Nucleotide repeat expansions are a common characteristic of Neurodegenerative disorders such as Huntington’s disease (HD), spinocerebellar ataxia, Fragile X syndrome and Frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS). The mechanisms by which these repeats confer toxicity remain largely elusive. Using a sensitized genetic screen in the Drosophila eye, we report a series of modifiers that interact with the toxicity of both the expanded CAG repeats (HD) and the expanded GGGGCC repeats (FTD/ALS), with synthetic lethality as a readout. Synthetic lethal interactions represent strong interactions that could indicate a functional relationship between genes. Our data suggests that common functional modules exist between HD and FTD/ALS.