Abstract

Tauopathies such as Alzheimer's disease and Frontotemporal Dementia-17 are diseases characterized by an abnormal amount of aggregated, hyperphosphorylated tau protein in the body. Tauopathies are one field of neuroscience which have not been studied as adamantly as others. For example, Alzheimer's disease is characterized by not only excess tau, but another hallmark is the presence of amyloid beta plaques. These amyloid-beta plaques have been studied extensively, whereas the tauopathic pathway of diseases like Alzheimer's has not been studied as thoroughly. This project covered how the removal of the MADD-2 gene and treatment with a supplement from grapes called Resveratrol can affect the amount of aggregated and hyperphosphorylated tau in Caenorhabditis elegans. This was accomplished through cDNA/ORF Clones of the MADD-2 gene, and then running a restriction digest, DNA purification, and ligation, and finally transformation of HT115 competent cells into an RNAi feeding strain to remove the MADD-2 gene. The results of this project rejected the null hypotheses because the amount of tau was lowered, and the locomotion assay showed that movement was much better after RNAi and resveratrol treatment of worms with excess tau. This study can be applied to further genetic research and neuroscience.