Peripheral inflammation induces neuroinflammation that alters neurotransmission and cognitive and motor function in hepatic encephalopathy: Underlying mechanisms and therapeutic implications
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Published on: April 18, 2011
Andrea Cabrera-Pastor1,2, Marta Llansola1, Carmina Montoliu2
1Laboratory of Neurobiology, Centro de Investigación Principe Felipe, Valencia, Spain.
Abstract:
Several million patients with liver cirrhosis suffer minimal hepatic encephalopathy (MHE), with mild cognitive and coordination impairments that reduce their quality of life and life span. Hyperammonaemia and peripheral inflammation act synergistically to induce these neurological alterations. We propose that MHE appearance is because of the changes in peripheral immune system, which are transmitted to brain, leading to neuroinflammation that alters neurotransmission leading to cognitive and motor alterations. We summarize studies showing that MHE in cirrhotic patients is associated with alterations in the immune system and that patients died with HE show neuroinflammation in cerebellum, with microglial and astrocytic activation and Purkinje cell loss. We also summarize studies in animal models of MHE on the role of peripheral inflammation in neuroinflammation induction, how neuroinflammation alters neurotransmission and how this leads to cognitive and motor alterations. These studies identify therapeutic targets and treatments that improve cognitive and motor function. Rats with MHE show neuroinflammation in hippocampus and altered NMDA and AMPA receptor membrane expression, which impairs spatial learning and memory. Neuroinflammation in cerebellum is associated with altered GABA transporters and extracellular GABA, which impair motor coordination and learning in a Y maze. These alterations are reversed by treatments that reduce peripheral inflammation (anti-TNFα, ibuprofen), neuroinflammation (sulphoraphane, p38 inhibitors), GABAergic tone (bicuculline, pregnenolone sulphate) or increase extracellular cGMP (sildenafil or cGMP). The mechanisms identified would also occur in other chronic diseases associated with inflammation, aging and some mental and neurodegenerative diseases. Treatments that improve MHE may also be beneficial to treat these pathologies.
Insights
Minimal hepatic encephalopathy (MHE) in liver cirrhosis patients involves peripheral inflammation causing neuroinflammation, altering neurotransmission and leading to cognitive/motor deficits. Treatments targeting inflammation show promise for MHE and related conditions.
Area of Science:
- Neuroscience
- Immunology
- Gastroenterology
Background:
- Millions with liver cirrhosis have minimal hepatic encephalopathy (MHE), experiencing cognitive and coordination impairments.
- Hyperammonaemia and peripheral inflammation synergistically drive these neurological changes in MHE.
- MHE is linked to peripheral immune system alterations that transmit to the brain, causing neuroinflammation.
Purpose of the Study:
- To explore the link between peripheral inflammation, neuroinflammation, and neurological alterations in MHE.
- To summarize evidence on MHE's immune system associations and neuroinflammatory changes in cirrhotic patients.
- To review animal model studies on MHE's mechanisms and potential therapeutic targets.
Main Methods:
- Summarized studies on MHE in cirrhotic patients and post-mortem HE cases.
- Reviewed animal models of MHE to investigate inflammation's role.
- Analyzed neuroinflammation, neurotransmission, and receptor expression in MHE models.
Main Results:
- MHE is associated with immune system alterations and neuroinflammation (microglial/astrocytic activation, Purkinje cell loss) in cirrhotic patients.
- Animal models show peripheral inflammation induces neuroinflammation, altering neurotransmission (NMDA, AMPA, GABA) and impairing cognitive/motor functions.
- Specific treatments targeting peripheral inflammation, neuroinflammation, GABAergic tone, or cGMP levels reversed MHE-related deficits.
Conclusions:
- Peripheral inflammation-induced neuroinflammation is a key mechanism in MHE's cognitive and motor impairments.
- Therapeutic strategies targeting these inflammatory and neurotransmission pathways offer potential for MHE treatment.
- Identified mechanisms may also be relevant for other inflammatory, aging, mental, and neurodegenerative diseases.
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