In a
fruit fly model, by targeting kynurenine 3-monooxygenase (
KMO) the authors were able to halt the development of the neurodegeneration associated with the
Huntington's disease mutation. Also by manipulating metabolites in the KMO cellular pathway they could manipulate the symptoms that the flies displayed.
KMO is enzyme 1.1.143.9 (in red) in this
KEGG pathway
This area of tryptophan metabolism can generate toxic NMDA receptor agonists (e.g.
quinolinic acid)or protective antagonists (
kynurenic acid).
No comments:
Post a Comment