This thesis explores the role of DNA repair enzyme 8-oxoguanine glycosylase (OGG1) in a Drosophila model through both genetic manipulation and the administration of small molecule agonists. Age- and neurodegeneration-related locomotor decline are significantly affected by Ogg1 RNAi knockdown and Ogg1 overexpression, while OGG1 agonists partially rescue deficits in an age-, sex-, and genotype-dependent manner. These findings support OGG1 as a potential therapeutic target, particularly in patients with genetic vulnerabilities to neurodegenerative disease.
