ArticleMetabolic brain disease2014
Microglial proliferation in the brain of chronic alcoholics with hepatic encephalopathy.
Article in Metabolic brain disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- The Interplay of Inflammatory Processes and Cognition in Alcohol Use Disorders-A Systematic Review.Frontiers in psychiatry · 2019Pooled it
- Context-dependent effects of microglial MyD88 removal on voluntary ethanol consumption in mice.Neuropharmacology · 2026Article
- Review
- Differential metabolic and cellular brain regional susceptibility in adult rats with chronic liver disease.Metabolic brain disease · 2026Article
- Quantification of the neuropathology of alcohol use disorder using tissue microarrays.Journal of neuropathology and experimental neurology · 2026Article
- Blood-brain barrier dysfunction in hepatic encephalopathy: pathophysiology, diagnostic assessment and therapeutic perspectives.Metabolic brain disease · 2025Review
- The New Phytocomplex AL0042 Extracted from Red Orange By-Products Inhibits the Minimal Hepatic Encephalopathy in Mice Induced by Thioacetamide.Biomedicines · 2025Article
- Ammonia and beyond - biomarkers of hepatic encephalopathy.Metabolic brain disease · 2025Review
- Review
- Molecular and biochemical pathologies in human alcohol-related cerebellar white matter degeneration.Advances in drug and alcohol research · 2025Article
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
- Infection, inflammation and hepatic encephalopathy from a clinical perspective.Metabolic brain disease · 2024Review
- Hepatic encephalopathy as a result of ammonia-induced increase in GABAergic tone with secondary reduced brain energy metabolism.Metabolic brain disease · 2024Review
- Substance Use and Addiction.Advances in neurobiology · 2024Review
- The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice.Brain sciences · 2023Article
- Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol-evoked neuropathic pain.British journal of pharmacology · 2023Article
- The role of brain inflammation and abnormal brain oxygen homeostasis in the development of hepatic encephalopathy.Metabolic brain disease · 2023Review
- Cellular Pathogenesis of Hepatic Encephalopathy: An Update.Biomolecules · 2023Review
- A mouse model of hepatic encephalopathy: bile duct ligation induces brain ammonia overload, glial cell activation and neuroinflammation.Scientific reports · 2022Article
- Hepatic encephalopathy.Nature reviews. Disease primers · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Hepatic encephalopathy (HE) is a common complication of chronic alcoholism and patients show neurological symptoms ranging from mild cognitive dysfunction to coma and death. The HE brain is characterized by glial changes, including microglial activation, but the exact pathogenesis of HE is poorly understood. During a study investigating cell proliferation in the subventricular zone of chronic alcoholics, a single case with widespread proliferation throughout their adjacent grey and white matter was noted. This case also had concomitant HE raising the possibility that glial proliferation might be a pathological feature of the disease. In order to explore this possibility fixed postmortem human brain tissue from chronic alcoholics with cirrhosis and HE (n = 9), alcoholics without HE (n = 4) and controls (n = 4) were examined using immunohistochemistry and cytokine assays. In total, 4/9 HE cases had PCNA- and a second proliferative marker, Ki-67-positive cells throughout their brain and these cells co-stained with the microglial marker, Iba1. These cases were termed 'proliferative HE' (pHE). The microglia in pHEs displayed an activated morphology with hypertrophied cell bodies and short, thickened processes. In contrast, the microglia in white matter regions of the non-proliferative HE cases were less activated and appeared dystrophic. pHEs were also characterized by higher interleukin-6 levels and a slightly higher neuronal density . These findings suggest that microglial proliferation may form part of an early neuroprotective response in HE that ultimately fails to halt the course of the disease because underlying etiological factors such as high cerebral ammonia and systemic inflammation remain.
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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.