Oral MS Drug Mechanism Known

An oral drug called laquinimod has been undergoing clinical trial and has so far been effective in treating relapsing-remitting MS. But the mechanism behind its effective treatment of MS has not been fully understood by researchers. A recent study on the oral MS drug will provide added insight on how the said drug works in treating the debilitating disease affecting millions of people worldwide.

According to researchers from St. Josef-Hospital Bochum and Ruhr-University Bochum in Germany, laquinimod works by triggering the immune cells within the central nervous system to produce and release a compound called brain-derived neurotrophic factor (BDNF) which contributes to the repair and stability of neurons, making it possible to limit damage to the brain. Neurotrophins like BDNF are important for the development and proper maintenance of neurons and axons in the central nervous system. Although they are known to be produced mainly by neurons, there are also several types of immune cells that are known to secrete BDNF. This suggests that the immune cells may also play a role in neuroprotection.

In order to understand better the effects of the oral drug laquinimod, the researchers evaluated the levels of BDNF in the serum of patients with relapsing-remitting MS who are being treated with the said oral MS drug. The researchers found a significant increase of BDNF levels in 76 percent of the patients. There was also an eleven-fold increase of BDNF serum levels seen in individual patients.

Results of experiments using animal models further strengthened the findings made on human patients. Mice induced with the experimental autoimmune encephalomyelitis, the animal model of MS. One group of mice was known to have BDNF deficiency in their immune cells (LLF mice) while another was composed of a wild-type control group. Both mice were treated with laquinimod. The treatment results showed a significant reduction in the incidence and severity of EAE in the wild control mice group. The effect of the said drug however was significantly reduced in the other mice group.

Added studies suggested that WT mice treated with suboptimal dose of the oral drug showed a significant reduction in the area of inflammation as well as in the level of demyelination. The WT mice also showed a reduction in macrophage infiltration as well as a significant number of axonal densities compared with the LLF mice. This data suggest that there is a BDNF-dependent mechanism of action for the drug laquinimod when it comes to autoimmune demyelination. The results of the study are published in the January 2012 issue of The American Journal of Pathology.

Source: Eureka Alert

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