Hyperammonemia-induced toxicity for the developing central nervous system

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_455534AF6BDE
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Hyperammonemia-induced toxicity for the developing central nervous system
Périodique
Brain Research Reviews
Auteur(s)
Cagnon L., Braissant O.
ISSN
0165-0173 (Print)
Statut éditorial
Publié
Date de publication
2007
Volume
56
Numéro
1
Pages
183-197
Notes
Review
Résumé
In pediatric patients, hyperammonemia can be caused by various acquired or inherited disorders such as urea cycle deficiencies or organic acidemias. The brain is much more susceptible to the deleterious effects of ammonium during development than in adulthood. Hyperammonemia can provoke irreversible damages to the developing central nervous system that lead to cortical atrophy, ventricular enlargement and demyelination, responsible for cognitive impairment, seizures and cerebral palsy. Until recently, the mechanisms leading to these irreversible cerebral damages were poorly understood. Using experimental models allowing the analysis of the neurotoxic effects of ammonium on the developing brain, these last years have seen the emergence of new clues showing that ammonium exposure alters several amino acid pathways and neurotransmitter systems, as well as cerebral energy metabolism, nitric oxide synthesis, oxidative stress, mitochondrial permeability transition and signal transduction pathways. Those alterations may explain neuronal loss and impairment of axonal and dendritic growth observed in the different models of congenital hyperammonemia. Some neuroprotective strategies such as the potential use of NMDA receptor antagonists, nitric oxide inhibitors, creatine and acetyl-l-carnitine have been suggested to counteract these toxic effects. Unraveling the molecular mechanisms involved in the chain of events leading to neuronal dysfunction under hyperammonemia may be useful to develop new potential strategies for neuroprotection.
Pubmed
Web of science
Open Access
Oui
Création de la notice
04/02/2008 9:49
Dernière modification de la notice
08/05/2019 17:53
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