Abstract: Genomic instability is one of the hallmarks of ageing. In general, DNA repair counteracts genomic instability, but here we show that too much DNA repair can be harmful and actually drive neuronal ageing. Specifically, we show that the base excision repair pathway generates genomic stress, and promotes age-related neurodegeneration in a Caenorhabditis elegans model of Parkinson Disease. Conversely, defects in the DNA glycosylase that initiates base excision repair leads to a remarkable neuroprotective phenotype. The mechanisms will be presented.