We utilized wildtype (Cd38+/+), heterozygous Cd38 (Cd38+/−), and knockout Cd38 (Cd38−/−) mice to evaluate transcriptional, metabolic, and functional changes associated with CD38 deficiency in the midbrain, a region enriched in dopaminergic neurons, which are vulnerable to dysfunction and cell loss in PD. This evidence concerns the gene CD38 and Parkinson disease.