My research interests lie within the area of hepatic encephalopathy (HE), a major neuropsychiatric complication of liver disease. As much as 80% of patients with cirrhosis suffer from HE which leads to substantial morbidity and mortality and has a significant impact on neurological outcome following liver

transplantation, the only curative approach to this day.
Translational research is the primary objective of our team and, therefore, our research program is based on a bench-to-bedside concept.

Throughout my career, I have been interested in identifying the pathogenic factors and the pathophysiological pathways involved in the development of cerebral complications associated with liver disease. Although ammonia is considered the main factor involved in the pathogenesis of HE, its correlation with the severity of HE remains controversial. Oxidative stress is another factor believed to play a role in the pathogenesis of this syndrome; it represents an imbalance between the production and neutralization of reactive oxygen species, which leads to cellular dysfunction.

In the setting of liver disease, oxidative stress represents a systemic phenomenon induced by several mechanisms. Data from both animal and human studies sustain that there is a synergistic effect between systemic oxidative stress and ammonia in the pathogenesis of HE, however the precise pathophysiological mechanisms remain undefined.

For all the above reasons, the ability to recognize pathogenic factors and mechanisms of the disease will lead to novel therapeutic approaches; an important goal in our research program. In turn, novel treatments will improve management of patients with liver disease and enhance neurological outcome following liver transplantation.