Author information

• ¹Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas, Austin, TX, USA.
• ²Department of Internal Medicine, Dell Medical School, The University of Texas, Austin, TX, USA.
• ³Research Division, Central Texas Veterans Healthcare System, Temple, TX, USA.
• ⁴CIBM Center for Biomedical Imaging, Lausanne, Switzerland.
• ⁵Animal Imaging and Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
• ⁶Institute for Liver and Digestive Health, University College London, Royal Free Campus, London, UK.
• ⁷General Medical Research, Neuropathology Section, R&D Service and South Florida VA Foundation for Research and Education Inc, Obstetrics, Gynecology and Reproductive Sciences, University of Miami School of Medicine, Miami, FL, USA.
• ⁸Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montreal, Canada.

Abstract

This working group of the International Society of Hepatic Encephalopathy and Nitrogen Metabolism (ISHEN) was commissioned to summarize and update current efforts in the development and characterization of animal models of hepatic encephalopathy (HE). As defined in humans, HE in animal models is based on the underlying degree and severity of liver pathology. Although hyperammonemia remains the key focus in the pathogenesis of HE, other factors associated with HE have been identified, together with recommended animal models, to help explore the pathogenesis and pathophysiological mechanisms of HE. While numerous methods to induce liver failure and disease exist, less have been characterized with neurological and neurobehavioural impairments. Moreover, there still remains a paucity of adequate animal models of Type C HE induced by alcohol, viruses and non-alcoholic fatty liver disease; the most common etiologies of chronic liver disease.