The biochemical pathways of central nervous system neural degeneration in niacin deficiency
- PMID: 25317166
- PMCID: PMC4192966
- DOI: 10.4103/1673-5374.139475
The biochemical pathways of central nervous system neural degeneration in niacin deficiency
Abstract
Neural degeneration is a very complicated process. In spite of all the advancements in the molecular chemistry, there are many unknown aspects of the phenomena of neurodegeneration which need to be put together. It is a common sequela of the conditions of niacin deficiency. Neural degeneration in Pellagra manifests as chromatolysis mainly in pyramidal followed by other neurons and glial cells. However, there is a gross lack of understanding of biochemical mechanisms of neurodegeneration in niacin deficiency states. Because of the necessity of niacin or its amide derivative NAD in a number of biochemical pathways, it is understandable that several of these pathways may be involved in the common outcome of neural degeneration. Here, we highlight five pathways that could be involved in the neuraldegeneration for which evidence has accumulated through several studies. These pathways are: 1) the tryptophan-kyneurenic acid pathway, 2) the mitochondrial ATP generation related pathways, 3) the poly (ADP-ibose) polymerase (PARP) pathway, 4) the BDNF-TRKB Axis abnormalities, 5) the genetic influences of niacin deficiency.
Keywords: BDNF-TRKB pathway; Niacin deficiency; biochemical pathways of degeneration; chromatolysis; kyneurenic acid; neural degeneration.
References
-
- Abdallah DM. Nicotinamide alleviates indomethacin induced gastric ulcers: a novel antiulcer agent. Eur J Pharmacol. 2010;627:276–280. - PubMed
-
- Anne M. Fagan, Guojun Bu, Yuling Sun, Alan Daughertyi, David M. Holtzman. Apolipoprotein E-containing high density lipoprotein promotes neurite outgrowth and is a ligand for the low density lipoprotein receptor-related protein. J Biol Chem. 1996;271:30121–30125. - PubMed
-
- Ayoub IA, Lee EJ, Ogilvy C, Flint BM, Maynard KI. Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in wistar rats. Neurosci Lett. 1999;259:21–24. - PubMed
Publication types
LinkOut - more resources
Full Text Sources
Other Literature Sources