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
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.
