HM568 Enhances NAD+ Biosynthesis to Ameliorate Mitochondrial Dysfunction and Neurotoxicity in Parkinson's Disease Models: A Putative Link to PARP1 Modulation - PubMed
3 hours ago
- #Parkinson's Disease
- #NAD+ Biosynthesis
- #Mitochondrial Dysfunction
- HM568 improves behavioral deficits, prevents dopaminergic neuron loss, and restores blood-brain barrier integrity and mitochondrial morphology in Parkinson's disease models.
- HM568 counteracts MPP+-induced inhibition of mitochondrial respiratory chain complexes I, III, and IV, restoring mitochondrial function.
- HM568 elevates intracellular NAD+ levels, downregulates PARP1 protein expression, and inhibits its enzymatic activity.
- Molecular docking and dynamics simulations show HM568 has high binding affinity and selective inhibition for PARP1 over PARP2.
- HM568 may correct mitochondrial dysfunction and energy imbalance via PARP1 inhibition and NAD+ metabolism modulation, suggesting therapeutic potential for Parkinson's disease.