Author Faculty (Discipline)

Nursing

Document Type

Article

Publication Date

2-6-2017

JOURNAL

Neural Regeneration Research

VOLUME NUMBER

12

ISSUE NUMBER

1

PAGE NUMBERS

39-42

ISSN

1876-7958

Embargo Period

1-12-2021

ANZSRC / FoR Code

110199 Medical Biochemistry and Metabolomics not elsewhere classified

Reportable Items (HERDC/ERA)

C1

Abstract

Immune-mediated activation of tryptophan (TRYP) catabolism via the kynurenine pathway (KP) is a consistent finding in all inflammatory disorders. Several studies by our group and others have examined the neurotoxic potential of neuroreactive TRYP metabolites, including quinolinic acid (QUIN) in neuroinflammatory 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 benefit 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 nucleotide, 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 neuroinflammatory disease.

Link to publisher version (DOI)

https://doi.org/10.4103/1673-5374.198971

Peer Review

Before publication

Comments

Used by permission: the author(s)

Creative Commons License

Creative Commons Attribution-Noncommercial-Share Alike 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License.


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