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research article

Ammonia toxicity to the brain

Braissant, Olivier
•
McLin, Valérie A.
•
Cudalbu, Cristina  
2013
Journal of inherited metabolic disease

Hyperammonemia can be caused by various acquired or inherited disorders such as urea cycle defects. The brain is much more susceptible to the deleterious effects of ammonium in childhood than in adulthood. Hyperammonemia provokes irreversible damage to the developing central nervous system: cortical atrophy, ventricular enlargement and demyelination lead to cognitive impairment, seizures and cerebral palsy. The mechanisms leading to these severe brain lesions are still not well understood, but recent studies show that ammonium exposure alters several amino acid pathways and neurotransmitter systems, cerebral energy metabolism, nitric oxide synthesis, oxidative stress and signal transduction pathways. All in all, at the cellular level, these are associated with alterations in neuronal differentiation and patterns of cell death. Recent advances in imaging techniques are increasing our understanding of these processes through detailed in vivo longitudinal analysis of neurobiochemical changes associated with hyperammonemia. Further, several potential neuroprotective strategies have been put forward recently, including the use of NMDA receptor antagonists, nitric oxide inhibitors, creatine, acetyl-L-carnitine, CNTF or inhibitors of MAPKs and glutamine synthetase. Magnetic resonance imaging and spectroscopy will ultimately be a powerful tool to measure the effects of these neuroprotective approaches.

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Type
research article
DOI
10.1007/s10545-012-9546-2
Web of Science ID

WOS:000321566900001

Author(s)
Braissant, Olivier
•
McLin, Valérie A.
•
Cudalbu, Cristina  
Date Issued

2013

Publisher

Springer Verlag

Published in
Journal of inherited metabolic disease
Volume

36

Issue

4

Start page

595

End page

612

Subjects

CIBM-AIT

Peer reviewed

REVIEWED

Written at

EPFL

EPFL units
CIBM  
Available on Infoscience
April 24, 2013
Use this identifier to reference this record
https://infoscience.epfl.ch/handle/20.500.14299/91732
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