Document Information


PMID 8858182  (  )
Title Oxidative stress and mitochondrial dysfunction in neurodegeneration.
Abstract Rapid advances are being made in our understanding of the pathogenesis of neurodegenerative diseases, particularly those in which specific DNA mutations have been identified. beta-amyloid has been shown to induce free radical formation both directly and via an effect on endothelial function. There is presuasive evidence for cytochrome oxidase dysfunction with oxidative stress and damage in the brains of patients with Alzheimer's disease. The confirmation of the complex II inhibitor 3-nitropropionic acid as a toxin model for Huntington's disease, together with the demonstration of reduced mitochondrial function in Huntington's disease caudate, supports the proposition that mutant huntingtin may exert its effect through an abnormality of energy metabolism. UK.

NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.



Targets by SciMiner Summary

HUGO ID Symbol Target Name #Occur ActualStr
620APPamyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)1amyloid beta protein |
4851HTThuntingtin1huntingtin |

 


Targets by SciMiner Full list

HUGO ID Symbol Name ActualStr Score FlankingText
4851HTThuntingtinhuntingtin1.0 3 nitropropionic acid as a toxin model for huntington's disease together with the demonstration of reduced mitochondrial function in huntington's disease caudate supports the proposition that mutant huntingtin may exert its effect through an abnormality of energy metabolism.
620APPamyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)amyloid beta protein1.0amyloid beta protein precursor|dna mitochondrial|free radicals|hd protein human|nerve tissue proteins|nuclear proteins|reactive oxygen species|electron transport complex iv|