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Stiripentol efficacy against status epilepticus and associated mortality in mice.
Heliyon
August 2024
Biocodex - Research and Development Center, Compiègne, France.
Stiripentol (STP, Diacomit©) is an antiseizure medication indicated for Dravet syndrome, a rare developmental and epileptic encephalopathy characterized by drug-resistant seizures, including status epilepticus (SE). SE is a life-threatening event that may lead to increased risk of morbidity and mortality. Here, we evaluated the effect of STP on SE and SE-associated mortality using a CBA mouse model induced by systemic administration of methionine sulfoximine (MSO), an irreversible inhibitor of glutamine synthetase.
View Article and Find Full Text PDFHyperammonemia induced gut microbiota dysbiosis and motor coordination disturbances in mice: new insight into gut‑brain axis involvement in hepatic encephalopathy.
Acta Neurobiol Exp (Wars)
July 2023
Nutritional Physiopathologies, Neuroscience and Toxicology Team, Laboratory of Anthropogenic, Biotechnology and Health, Faculty of Sciences, Chouaib Doukkali University, El Jadida, Morocco,
Hepatic encephalopathy (HE) is a neuropsychiatric hepatic‑induced syndrome in which several factors are involved in promoting brain perturbations, with ammonia being the primary factor. Motor impairment, incoordination, and gut dysbiosis are some of the well‑known symptoms of HE. Nevertheless, the link between the direct effect of hyperammonemia and associated gut dysbiosis in the pathogenesis of HE is not well established.
View Article and Find Full Text PDFHyperammonemic Encephalopathy in a Patient with Pancreatic Neuroendocrine Tumor and Portosystemic Shunt.
Diagnostics (Basel)
February 2023
Department of Radiology, University Medical Centre Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Hyperammonemia can lead to encephalopathy and may be accompanied by a diagnostic dilemma. Imaging as well as biochemical analyses are the cornerstone for identifying possible underlying causes such as severe liver disease or urea cycle defect. We report a case of a patient that presented with neurological deficits based on hyperammonemia in the presence of a large pancreatic neuroendocrine tumor (PNET) and portosystemic shunts in the liver.
View Article and Find Full Text PDFEnhanced recruitment of glutamate receptors underlies excitotoxicity of mitral cells in acute hyperammonemia.
Front Cell Neurosci
October 2022
Department of Otorhinolaryngology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Article Synopsis
- Hepatic encephalopathy (HE), a serious liver condition, has been linked to olfactory dysfunction due to high levels of ammonia in the blood and cerebrospinal fluid.
- Research using mouse models showed that increased ammonium levels altered the activity of mitral cells in the olfactory bulb, suggesting that glutamate receptors play a key role in this dysfunction.
- The study found that elevated ammonia levels caused neuronal excitotoxicity by enhancing glutamate receptor activity, leading to cell death and providing insights into the potential causes of olfactory defects in HE patients.
Enhanced BDNF and TrkB Activation Enhance GABA Neurotransmission in Cerebellum in Hyperammonemia.
Int J Mol Sci
October 2022
Laboratory of Neurobiology, Centro Investigación Príncipe Felipe, 46012 Valencia, Spain.
Hyperammonemia is a main contributor to minimal hepatic encephalopathy (MHE) in cirrhotic patients. Hyperammonemic rats reproduce the motor incoordination of MHE patients, which is due to enhanced GABAergic neurotransmission in the cerebellum as a consequence of neuroinflammation. In hyperammonemic rats, neuroinflammation increases BDNF by activating the TNFR1-S1PR2-CCR2 pathway.
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