Dynamics and heterogeneity of brain damage in multiple sclerosis
Publication Date
October 26, 2017
Authors
Ekaterina Kotelnikova, Narsis A. Kiani, Elena Abad, Elena H. Martinez Lapiscina, et al
Volume
13
Issue
10
Pages
e1005757
DOI
https://dx.plos.org/10.1371/journal.pcbi.1005757
Publisher URL
http://journals.plos.org/ploscompbiol/article?id=10.1371%2Fjournal.pcbi.1005757
Scopus
85032617603
Mendeley
http://www.mendeley.com/research/dynamics-heterogeneity-brain-damage-multiple-sclerosis
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Mendeley | Further Information

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However, it is not well under-stood how these events interact and evolve to evoke such a highly dynamic and heteroge-neous disease. We established a hypothesis whereby the variability in the course of MS is driven by the very same pathogenic mechanisms responsible for the disease, the autoim-mune attack on the CNS that leads to chronic inflammation, neuroaxonal degeneration and remyelination. We propose that each of these processes acts more or less severely and at different times in each of the clinical subgroups. To test this hypothesis, we developed a mathematical model that was constrained by experimental data (the expanded disability sta-tus scale [EDSS] time series) obtained from a retrospective longitudinal cohort of 66 MS patients with a long-term follow-up (up to 20 years). Moreover, we validated this model in a second prospective cohort of 120 MS patients with a three-year follow-up, for which EDSS data and brain volume time series were available. The clinical heterogeneity in the datasets was reduced by grouping the EDSS time series using an unsupervised clustering analysis. We found that by adjusting certain parameters, albeit within their biological range, the math-ematical model reproduced the different disease courses, supporting the dynamic CNS damage hypothesis to explain MS heterogeneity. Our analysis suggests that the irreversible axon degeneration produced in the early stages of progressive MS is mainly due to the higher rate of myelinated axon degeneration, coupled to the lower capacity for remyelina-tion. However, and in agreement with recent pathological studies, degeneration of chroni-cally demyelinated axons is not a key feature that distinguishes this phenotype. 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Scopus | Further Information

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