Brain tissue ammonia and Alzheimer type 2 astrocytosis in human liver cirrhosis

Abstract

Hepatic encephalopathy (HE) is among key manifestations of decompensated liver cirrhosis (LC) and is typical for 30-45% of patients [1], reducing their survival rate up to 2 years. The neurotoxic effect of ammonia is central in the pathophysiology of HE [2]. In astrocytes, high ammonia concentration with glutamate are metabolized in osmotically active glutamine, accumulation of which causes astrocytes swelling and subsequent generalized brain edema [3].