7 de febrero 2014. Seminario Neuroinflammation in hepatic encephalopathy: role in the cognitive and motor alterations.
El Seminario, que será impartido por el Dr. Vicente Hernández Rabaza se realizará en el Salón de Actos del Centro de Investigación Príncipe Felipe el próximo viernes 7 a las 13 horas.
Liver failure affects brain function, leading to neurological and psychiatric alterations; such alterations are referred to as hepatic encephalopathy (HE). However, HE is not a single syndrome. Different types of liver disease, such as liver cirrhosis (the most frequent) or acute liver failure, lead to different cerebral and neurological alterations and, thus, to different forms of HE which are mediated by different mechanisms. HE is a serious health, social and economic problem. The mechanisms underlying HE are beginning to be identified in animal models. The two main factors responsible for the neurological alterations in HE are hyperammonemia and inflammation.
Our group is investigating, both in animal models and in patients, the mechanisms underlying the cognitive and motor alterations in HE, with the aim to design new therapeutic strategies. We have shown that hyperammonemia per se induces neuroinflammation. Rats with chronic hyperammonemia without liver failure show microglial activation and neuroinflammation. Treatment of these rats with anti-inflammatory drugs restores cognitive function indicating that hyperammonemia-induced neuroinflammation mediates neurological impairment in HE. We have also shown that anti-inflammatory drugs, such as Ibuprofen and MAPK p38 inhibitors, reduce neuroinflammation and restores learning ability and motor function in rats with liver failure and HE. Together, these results indicate that targeting neuroinflammation may be a key strategy to restore cognitive and motor function in patients with chronic liver diseases and HE.
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