Kynurenine pathway metabolism and neuroinlfammator y disease
Nady Braidy
Ross Grant
摘要：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.
机标关键词：neurological disordersbrain dysfunctionquinolinic acidimmune responseDNA damagecell death
论文发表日期：2017-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：4( 39-42 )
英文信息