The regeneration of infarcted brain tissue has been a sought after feat in the neuroscience field since the conceptualization of stroke. This challenging and often elusive goal has been likened to a “holy grail” for those most concerned with this endeavor. Hundreds of molecules have been potential solutions to this puzzle, but only few have proven worthy of pursuit. One such molecule is actually an antibody called GSK249320. This antibody blocks the axon outgrowth inhibition molecule known as myelin-associated glycoprotein (MAG). So, it’s an anti-MAG antibody. MAG is a good target since it has been shown to be up-regulated in peri-infarct tissue after ischemic damage.
In 2013, Cramer and colleagues published a study in Stroke proclaiming the safety and tolerability of escalating doses of GSK249230 in 42 post-stroke patients. In the present study, Barbay et al set out to move toward proving efficacy of GSK249320 by showing its ability to enhance recovery of skilled use of the forelimb in a non-human primate model of focal cortical ischemia. Essentially, the goal was to find out if the effects are evident in the organization of movement representations in spared cortical areas.
The study involved 9 monkeys that were either assigned to receiving the drug or placebo. First the monkeys were all taught a specific task that required the use of their distalThey were all taken to the OR and given a stroke in the distal forelimb representations (DFLs) in primary motor cortex. Afterward, they either got the drug or placebo at 24-hours post-stroke, and then weekly for seven weeks. At the end of this time period, the two groups were compared to evaluate for their ability to complete the previously learned task. Then, the monkey brains were analyzed to see if there were anatomic and histologic correlations.
This study found that the experimental group had almost immediate improvements compared with the control group. Their functional outcome was significantly improved at day 3 and day 9 (second treatment). There were some discrepancies in the analysis of the cortical areas that were explained by the length of the study. But, overall there were also significant changes neurophysiologically in the experimental groups stroke sites.
