Lou Gehrig's Disease Advance... Possibly

In a series of experiments reported today in the Journal of Neuroscience, a University of Wisconsin-Madison pharmacy researcher was able to prolong life and slow nerve deterioration in a mouse with a genetic form of ALS, or amyotrophic lateral sclerosis. Marcelo Vargas, a postdoctoral fellow in the laboratory of Jeff Johnson, professor in the School of Pharmacy, tested mice that carried an extra gene that pushed support cells for the neurons into overdrive, causing them to pump out extra quantities of the anti- oxidant glutathione.
The gene in question, called Nrf2, has long been a research focus for Johnson, who is also a Waisman Center investigator.
Although oxidation is a major cause of cell death in Parkinson's disease and Alzheimer's disease as well as ALS, antioxidant treatments have failed to slow these diseases.
But the mice with extra copies of Nrf2 produced glutathione right alongside the vulnerable neurons, and that made all the difference, says Johnson. These special mice were engineered in collaboration with Albee Messing, a professor in the UW-Madison School of Veterinary Medicine and also an investigator at the Waisman Center. "It's extremely difficult to increase glutathione in the central nervous system," Johnson says. "You can't just shoot it into people or animals. But we found a 25 percent increase in the molecule in the spinal cords."
Although the mice did eventually die of ALS, they lived longer, and the disease appeared 17 days later than in mice that lacked the extra Nrf2 gene, Johnson says. "This was a very aggressive model of ALS, so a life extension of 21 days is thought to be pretty significant, roughly equivalent to five to 10 years in human patients."
http://www.physorg.com/news148067707.html

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