In ataxia-telangiectasia models, persistent DNA damage causes PARP1 hyperactivation, NAD+ depletion, and reduced SIRT1 activity, whereas NAD+ replenishment with NR or related interventions restores SIRT1-dependent deacetylation, improves mitochondrial function and mitophagy, and prolongs health span [53]. This evidence concerns the gene SIRT1 and Ataxia-telangiectasia.