title: Natalizumab strongly suppresses cortical pathology in relapsing-remitting multiple sclerosis.
abstract: 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 togli spazio, 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.
authors.affiliation: The Multiple Sclerosis Centre of Veneto Region, Department of Neurology, University Hospital of Padova, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Rinaldi
authors.forename: M
authors.initials: M
authors.lastname: Calabrese
authors.forename: D
authors.initials: D
authors.lastname: Seppi
authors.forename: M
authors.initials: M
authors.lastname: Puthenparampil
authors.forename: P
authors.initials: P
authors.lastname: Perini
authors.forename: P
authors.initials: P
authors.lastname: Gallo
mesh_terms: D000293:Adolescent; D000328:Adult; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D002540:Cerebral Cortex / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D000068717:Glatiramer Acetate; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D007155:Immunologic Factors / Q000627:therapeutic use; D016899:Interferon-beta / Q000627:therapeutic use; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000188:drug therapy* / Q000473:pathology*; D000069442:Natalizumab; D010455:Peptides / Q000627:therapeutic use; D055815:Young Adult
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D007155:Immunologic Factors; D000069442:Natalizumab; D010455:Peptides; D000068717:Glatiramer Acetate; D016899:Interferon-beta