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Hepatic Encephalopathy as a Gliopathy: The Mechanisms of Alzheimer Type II Astrocytosis
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Author(s): Bilal El-Mansoury (Faculty of Sciences, Chouaib Doukkali University, Morocco), Omar El Hiba (Faculty of Sciences, Chouaib Doukkali University, Morocco), Abdelaati El Khiat (Higher Institute of Nursing Professions and Health Techniques, Ouarzazate, Morocco & Cadi Ayyad University, Morocco), El Baz Soraia (Faculty of Science Semlalia, Cadi Ayyad University, Morocco)and Arumugam Radhakrishnan Jayakumar (Miller School of Medicine, University of Miami, USA)
Copyright: 2024
Pages: 20
Source title:
Physiology and Function of Glial Cells in Health and Disease
Source Author(s)/Editor(s): Bilal El-Mansoury (Faculty of Sciences, Chouaib Doukkali University, Morocco), Omar El Hiba (Chouaib Doukkali University, Morocco)and Arumugam Radhakrishnan Jayakumar (University of Miami, USA)
DOI: 10.4018/978-1-6684-9675-6.ch012
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Abstract
Hepatic encephalopathy (HE) is defined as a wide spectrum of neuropsychiatric abnormalities caused by liver dysfunction (acute or chronic) and/or portal-systemic shunting. The histopathologic hallmark of HE is astrocyte swelling following acute liver failure (ALF) or the presence of the so-called Alzheimer type 2 astrocytosis under chronic liver disease. HE can be classified according to the undelaying cause into three types: type A as an essential component of acute liver failure, type B as a consequence of porto-systemic shunts in the absence of liver dysfunction, and type C in patients with liver cirrhosis and porto-systemic bypass. While ammonia, manganese, proinflammatory cytokines, and other precipitating factors play a role in the pathogenesis of HE, the exact mechanisms leading to the development of HE are not fully elucidated. This chapter provides a brief overview of HE with a focus on the mechanisms of AT2A.
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