BDNF (Brain-Derived Neurotrophic Factor) May Be Involved in Lesion Resolution and Recovery
November 17, 2003
Kansas City, MO
Researchers at the University of Maryland School of Medicine have shown that Copaxone® (glatiramer acetate injection), used to treat relapsing-remitting multiple sclerosis (RRMS), stimulates anti-inflammatory lymphocytes (T-cells) to produce a neuroprotective protein, brain-derived neurotrophic factor (BDNF). Results published in the November issue of the Journal of Neurological Sciences demonstrated that in cell lines originating from the same patients, Copaxone®-reactive T-cells produced significantly higher levels of BDNF than T-cells reactive to other compounds (p=0.033).
In the study, BDNF production was examined in 73 Copaxone®-reactive, 13 Myelin Basic Protein-reactive, and 22 Tetanus toxoid-reactive T-cell lines generated from 12 patients treated with Copaxone®. Of these, the Copaxone®-reactive T-cell lines produced significantly higher BDNF levels compared to the other T-cell lines after stimulation with their respective antigens (p= 0.033).
Suhayl Dhib-Jalbut, M.D., professor of neurology, University of Maryland, and corresponding author of the paper, discussed the significance of these findings. "It is important to further understand mechanisms that produce clinical effects of drugs used to treat MS. Our findings seem to suggest a possible neuroprotective mechanism for Copaxone® based on its ability to stimulate production of BDNF, a potent neurotrophin that has profound effects on neuronal survival and repair."
There are several possible effects of BDNF in MS. First, BDNF could support neuronal survival and enhance neuronal and axonal repair. In addition, locally produced BDNF might affect remyelination. These mechanisms are of particular importance in a disease such as MS, in which the loss of axons is believed to underlie the clinical deficit a patient may acquire over time.
"While the exact mechanism of action of Copaxone® (glatiramer acetate injection) is not fully understood in MS, if BDNF provides a neuroprotective effect in MS, then Copaxone®, may work through a dual action of anti-inflammatory and neuroprotective mechanism via activation of T-cells which enter the brain and protect axons from long-term degeneration. Correlation of BDNF production with clinical outcome measures of treatment efficacy is not possible due to the small sample size and was not intended as an objective of this study. However, given the heterogeneity of BDNF production among the 12 patients, such correlations are warranted in prospective clinical trials with Copaxone®," said Dr. Dhib-Jalbut.
Copaxone® is indicated for the reduction of the frequency of relapses in relapsing-remitting MS. The most common side effects of Copaxone® are redness, pain, swelling, itching, or a lump at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.
Copaxone® is now approved in 42 countries worldwide, including the U.S., Canada, Australia, Israel, and all the European countries. In Europe, Copaxone® is marketed by Teva Pharmaceutical Industries Ltd., and Aventis Pharma. In North America, Copaxone® is marketed by Teva Neuroscience, Inc.
Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 30 pharmaceutical companies in the world. The company develops, manufactures, and markets generic and branded human pharmaceuticals and active pharmaceutical ingredients. Close to 90 percent of Teva's sales are in North America and Europe. Teva's innovative R&D focuses on developing novel drugs for diseases of the central nervous system.
Teva Pharmaceuticals USA is a subsidiary of Teva Pharmaceutical Industries Ltd. Teva Neuroscience, Inc. is a subsidiary of Teva Pharmaceutical Industries Ltd. Teva Neuroscience, Inc. markets Copaxone® (glatiramer acetate injection).
Copaxone® is a registered trademark of Teva Pharmaceutical Industries Ltd.
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