ArticleNeuropharmacology2018
Minocycline protects developing brain against ethanol-induced damage.
Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- Postnatal Day 7 Ethanol Exposure is Associated with Apoptosis-Related Changes in GAD67-Positive Neurons and Candidate CaMKII/GSK-3β/BAX Signaling in the Mouse Spinal Dorsal Horn.Substance abuse and rehabilitation · 2026Article
- Alcohol addiction and Alzheimer's disease: a molecular collision course.Translational psychiatry · 2025Review
- Alcohol-Induced Oxidative Stress and Gut-Liver-Brain Crosstalk: Expanding the Paradigm from ALD to MetALD.Antioxidants (Basel, Switzerland) · 2025Review
- Gut Microbiome, Neuroinflammation, and Fetal Alcohol Spectrum Disorders: Insights from Rodent Models.Biology · 2025Review
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- Novel Interventions on Comorbidities in Patients with Fetal Alcohol Spectrum Disorder (FASD): An Integrative Review.Biomedicines · 2024Review
- Binge ethanol exposure in advanced age elevates neuroinflammation and early indicators of neurodegeneration and cognitive impairment in female mice.Brain, behavior, and immunity · 2024Article
- Detrimental Effects of Alcohol-Induced Inflammation on Brain Health: From Neurogenesis to Neurodegeneration.Cellular and molecular neurobiology · 2023Review
- Nicotinamide ameliorates mitochondria-related neuronal apoptosis and cognitive impairment via the NADSchizophrenia (Heidelberg, Germany) · 2023Article
- Nicotinamide reverses deficits in puberty-born neurons and cognitive function after maternal separation.Journal of neuroinflammation · 2022Article
- Chemokine (C-C motif) receptor 2 is associated with the pathological grade and inflammatory response in IgAN children.BMC nephrology · 2022Article
- Do We Have Viable Protective Strategies against Anesthesia-Induced Developmental Neurotoxicity?International journal of molecular sciences · 2022Review
- Minocycline attenuates neuronal apoptosis and improves motor function after traumatic brain injury in rats.Experimental animals · 2021Article
- Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Review
- Ethanol affects behavior and HPA axis activity during development in zebrafish larvae.Scientific reports · 2020Article
- Transcriptomic analysis reveals moderate modulation of macrophage migration inhibitory factor superfamily genes in alcohol use disorders.Experimental and therapeutic medicine · 2020Article
- Fact versus Fiction: a Review of the Evidence behind Alcohol and Antibiotic Interactions.Antimicrobial agents and chemotherapy · 2020Review
- Involvement of AMP-activated protein kinase in neuroinflammation and neurodegeneration in the adult and developing brain.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during the pregnancy and is the leading cause of mental retardation. Ethanol exposure during the development results in the loss of neurons in the developing brain, which may underlie many neurobehavioral deficits associated with FASD. It is important to understand the mechanisms underlying ethanol-induced neuronal loss and develop appropriate therapeutic strategies. One of the potential mechanisms involves neuroimmune activation. Using a third trimester equivalent mouse model of ethanol exposure, we demonstrated that ethanol induced a wide-spread neuroapoptosis, microglial activation, and neuroinflammation in C57BL/6 mice. Minocycline is an antibiotic that inhibits microglial activation and alleviates neuroinflammation. We tested the hypothesis that minocycline may protect neurons ethanol-induced neuron death by inhibiting microglial activation and neuroinflammation. We showed that minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and the expression of pro-inflammatory cytokines. In contrast, minocycline reversed ethanol inhibition of anti-inflammatory cytokines. Minocycline blocked ethanol-induced activation of GSK3β, a key mediator of neuroinflammation and microglial activation in the developing brain. Consistent with the in vivo observations, minocycline inhibited ethanol-induced the expression of pro-inflammatory cytokines and activation of GSK3β in a microglia cell line (SIM-9). GSK3β inhibitor eliminated ethanol activation of pro-inflammatory cytokines in SIM-9 cells. Co-cultures of cortical neurons and SIM-9 microglia cells sensitized neurons to alcohol-induced neuronal death. Minocycline protected neurons against ethanol-induced neuronal death in neurons/microglia co-cultures. Together, these results suggest that minocycline may ameliorate ethanol neurotoxicity in the developing by alleviating GSK3β-mediated neuroinflammation.
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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.