An article published in the journal BMC Neuroscience in the August 2008 edition caught my eye this week. The article was about a compound called edaravone (chemical name- 3-methyl-1-phenyl-2-pyrazolin-5-one) that is used in ischemic stroke patients to protect neurons in the brain. Scientists think that edaravone may be neuroprotective because it will scavenge free radicals in the brain. The researchers in this study thought that this neuroprotective behavior might help in Parkinson’s Disease.
So what’s a free radical exactly? (No, it’s not a political extremist running amok in society as my husband likes to say every time I say something about free radicals and PD.) Free radicals are molecules that have an “extra” electron that is not paired with another electron. This “extra” electron does not like being unpaired so it looks for other molecules that it can “take” electrons from. When a free radical “takes” these electrons it can cause a host of issues for the “donor” molecule including cell death. Obviously the more free radicals that exist in someone’s brain the more cells that can be adversely affected. Edaravone is thought to essentially “eat up” these free radicals by binding with the “extra” electrons itself.
Now on to the actual study and how edaravone may help Parkinson’s Disease.
The study was conducted in two phases. First a known dopamine neuron toxin called 6-OHDA (6-hydroxydopamine) was applied to cells in-vitro (outside of a living organism) and then either edaravone or regular old saline was applied to the cells and the number and/or concentration of dopamine neurons was measured to see which group contained more dopamine cells. Second, an animal model of PD was used. In the second phase 6-OHDA was injected into several rats’ brains and then either edaravone or saline was administered intravenously at one of two different time periods. The first group received either edaravone or saline 30 minutes after the 6-OHDA injection and the second was administered edaravone or saline 24 hours after the initial 6-OHDA injection. The study was looking at two things: 1) Did the edaravone rats maintain more dopamine neurons than the saline rats and 2) Did those who received the edaravone at 30 minutes maintain more dopamine than those who received it at 24 hours.
The results of the study bode well for edaravone helping to protect dopamine neurons. First, the in-vitro part of the study showed a statistically significant increase in the number of surviving dopamine neurons in the edaravone infused cells over the saline infused controls. Second, the rats that received edaravone at either 30 minutes or 24 hours both had statistically significant higher amounts of dopamine cells when measured against those rats that only received saline. Also, those rats that received the edaravone at 30 minutes had statistically significant more dopamine neurons than those that received the same dosage at 24 hours.
The study’s authors concluded that edaravone did three things that might protect cells. First, it decreased oxidative stress by scavenging those nasty free radicals. Second, it decreased apoptosis (essentially cell suicide) and lastly it decreased inflammation in the brain.
So what implications does this have for Parkinson’s Disease? At this moment, not a lot, but possibly over a few years this compound could be used to help delay onset or help slow progression by “eating up” free radicals. Edaravone might also be helpful by increasing the survival of transplanted stem cells by decreasing apoptosis (cell suicide) and it might help decrease the inflammatory reaction due to surgery in the brain. All of these avenues offer hope for potential drugs or PD treatments that could help millions of Parkinson’s patients in the future. I will be watching for updates on edaravone and any applications it may have to Parkinson’s Disease.
As always here is a link to the study. A link to the full article is at the end of this abstract.
Edaravone Study
Wednesday, September 17, 2008
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2 comments:
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