ArticleNeurobiology of disease2013
Microglial activation is not equivalent to neuroinflammation in alcohol-induced neurodegeneration: The importance of microglia phenotype.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.
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Who cites it
159 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.
- The Interplay of Inflammatory Processes and Cognition in Alcohol Use Disorders-A Systematic Review.Frontiers in psychiatry · 2019Pooled it
- Early abstinence in severe alcohol use disorder: MCP-1 decline, choroid plexus shrinkage, and region-specific grey-matter volume changes.Translational psychiatry · 2026Article
- Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026Review
- Sex differences in the neuroimmune response following heavy, binge-like alcohol exposure in adolescent rats.Journal of neuroimmunology · 2025Article
- Impact of adolescent ethanol binge on serotonin signaling and pain sensitivity post-withdrawal.Alcohol (Fayetteville, N.Y.) · 2025Article
- Deep Proteomic Profiling of Human Stem Cell-Derived Microglia: Insights Into Inflammatory and Alcohol-Induced Reactivity.Research square · 2025Article
- Targeting IL-6 as a novel therapeutic approach for alcohol abstinence - related mechanical allodynia.Neuropharmacology · 2025Article
- Chronic alcohol consumption induces phenotypic and functional alterations consistent with a hyper-inflammatory state in peripheral blood mononuclear cell-derived microglia in a rhesus macaque model.Brain, behavior, and immunity · 2025Article
- Potential roles for microglia in drug addiction: Adolescent neurodevelopment and beyond.Journal of neuroimmunology · 2025Review
- Binge alcohol and the neuroendocrinology of the aging female.Frontiers in neuroendocrinology · 2025Review
- Chronic alcohol exposure during young adulthood attenuates microglial reactivity and downstream immune response pathways in a mouse model of tauopathy later in life.Alcohol, clinical & experimental research · 2025Article
- Sex differences in the microglial response to stress and chronic alcohol exposure in mice.Biology of sex differences · 2025Article
- Pharmacological Depletion of Microglia Protects Against Alcohol-Induced Corticolimbic Neurodegeneration During Intoxication in Male Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Excessive Alcohol Use as a Risk Factor for Alzheimer's Disease: Epidemiological and Preclinical Evidence.Advances in experimental medicine and biology · 2025Review
- Investigation of Uncovering Molecular Mechanisms of Alcohol-Induced Female Infertility-A Rational Approach.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Polygenic risk for alcohol use disorder affects cellular responses to ethanol exposure in a human microglial cell model.Science advances · 2024Article
- Ethanol Exacerbates the Alzheimer's Disease Pathology in the 5xFAD Mouse Model.Neuroglia (Basel, Switzerland) · 2024Article
- Effects of isolation stress and voluntary ethanol exposure during adolescence on ethanol and nicotine co-use in adulthood using male rats.Drug and alcohol dependence reports · 2024Article
- Effects of Ketogenic Diet on Increased Ethanol Consumption Induced by Social Stress in Female Mice.Nutrients · 2024Article
- Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice.International journal of molecular sciences · 2024Article
99 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Excessive alcohol intake, a defining characteristic of an alcohol use disorder (AUD), results in neurodegeneration in the hippocampus and entorhinal cortex that has been linked to a variety of cognitive deficits. Neuroinflammation is thought to be a factor in alcohol-induced neurodegeneration, and microglia activation is a key but not sole component of an inflammatory response. These experiments investigate the effects of ethanol exposure in a well-accepted model of an AUD on both microglial activation and blood brain barrier disruption (BBB) in order to understand their relationship to classical definitions of inflammation and alcohol-induced neurodegeneration. Following a four-day binge ethanol paradigm, rat hippocampal and entorhinal cortex tissue was examined using three distinct approaches to determine microglia phenotype and BBB disruption: immunohistochemistry, autoradiography, and ELISA. After ethanol exposure, there was an increase in [(3)H]-PK-11195 binding and OX-42 immunoreactivity indicative of microglial activation; however, microglia were not fully activated since both OX-6 and ED-1 immunoreactive microglia were absent. This data was supported by functional evidence as there was no increase in the proinflammatory cytokines IL-6 or TNF-α, but a 26% increase in the anti-inflammatory cytokine, IL-10, and a 38% increase in the growth factor, TGF-β, seven days after exposure. Furthermore, there was no evidence of a disruption of the BBB. These data suggest that the four-day binge model of an AUD, which produces neurodegeneration in corticolimbic regions, does not elicit classical neuroinflammation but instead produces partially activated microglia. Partial activation of microglia following binge ethanol exposure suggest that microglia in this model have beneficial or homeostatic roles rather than directly contributing to neurodegeneration and are a consequence of alcohol-induced-damage instead of the source of damage.
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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.