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A number of research confirmed a strong involvement of oxidative stress in the pathophysiology of neurodegenerative diseases through a variety of mechanisms including induction of oxidation of macromolecules such as nucleic acids, proteins, lipids, mitochondrial dysfunction, glial cell activation, amyloid deposition, apoptosis, and proteasome dysfunction [3, 5, 10, 11]

This local hepatic inflammation leads to further recruitment of systemic inflammatory cells, such as neutrophils, T-cells and monocytes, which perpetuate additional inflammation, hepatic fibrosis, hepatocyte cell death (68, 72, 73) that ultimately leads to rapid progression to multiple organ failure (74)