| Each year, neurodegeneration affects over 10 million individuals worldwide. It is the fourth leading cause of death in industrialized nations. This number is anticipated to increase by 20% over the next 10 years as the aging population continues to expand (Spuch, Ortolano, & Navarro, 2012). The pathogenesis of Alzheimer's disease (AD) is a poorly understood, complex mechanism. It is the most common age-related neurodegenerative disease in the United States (Alzheimer's Association, 2014). Advancing age is the single greatest risk factor for the development of Alzheimer's. Therefore, as the median population in the United States increases, the prevalence of AD continues to rise. Consequently, research involving the impact of anesthesia on cognitive function has gained attention. The need to explore anesthetic agents and their potential contribution to the pathogenesis of AD is pertinent so that certain agents may be avoided in at risk populations in the future. This research examines the effects of the most widely used volatile anesthetic agent, sevoflurane, on the gene expression of tau protein kinase II (TPK II). This enzyme is responsible for the phosphorylation of a microtubule associated protein, tau. Hyperphosphorylation of tau is a key characteristic in AD development (Imahori & Uchilda, 1996). Pheochromocytoma cells (PC-12) were exposed to varying concentrations of sevoflurane. The impact on tau phosphorylation will be measured by quantitative real time polymerase chain reaction (RT-PCR). |
