Molecular mechanisms of the (cognitive and motor) alterations in hyperammonemia and hepatic encephalopathy. Therapeutic implications.

Patients with liver disease (e.g., cirrhosis) may present with hepatic encephalopathy (HE), an alteration of brain function that is a consequence of a previous failure of liver function. Patients with minimal or clinical HE have different levels of cognitive impairment.

Acronym

Molecular-mechanisms-2021-2025

Reference code

CIPROM/2021/82

Description

Hyperammonemia is considered to be a major contributor to neurological alterations in HE. Animal models of chronic HE (e.g., rates with 'portacaval' sunts) or “pure” hyperammonemia also show impairment of cognitive function. The studies summarized here demonstrate that the impairment of some types of cognitive function in chronic HE is due to impaired function of the glutamate-nitric oxide-GMPC pathway in the brain.

Developers of the project

Laboratory of Social Cognitive Neuroscience (LabNSC)

www.uv.es/labnsc

labnsc@uv.es

labnscuv@uv.es

Keywords

Hepatic encephalopathy, Hyperammonemia, Cognitive function GMPN Receptors, MDA, Nitrogen oxide, Neuroinflammation

Non-UV principal researchers

Vicente Felipo.

Non-UV participating researchers

Pilar Monfort, Omar Cauli, Carmina Montoliu, Regina Rodrigo, Marta Llansola, Blanca Piedrafita, Nisrin el Mlili, Jordi Boix, Ana Agustí,

Start date