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Abstract
Abstract The DNA of neurons is continually damaged due to lifelong, high-level metabolic and transcriptional activity. In addition, recent studies have demonstrated extensive “programmed” DNA damage and somatic mutation in differentiating post-mitotic neurons. Here, we identify these endogenous lesions as single strand break intermediates of thymine DNA glycosylase (TDG)-mediated removal of oxidized methylcytosines during active DNA demethylation. Interrupting active DNA demethylation using anti-neoplastic cytosine analogs triggers TDG-dependent neuronal cell death. This suggests that the well-known neurotoxic side effects of certain chemotherapies, also called “chemobrain,” could be linked to DNA repair processes intrinsic to normal neuronal differentiation. In this presentation, we discuss the implications of these findings to neurodegeneration and cancer. Citation Format: Andre Nussenzweig. Neuronal Genome Stability and Plasticity [abstract]. In: Proceedings of the AACR Special Conference: Aging and Cancer; 2022 Nov 17-20; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_1):Abstract nr IA003.
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