Hospital, San Diego, CA, USA 
d Division of Neurology, Department of Medicine, Li Ka Shing Knowledge Institute, St Michael’s Hospital, University of Toronto, Toronto, ON, Canada 
e Department of Neurology, Cleveland Clinic, Lou Ruvo Center for Brain Health, Las Vegas, NV, USA 
f Department of Neurology, Johns Hopkins University, Baltimore, MD, USA 
g Division of Neuroscience, IRCCS San Raffaele Scientific Institute and Vita-Salute San Raffaele University, Milan, Italy 
h Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK 
i Department of Neurology and the Neuroscience Research Institute, The Ohio State University, Columbus, OH, USA 

* Correspondence to: Assoc Prof Jennifer S Graves, Department of Neurosciences, University of California, San Diego, CA 92037, USA Department of Neurosciences University of California San Diego CA 92037 USA

Summary

The factor that is most relevant and strongly associated with the clinical course of multiple sclerosis is chronological age. Very young patients exclusively have relapsing remitting disease, whereas those with later onset disease face a more rapid development of permanent disability. For people with progressive multiple sclerosis, the poor response to current disease modifying therapies might be related to ageing in the immune system and CNS. Ageing is also associated with increased risks of side-effects caused by some multiple sclerosis therapies. Both somatic and reproductive ageing processes might contribute to development of progressive multiple sclerosis. Understanding the role of ageing in immune and neural cell function in patients with multiple sclerosis might be key to halting non-relapse-related progression. The growing literature on potential therapies that target senescent cells and ageing processes might provide effective strategies for remyelination and neuroprotection.

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Vol 22 - N° 1

P. 66-77 - janvier 2023 Regresar al número
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