Immunohistochemical study of GFAP, GS and AQP4 levels in the postmortem brain of cirrhotic patients

Abstract

One of the most dangerous liver cirrhosis-associated disturbances is hepatic encephalopathy (HE), defined as brain dysfunction caused by liver failure. HE manifests as a neuropsychiatric disorder and causes high rates of lethal outcome [1]. Current knowledge on HE is linked to hyperammonemia, neuroinflammation, oxidative/nitrosative stress, abnormal neurotransmission and brain edema of different degree [2]. It is considered that in HE, the most vulnerable cells in the brain appear astrocytes being the only cells to ammonia neutralization [3].