Source: David Stauth
Distinguished biochemistry and biophysics professor Joe Beckman and his research team recently determined that a copper compound known for decades may treat amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease.
Beckman collaborated with scientists from Australia and the United Kingdom on this study just published in the Journal of Neuroscience that showed oral intake of this compound significantly extended the lifespan and improved the locomotor function of transgenic mice that are genetically engineered to develop this debilitating and terminal disease.
No human therapy for ALS has ever been discovered that could extend lifespan beyond a few months. Linus Pauling Institute researchers say this approach has the potential to change that and may help treat Parkinson’s disease as well.
“We believe that with further improvements, and following necessary human clinical trials for safety and efficacy, this could provide a valuable new therapy for ALS and perhaps Parkinson’s disease,” said Joe Beckman, principal investigator and Ava Helen Pauling Chair at the Linus Pauling Institute as well at the Director of the Environmental Health Sciences Center.
ALS was first identified as a progressive and fatal neurodegenerative disease in the late 1800s and gained international recognition in 1939 when it was diagnosed in American baseball legend Lou Gehrig. It’s known to be caused by motor neurons in the spinal cord deteriorating and dying, and has been traced to mutations in copper, zinc superoxide dismutase, or SOD1. Ordinarily, superoxide dismutase is an antioxidant whose proper function is essential to life.
Collaborators on this research include OSU, the University of Melbourne, University of Technology/Sydney, Deakin University, the Australian National University, and the University of Leeds in the United Kingdom. The lead author on the new study is Blaine Roberts from the University of Melbourne, who received his doctorate from OSU studying under Beckman.
Funding has been provided by the Australian National Health and the Medical Research Council, the U.S. National Institutes of Health, the Linus Pauling Institute and other groups in Australia and Finland.
Joe Beckman et. al. Oral Treatment with CuII(atsm) Increases Mutant SOD1 In Vivo but Protects Motor Neurons and Improves the Phenotype of a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis. J Neurosci. 2014 Jun 4;34(23):8021-31. doi: 10.1523/JNEUROSCI.4196-13.2014.
See the video and story from KEZI
Read the post on the Linus Pauling Institute blog. When Copper Meets SOD: An ALS Story
