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Interferon beta-1a slows progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by

R Zivadinov1, L Locatelli, D Cookfair

  • 1Department of Neurology, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. rzivadinov@thejni.org

Multiple Sclerosis (Houndmills, Basingstoke, England)
|April 28, 2007
PubMed
Abstract

Insights

Interferon beta-1a (IFN beta-1a) therapy slowed brain atrophy and gray matter loss in multiple sclerosis (MS) patients over three years. This treatment also reduced T1-lesion accumulation compared to controls.

Area of Science:

  • Neurology
  • Radiology

Background:

  • Brain atrophy, including white matter (WM) and gray matter (GM) loss, is linked to disability in multiple sclerosis (MS).
  • The clinical impact of GM atrophy in MS requires further investigation.

Purpose of the Study:

  • To evaluate the effect of intramuscular interferon beta-1a (IFN beta-1a) on brain atrophy and lesion progression in MS patients.
  • To compare three-year outcomes between patients receiving IFN beta-1a and an untreated control group.

Main Methods:

  • A three-year open-label study involving 26 patients on IFN beta-1a and 28 controls.
  • Quantitative MRI scans assessed brain parenchymal fraction (BPF), GM fraction (GMF), and WM fraction (WMF).
  • T1- and T2-lesion volumes (LVs) and clinical assessments were monitored.

Main Results:

  • IFN beta-1a treatment significantly slowed the decrease in BPF (-1.3% vs -2.5%) and GMF (+0.2% vs -1.4%) compared to controls.
  • The IFN beta-1a group showed a significant reduction in T1-lesion volume (-9.3% vs +91.6%).
  • Both groups experienced within-patient decreases in BPF, with significant WMF decrease in the IFN beta-1a group and GMF decrease in the control group.

Conclusions:

  • Interferon beta-1a therapy significantly mitigated whole-brain and GM atrophy progression over three years.
  • IFN beta-1a also demonstrated a significant effect in slowing the accumulation of T1-hypointense lesions.
  • These findings highlight the neuroprotective potential of IFN beta-1a in managing MS.

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