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Grant strengthens research arm of Penn State Hershey Medical Center's ALS Clinic

lar diseases and look for the prevalence of the mutated form of the Hfe gene in the two groups. A mutation in the Hfe gene has been linked with a condition called hemachromatosis, which causes too much iron to accumulate in the tissues. People can be carriers of the mutant Hfe gene and yet have no symptoms of hemachromatosis. However, the organs (e.g. liver, heart, brain) of these individuals may still mishandle iron and as a result can produce free radicals. Free radicals are toxic forms of oxygen that result when iron interacts with oxygen in the body. These toxins can indiscriminately kill healthy cells. This process, called oxidative stress, is considered a contributor to the disease process in ALS.

Connor and Simmons will test the hypothesis that Hfe mutations are associated with an earlier onset of ALS and a more rapid disease progression. A second part of the study will investigate distribution and levels of expression of Hfe in tissue collected at autopsy from the brains and spinal cords of those with and without ALS. Finally, because the researchers hypothesize that the presence of an Hfe mutation increases the amount of oxidative damage, they will measure the amount of oxidative stress markers in autopsy samples from those with ALS and the Hfe mutation, and compare it to samples from patients with ALS without the mutation. An important component of ALS research is organ and tissue donation when a person with ALS dies.

"We deeply appreciate such donations, and fully realize what valuable gifts these are," Simmons said. "We believe there are exciting therapeutic opportunities that may result from our study. If our hypothesis proves correct, those patients with ALS who possess the Hfe mutation could be counseled to reduce dietary iron intake and may respond particularly well to antioxidant therapy."


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Contact: Valerie Gliem
vgliem@psu.edu
814-865-9481
Penn State
28-Jul-2003


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