Abstract #3865

Novel urease inhibitor as potential treatment of hepatic encephalopathy led to brain glutamine decrease

Dunja Simicic^1,2, Diana Evstafeva³, Filip Ilievski³, Yinyin Bao³, Sunghyun Kang³, Dario Sessa⁴, Stefanita-Octavian Mitrea^1,2, Katarzyna Pierzchala^1,2,5, Jean-Christophe Leroux³, and Cristina Cudalbu^1,2

¹CIBM Center for Biomedical Imaging, Lausanne, Switzerland, ²Animal Imaging and Technology, EPFL, Lausanne, Switzerland, ³Institute of Pharmaceutical Sciences, ETH Zurich, Zurich, Switzerland, ⁴Swiss Center for Liver Disease in Children, University Hospitals Geneva, Geneva, Switzerland, ⁵Laboratory of Functional and Metabolic Imaging, EPFL, Lausanne, Switzerland

Synopsis

Keywords: Spectroscopy, Brain, Metabolism, Hepatic Encephalopathy, proton

Type C hepatic encephalopathy (HE) is a severe neuropsychiatric disorder associated with chronic liver disease. Ammonia (partially produced in the gut by bacterial urease activity) has been pinpointed to explain the observed neurological alterations in HE and connected with the increase in brain Gln measured using ¹H-MRS. As such current treatment strategies focus on either reducing ammonia production and absorption or on promoting its elimination. We showed that targeting urease activity using the urease inhibitor 2-octynoHA has a beneficial effect in reducing blood ammonia levels and reducing brain Gln measured using ¹H-MRS at 9.4T in the cerebellum.

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