Topic: hyperammonemia

Cirrhotic patients may show minimal hepatic encephalopathy (MHE), with mild cognitive impairment and motor deficits. Hyperammonemia and inflammation are the main contributors to the cognitive and motor alterations of MHE. Hyperammonemic rats reproduce these alterations. There are no specific treatments for the neurological alterations of MHE. Extracellular vesicles from mesenchymal stem cells (MSC-EVs) are promising to treat inflammatory and immune diseases.We aimed to assess whether treatment of hyperammonemic rats with MSC-EVs reduced neuroinflammation in cerebellum and restored motor coordi

Patients with liver cirrhosis show hyperammonemia and peripheral inflammation and may show hepatic encephalopathy with cognitive impairment, reproduced by rats with chronic hyperammonemia. Peripheral inflammation induces neuroinflammation in hippocampus of hyperammonemic rats, altering neurotransmission and leading to cognitive impairment. Extracellular vesicles (EVs) may transmit pathological effects from the periphery to the brain. The aims were to assess whether EVs from plasma of hyperammonemic rats (HA-EVs) induce cognitive impairment and to identify the underlying mechanisms.HA-EVs were

GABAergic neurotransmission is enhanced in the cerebellum of hyperammonemic rats, an animal model of hepatic encephalopathy, and this induces motor incoordination. There is an interplay between neuroinflammation and GABAergic neurotransmission, but the underlying mechanisms remain unclear. This work aimed to unveil the molecular mechanisms by which GABAergic neurotransmission modulates neuroinflammation in the cerebellum.Ex-vivo experiments were performed using cerebellar slices from control and hyperammonemic rats treated or not with bicuculline. We analyzed by immunohistochemistry microglia