Research: Tysabri inhibits grey matter Damage

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Background: Since cortical pathology has been indicated to play a relevant role in the physical and cognitive disability of multiple sclerosis (MS) patients, this study aims to analyze the efficacy of natalizumab in slowing down its progression.

Methods: A total of 120 relapsing-remitting MS patients completed a 2-year prospective study: 35 received natalizumab, 50 received interferon beta-1a or glatiramer acetate (immunomodulatory agents – IMA) and 35 remained untreated. Forty healthy subjects constituted the reference population. Clinical and magnetic resonance imaging (MRI) evaluations (including cortical lesions and atrophy) were performed at baseline and after 2 years.

Results: Natalizumab significantly reduced accumulation of new cortical lesions (0.2±0.6, range 0-3) compared to immunomodulatory agents (1.3±1.1, range 1-6, p=0.001) and no treatment (2.9±1.5, range 1-8, p<0.001). The percentage of patients with new cortical lesions was also lower in natalizumab-treated patients (20%) compared to IMA-treated and untreated patients (68.0% and 74.2%; p<0.001 for both comparisons). Furthermore, the progression of cortical atrophy was significantly reduced by natalizumab (% change=1.7%) compared to IMA (3.7%, p=0.003) and no therapy (4.6%, p<0.001). Finally, a greater percentage (51.4%) of natalizumab-treated patients remained disease-free (no clinical or MRI evidence of disease activity or progression) compared to IMA-treated (18%, p=0.001) and untreated patients (5.7%, p<0.001).

Conclusions: Natalizumab treatment significantly decreases cortical lesion accumulation and cortical atrophy progression in severe relapsing-remitting MS. While supporting the inflammatory origin of cortical lesions, our results highlight the significant impact of natalizumab on cortical pathology.

This study shows that blocking inflammation in the brain with tysabri can inhibit the accumulation of loss of nerves in the grey matter in the cortext of the brain.

Grey matter lesions in MS are not associated with a lot of infilration from the blood in contrast to the white matter, so is the Tysabri working at this level and there is a low amount of white blood cell traffic into the brain or is it because that Tysabri quells the inflammation elsewhere, such that it was reported to dampen antibody production in the cerebrospinal fluid.

This yet another example of  the advantages to blocking the accumulation of inflmmatory cells in the brain

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