Molecular-mechanisms-2021-2025
CIPROM/2021/82
DESCRIPTION
Hyperammonemia is considered to contribute primarily to neurological impairments in SSc. Animal models of chronic SSc (e.g., rats with 'portal-caval' shunts) or of 'pure' hyperammonemia also show impaired cognitive function. The studies summarized here demonstrate that impairment of some types of cognitive function in chronic SSc is due to impaired function of the glutamate-nitric oxide-GMPC pathway in the brain.
DEVELOP THE PROJECT
Laboratory of Cognitive Social Neuroscience (LabNSC)
Email: labnsc@uv.es / labnscuv@uv.es
Hepatic encephalopathy, Hyperammonemia, Cognitive function GMPN Receptors, MDA, Nitrogen oxide, Neuroinflammation
- Salvador Fernandez-montejo, Otilia Alicia
- PDI-Catedratic/a d'Universitat
Vicente Felipo.
Pilar Monfort, Omar Cauli, Carmina Montoliu, Regina Rodrigo, Marta Llansola, Blanca Piedrafita, Nisrin el Mlili, Jordi Boix, Ana Agustí,
- Generalitat Valenciana.
- Laboratory of Neurobiology, Centro de Investigacion Principe Felipe, Valencia.
- Fundación Hospital Clínico Universitario, Valencia.