Neurological deterioration in Parkinson’s disease (PD) and resulting motor dysfunction arises from Lewy body formation and dopaminergic neuronal death in the substantia nigra. Two factors contributing to PD-related apoptosis and subsequent motor dysfunction involve improper cellular metabolism of reactive oxygen species (ROS) and impaired mitochondrial functionality. The co-factor Nicotinamide Adenine Dinucleotide (NAD+), reduction of which has been implicated in the development of neurodegenerative disease, is a critical player in maintaining cellular redox metabolism and mitochondrial function. We present a case study of a PD patient who has become near asymptomatic through the use of intravenous (I.V.) NAD+. This report documents the patient’s initial symptom changes while receiving I.V. NAD+ over the course of eight treatment days, with two non-treatment days in between. The treatment entailed 1500 mg. I.V. NAD+ on day one, 1000 mg. I.V. NAD+ on day two, and 750 mg. I.V. NAD+ on day three. Symptoms were documented by medical staff for the next two days of non-treatment. Following this, 750 mg. I.V. NAD+ was administered on treatment days four and five, 500 mg. I.V. NAD+ on treatment days six and seven, and 750 mg. I.V. NAD+ on treatment day eight. Over the course of treatment, the patient’s hand tremors decreased to a mild level, permitting coordinated use of a pen and utensils. Hand tremors were absent on days one and six. Visual hallucinations were absent on days two through seven. To maintain tremors at a tolerable level, aftercare involved I.V. NAD+ every four to six weeks, with a daily regimen of 300 mg/ml NAD+ nasal spray. Moreover, the patient discontinued PD-related medication, thereby preventing visual hallucination side effects. Although more research on NAD+ in clinical use is needed, the evidence obtained from these symptom improvements indicates NAD+ as having the potential for clinical use in at least a subset of PD sufferers.