Impaired brain glymphatic flow in experimental hepatic encephalopathy

The mechanisms underlying the pathogenesis of hepatic encephalopathy (HE) in patients with cirrhosis (chronic liver disease) are not completely understood. Data available in the literature suggest that noxious substances and metabolites such as lactate, glutamate, bile acids and drugs accumulate in the brain of HE patients[1]. The currently prevailing hypothesis proposes that this occurs due to metabolic and transporter defects induced by hyperammonemia, inflammation and alterations in blood brain barrier (BBB) function [2,3].

Source: Journal of Hepatology - September 7, 2018 Category: Gastroenterology Authors: Anna Hadjihambi, Ian F. Harrison, Marta Costas-Rodr íguez, Frank Vanhaecke, Natalia Arias, Rocío Gallego-Durán, Svetlana Mastitskaya, Patrick S. Hosford, Steven W.M. Olde Damink, Nathan Davies, Abeba Habtesion, Mark F. Lythgoe, Alexander V. Gourine, Ra Source Type: research