Published on November 18, 2008 at 4:11 AM
Maas Biolab researchers CSO Eskil Elmer, M.D., Ph.D. and neuroscientist Magnus Hansson, M.D., Ph.D., and colleagues have for the first time ever demonstrated the mitochondrial permeability transition (mPT) or "megapore" occurs in viable adult human neuron mitochondria and the ability of cyclosporin-A to block its formation.
These effects had previously been well characterized in animal neuroprotection studies and have now been validated in human brain tissue. The findings were presented at the Society for Neuroscience annual meeting in Washington, D.C. on Saturday, November 15, 2008. 32,000 attended this meeting, the premiere venue for world neuroscientists' cutting-edge research.
Cyclosporin-A is neuroprotective through its effects on mitochondria. Attacked mitochondria normally stop making ATP and release toxic factors that activate caspases and apoptosis genes, killing the neuron. This cell death is caused by the formation of the mPT megapore. The mPT megapore can only form if it has cyclo philin -D available. Cyclosporin-A binds up all cyclophilin-D within each mitochondrion. Cyclosporin-A treated mitochondria continue to function normally, even while under attack, from conditions ranging from amyotrophic lateral sclerosis (ALS) to brain trauma. This is now confirmed in the human brain, reinforcing the expected effectiveness for cyclosporin-A in people with neurological diseases.
Cyclosporin-A is the active ingredient in Maas Biolab's Mitogard intrathecal formula developed to treat ALS. Maas partner NeuroVive Pharmaceutical AB is producing NeuroSTAT, an intravenous cyclosporin-A formula for the treatment of traumatic brain injury. This research confirms cyclosporin-A is an effective human neuromitochondrial protectant.
http://www.neurovive.com