ReviewNeurotoxicity research2012
Alterations of blood brain barrier function in hyperammonemia: an overview.
Review in Neurotoxicity research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 106 citations in OpenAlex.
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- Consequences of Western and Mediterranean Diets' Nutrients on the Microbiota-Gut-Brain Axis.Nutrients · 2026Review
- The Influence of Metabolic Dysfunction-Associated Steatotic Liver Disease and Body Mass Index on the Incidence of Alzheimer Disease: A Nationwide Cohort Study.Gut and liver · 2026Article
- Article
- Glutamine and Albumin Levels in Cerebrospinal Fluid Are Correlated with Neurological Severity in an Experimental Model of Acute Hepatic Encephalopathy.Metabolites · 2025Article
- Soil to Synapse: Molecular Insights into the Neurotoxicity of Common Gardening Chemicals in Alzheimer's and Parkinson's Disease.International journal of molecular sciences · 2025Review
- Blood-brain barrier dysfunction in hepatic encephalopathy: pathophysiology, diagnostic assessment and therapeutic perspectives.Metabolic brain disease · 2025Review
- Ammonia-induced stress response in liver disease progression and hepatic encephalopathy.Nature reviews. Gastroenterology & hepatology · 2024Review
- Efficacy and safety of albumin for the treatment of hepatic encephalopathy: an updated systematic review and meta-analysis of randomized controlled trials.Annals of medicine and surgery (2012) · 2024Article
- Brain energy metabolism: A roadmap for future research.Journal of neurochemistry · 2024Review
- Could the Urease of the Gut BacteriumMicroorganisms · 2023Article
- Dementia and non-alcoholic fatty liver disease - An unprecedented relationship.Annals of medicine and surgery (2012) · 2022Article
- Article
- Effects of platelet-rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy.Brain and behavior · 2022Article
- Neuromyelitis Optica Complicated by Ornithine Transcarbamylase Deficiency Treated Safely with Pulse Steroid Therapy.Internal medicine (Tokyo, Japan) · 2021Article
- Comparative Proteome Research in a Zebrafish Model for Vanishing White Matter Disease.International journal of molecular sciences · 2021Article
- Cognitive-Behavioural Correlates of Dysbiosis: A Review.International journal of molecular sciences · 2020Review
- L-Aspartate, L-Ornithine and L-Ornithine-L-Aspartate (LOLA) and Their Impact on Brain Energy Metabolism.Neurochemical research · 2020Article
- Astroglia in Sepsis Associated Encephalopathy.Neurochemical research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ammonia is a neurotoxin involved in the pathogenesis of neurological conditions associated with hyperammonemia, including hepatic encephalopathy, a condition associated with acute--(ALF) or chronic liver failure. This article reviews evidence that apart from directly affecting the metabolism and function of the central nervous system cells, ammonia influences the passage of different molecules across the blood brain barrier (BBB). A brief description is provided of the tight junctions, which couple adjacent cerebral capillary endothelial cells to each other to form the barrier. Ammonia modulates the transcellular passage of low-to medium-size molecules, by affecting their carriers located at the BBB. Ammonia induces interrelated aberrations of the transport of the large neutral amino acids and aromatic amino acids (AAA), whose influx is augmented by exchange with glutamine produced in the course of ammonia detoxification, and maybe also modulated by the extracellularly acting gamma-glutamyl moiety transferring enzyme, gamma-glutamyl-transpeptidase. Impaired AAA transport affects neurotransmission by altering intracerebral synthesis of catecholamines (serotonin and dopamine), and producing "false neurotransmitters" (octopamine and phenylethylamine). Ammonia also modulates BBB transport of the cationic amino acids: the nitric oxide precursor, arginine, and ornithine, which is an ammonia trap, and affects the transport of energy metabolites glucose and creatine. Moreover, ammonia acting either directly or in synergy with liver injury-derived inflammatory cytokines also evokes subtle increases of the transcellular passage of molecules of different size (BBB "leakage"), which appears to be responsible for the vasogenic component of cerebral edema associated with ALF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.