Multiple Sclerosis (MS) Support Group

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Main Category: Multiple Sclerosis
Also Included In: Neurology / Neuroscience
Article Date: 29 Apr 2009 - 7:00 PDT


New data presented provided evidence that long-term treatment with COPAXONE® (glatiramer acetate injection) may offer sustained protection from neuronal/axonal injury. This protective effect was reflected biologically by a significant increase in N-acetylaspartate (NAA), a specific marker of neuronal mitochondrial function, in treated versus non-treated relapsing-remitting multiple sclerosis (RRMS) patients. These six-year results augment previously published findings suggesting that treatment with COPAXONE® may provide a neuroprotective effect in RRMS patients1, 2.

The study, "Six-Year Prospective Multi-Voxel Brain MRS Study of Two Cohorts in RRMS To Examine the Effect of Glatiramer Acetate on Neuronal/Axonal Metabolic Injury," is the largest (n=46) and longest study of its kind to date. In the study, patients taking COPAXONE® for six years experienced an improvement in neuronal mitochodrial function, as quantified by an increase in neuronal NAA levels and evaluated by 1H- Magnetic Resonance Spectroscopy (1H-MRS). Decreased neuronal NAA levels are reflective of neuronal/axonal injury.

"The potential ability to prevent or repair brain tissue damage in RRMS patients is an important treatment consideration given the degenerative pathology of this life-long condition," said Omar Khan, M.D., Professor of Neurology, Director, Multiple Sclerosis Center, Wayne State University and lead investigator of the study. "These data further substantiate our previous research into the potential neuroprotective effect of COPAXONE®, as well as the use of NAA measures as a reliable marker for assessing a patient's disease progression and response to treatment."

Similar results were reported from a different study examining the effect of COPAXONE® in Clinically Isolated Syndrome (CIS) patients. The study demonstrated patients who received COPAXONE® improved in their cerebral neuroaxonal integrity relative to patients treated with placebo. Patients on placebo showed a decline in NAA consistent with that demonstrated in historical control studies.

1. Khan, O. (2008). Long-Term Study of Brain 1H-MRS Study in Multiple Sclerosis: Effect of Glatiramer Acetate Therapy on Axonal Metabolic Function and Feasibility of Long-Term 1H-MRS Monitoring in Multiple Sclerosis. Neuroimaging 2008.

2. Arnold, D. et al. (2008, September). Treatment with Glatiramer Acetate Protects Axons in Patients with Clinically Isolated Syndromes: Evidence from the PreCISe trial. Presented at ECTRIMS, Montreal, Canada. Multiple Sclerosis 2008 14 (Suppl 1): S5.

About the Study

Forty-nine patients, divided into two cohorts of previously treatment-naïve RRMS patients, underwent serial brain 1H-MRS scanning. Group 1 (n=22) included patients who started COPAXONE® therapy at enrollment (n=18) and during the course of the study (n=4). Mean age, disease duration and Expanded Disability Status Scale (EDSS) were 43.5 years, 8.2 years and 2.77, respectively. Mean NAA/Cr at baseline was 1.97 + 0.24 and 2.20 + 0.16 (+11.6 percent) at year 6 (p
Posted on 04/29/09, 04:04 pm