In neurodegenerative diseases, such as Alzheimer’s disease, tau protein aggregation is observed. In Alzheimer’s disease and related conditions, accumulation of insoluble tau impairs physiological function that ultimately leads to neuron loss. Using a transgenic Caenorhabditis elegans model that expresses human tau protein in neurons, we are able to see accumulated, insoluble, phosphorylated tau, and uncoordinated movement (Unc) phenotypes in these organisms. To identify genes participating in aggregated tau and Unc phenotypes, we conducted a mutagenesis; an estimated 20,000 worm genomes were screened and we isolated seven promising strains of C. elegans that carried loss of function genes suppressing the tau-induced phenotypes. These strains are currently being sequenced to determine the identity of the loss of function genes, which may represent novel suppressors of tau pathology. Currently, the Kraemer lab has identified two genes suppressing tau-induced Unc phenotype and called them suppressor of tau 1 (sut-1) and suppressor of tau 2 (sut-2). Animals with sut-1 and/or sut-2 mutations are resistant to the negative effects of tau, meaning that the proteins made by these genes are necessary for tau phenotypes. With this knowledge and the additional information to be gained from the sequencing of seven novel sut alleles, we hope that potential neuroprotective approaches for treatment can be developed.