Moreover, mice with reduced DNA repair capability as a result of genetic deletion of BER proteins (OGG1, NEIL1, Xrcc 1, and Polβ) exhibit increased neuronal vulnerability to metabolic stress (Liu et al., 2011; Canugovi et al., 2012; Ghosh et al., 2015), and metabolic stress is implicated in neuronal dysfunction and death in AD (Mattson et al., 2008). The gene discussed is POLB; the disease is Alzheimer disease.