Effect of Metal Ions and EDTA on Catalase Activity-Potential in Alzheimer's Treatment

Friday, 13 February 2015
Exhibit Hall (San Jose Convention Center)
Jack Zhang, Blue Bell, PA
Research on Alzheimer's disease has indicated that the etiology of AD includes (although is not restricted to) marked accumulation of metals, amyloid-beta deposition, severe oxidative stress, and metal - amyloid-beta interactions. The neurodegenerative damage may in part be caused by the inhibited activity of catalase, the anti-oxidant enzyme responsible for preventing oxidative damage. This study sought to measure the effects of metal ions and EDTA on an enzyme-catalyzed reaction in a controlled experiment, and explain how these factors affect rates of enzyme-catalyzed reactions. Based on experimental results, it was cautiously extrapolated that chelation therapy, as a metal-targeting treatment, could hold attractive implications for the treatment of AD. The methodology of a simple disc-gas system was utilized to measure the rate of the release of oxygen gas from the decomposition of hydrogen peroxide. Three metal ions, aluminum, lead, and copper, all of which commonly associated with AD, were found to inhibit the rate of catalase oxidation. However, the presence of EDTA was measured to have a marked effect by decreasing the inhibition of the metal ions on catalase activity. Thus, this observation renders chelation therapy an attractive potential pharmacological option for the treatment of AD. However, this study does not prove, but only suggests, the viability of chelation therapy, as there is still a substantial lack of reliable data as well as definitive conclusions regarding the clinical advantages of chelation in neurodegenerative conditions, and a number of must still be fulfilled if chelation therapy is to be adapted to AD.