Abstract
Cirrhotic patients can present hepatic encephalopathy (HE), showing motor and cognitive deficits. Hyperammonemia and peripheral inflammation are known to induce neuroinflammation and alter neurotransmission, which finally induces neurological impairment in HE. However, the mechanisms by which the deleterious effects of peripheral inflammation are transmitted to the brain are not well understood. Extracellular vesicles (EVs) have recently emerged as a new mediator between the periphery and the brain, particularly in pathologies associated with sustained inflammation and in neurological disorders. In this work, we summarized the main findings on the role of plasma EVs in hyperammonemia and HE and discussed its potential implication in the pathogenesis of hepatic encephalopathy.