by Isabella Colonna
For March we selected Lazzarotto A, Hamzaoui M, Tonietto M, Dubessy AL, Khalil M, Pirpamer L, Ropele S, Enzinger C, Battaglini M, Stromillo ML, De Stefano N, Filippi M, Rocca MA, Gallo P, Gasperini C, Stankoff B, Bodini B; MAGNIMS Study Group. Time is myelin: early cortical myelin repair prevents atrophy and clinical progression in multiple sclerosis. Brain. 2024 Jan 24:awae024. doi: 10.1093/brain/awae024. Epub ahead of print. PMID: 38267729.
Demyelination is considered one of the main neuropathological features of Multiple Sclerosis; therefore, changes in myelin content over time may have a relevant impact on neurodegeneration and disease progression. Few neuropathological studies have explored the extent of cortical remyelination in patients with MS, finding high variability between patients and between cortex and white matter lesions. This multicenter study is the first work to explore in-vivo cortical remyelination in patients with MS using quantitative MRI; the aim of the study was to identify the main determinants of myelin loss and repair in all MS phenotypes and to evaluate their role in predicting cortical atrophy after one year as well as clinical progression after five years.
One-hundred-forty patients with MS (37 clinically isolated syndromes, 71 relapsing-MS, 32 progressive-MS) from four European neurological centers (Graz, Milan, Paris and Siena) were investigated in this retrospective longitudinal study. Each patient underwent clinical assessment using the Expanded Disability Status Scale (EDSS) at baseline and after 5 years as well as 3T-MRI protocol including magnetization transfer imaging, technique that has been previously shown to be sensitive to myelin content changes in the cortex, at baseline and after one year of follow-up. Eighty-four healthy controls were included in the study and underwent the same MRI protocol as the patients.
The authors found that cortical demyelination increases with disease duration and is predictive of short-term cortical atrophy as well as long-term clinical progression in all patients with MS. However, cortical remyelination occurred in half of the patients and in the majority of the demyelinated cortical regions, independent of age, disease duration or clinical phenotype. Moreover, higher extent of cortical remyelination was associated with lower cortical atrophy after one year and with a significantly reduced risk of long-term clinical disability in patients with short disease duration and with limited extent of cortical demyelination.
In conclusion, this study emphasizes the important role of cortical myelin dynamics in determining neurodegeneration and clinical progression in MS; furthermore, it shows that cortical remyelination occurring at early stages of the disease may prevent short-term cortical atrophy and long-term clinical progression. These findings suggest that interventions aimed to prevent demyelination and to promote remyelination early in the disease course may help in preventing clinical progression in patients with MS.
