Immune-mediated activation of tryptophan (TRYP) catabolism via the kynurenine pathway (KP) is a con-sistent ifnding in all inlfammatory disorders. Several studies by our group and others have examined the neurotoxic potential of neuroreactive TRYP metabolites, including quinolinic acid (QUIN) in neuroinlfam-matory neurological disorders, including Alzheimer’s disease (AD), multiple sclerosis, amylotropic lateral sclerosis (ALS), and AIDS related dementia complex (ADC). Our current work aims to determine whether there is any beneift to the affected individuals in enhancing the catabolism of TRYP via the KP during an immune response. Under physiological conditions, QUIN is metabolized to the essential pyridine nucle-otide, nicotinamide adenine dinucleotide (NAD+), which represents an important metabolic cofactor and electron transporter. NAD+also serves as a substrate for the DNA‘nick sensor’ and putative nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP). Free radical initiated DNA damage, PARP activation and NAD+depletion may contribute to brain dysfunction and cell death in neuroinlfammatory disease.