I say 'potentially' because this study, like many others, was supported by the drug co. that developed, produces, markets and distributes Copaxone. So I guess we take the info with a grain of salt, and hope that the study was designed appropriately and objectively, and that results are reported accurately and ethically. If so, and the encouraging results are repeated in future studies, then it really would be great news for Copaxone users. Anything that may change the course of the disease for the better, is something we would all welcome!
www. medicalnewstoday. com/articles/148146.php
Long-Term Study With COPAXONE(R) Indicated Protective Effect On Brain Tissue In Multiple Sclerosis Patients 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<0.05). Group 2 (n=31) included patients who started GA therapy at enrollment. Mean age, disease duration and EDSS were 35.1 years, 5.8 years and 2.53, respectively. Mean NAA/Cr at baseline was 1.99 + 0.1 and 2.12 + 0.08 (+6.53 percent) at year 6 (p<0.05). Twelve untreated RRMS patients were also scanned for two years and showed a significant decline in NAA/Cr over the two years of follow-up. Additionally four untreated patients initiated COPAXONE® during the course of the study and demonstrated considerable improvement in the mean NAA/Cr ratio, as well as clinical stability during total study observation. Finally, nine healthy volunteers were scanned annually for controls. Further analysis is ongoing. The study was in part supported by Teva Neuroscience.
COPAXONE® is indicated for the reduction of the frequency of relapses in RRMS, including patients who have experienced a first clinical episode and have MRI (Magnetic Resonance Imaging) features consistent with multiple sclerosis. The most common side effects of COPAXONE® are redness, pain, swelling, itching, a lump or an indentation at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.
COPAXONE® is now approved in 52 countries worldwide, including the United States, Canada, Mexico, Australia, Israel and all European countries. In North America, COPAXONE® is marketed by Teva Neuroscience, Inc., which is a subsidiary of Teva Pharmaceutical Industries Ltd. (NASDAQ:TEVA). In Europe, COPAXONE® is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis. COPAXONE® is a registered trademark of Teva Pharmaceutical Industries Ltd.
See additional important information at http://www.copaxone.com/pi/index.html or call 1-800-887-8100 for electronic releases. For hardcopy releases, please see enclosed full prescribing information."