Parkinson’s disease (PD) is a neurodegenerative disorder characterized by dopaminergic neuronal loss, mitochondrial dysfunction, and neuroinflammation.1 Hyperactivation of poly(ADP-ribose) polymerase 1 (PARP1) contributes to PD pathology by depleting nicotinamide adenine dinucleotide (NAD+) and promoting cell death. While PARP1 inhibitors like PJ34 can attenuate neurodegeneration, their efficacy may be limited when used alone.2 NAD+ supplementation has shown promise in maintaining mitochondrial integrity and reducing inflammation, but has not been extensively combined with PARP1 inhibition.3 This study explores the therapeutic synergy of co-administering NAD+ and PJ34 in a 6-hydroxydopamine (6-OHDA)-induced PD model.4 We demonstrate that this combination enhances neuronal survival, suppresses neuroinflammation, and promotes autophagic flux more effectively than monotherapies, providing a compelling strategy to concurrently target energy metabolism and DNA repair pathways.