Cynthia J.M. Kane
Professor Emeritus
Also affiliated: Texas Tech University (2005); Dartmouth–Hitchcock Medical Center (2005); Stanford Medicine (1991); Texas Tech University Health Sciences Center (2005); Stanford University (1988–1992)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Cynthia J.M. Kane's research focuses on the neurobiological effects of ethanol exposure, particularly during critical developmental periods. Her work investigates how alcohol impacts neuroinflammation, myelination, and gene expression in the cerebellum and hippocampus, utilizing mouse models to study both fetal alcohol spectrum disorders (FASD) and alcohol use disorder (AUD).
Her recent publications explore the molecular signaling pathways, such as TLR4 and MyD88, involved in ethanol-induced neuroinflammation. Kane also examines the long-term consequences of developmental ethanol exposure on brain development and function, with a specific interest in cerebellar transcriptomic changes that may relate to disease onset. Her research group collaborates with other faculty members at the University of Arkansas for Medical Sciences, including Paul D. Drew, James C. Douglas, Tonya Rafferty, and Kalee N. Holloway, on shared publications.
Kane has an h-index of 26 and has authored 56 publications with over 2,400 citations. She is recognized as a highly cited researcher.
Metrics
- h-index: 26
- Publications: 56
- Citations: 2,453
Positions
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Professor Emeritus publications 1988–2023University of Arkansas for Medical Sciences Institution web page
Selected Publications
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Ethanol Induces Neuroinflammation in a Chronic Plus Binge Mouse Model of Alcohol Use Disorder via TLR4 and MyD88-Dependent Signaling (2023)
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Ethanol-induced cerebellar transcriptomic changes in a postnatal model of fetal alcohol spectrum disorders: Focus on disease onset (2023)
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Cerebellar Transcriptomic Analysis in a Chronic plus Binge Mouse Model of Alcohol Use Disorder Demonstrates Ethanol-Induced Neuroinflammation and Altered Glial Gene Expression (2023)
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Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation (2022)
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Ethanol effects on cerebellar myelination in a postnatal mouse model of fetal alcohol spectrum disorders (2021)
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Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders (2021)
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Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period (2021)
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Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders (2021)
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Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders (2020)
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Prenatal Ethanol Exposure and Postnatal Environmental Intervention Alter Dopaminergic Neuron and Microglia Morphology in the Ventral Tegmental Area During Adulthood (2019)
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PPAR-γ agonists suppress neuroinflammation in a FASD animal model (2017)
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Protection against alcohol-induced neuronal and cognitive damage by the PPARγ receptor agonist pioglitazone (2017)
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Peroxisome Proliferator-Activated Receptor-γ Agonists: Potential Therapeutics for Neuropathology Associated with Fetal Alcohol Spectrum Disorders (2016)
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Inflammatory responses to alcohol in the CNS: nuclear receptors as potential therapeutics for alcohol-induced neuropathologies (2016)
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Alcohol and Neuroimmune Interactions (2016)
Collaboration Network
Top Collaborators
- Pioglitazone Blocks Ethanol Induction of Microglial Activation and Immune Responses in the Hippocampus, Cerebellum, and Cerebral Cortex in a Mouse Model of Fetal Alcohol Spectrum Disorders
- Effects of Ethanol on Immune Response in the Brain: Region-Specific Changes in Adolescent Versus Adult Mice
- Protection of neurons and microglia against ethanol in a mouse model of fetal alcohol spectrum disorders by peroxisome proliferator-activated receptor-γ agonists
- Fetal Alcohol Spectrum Disorders and Neuroimmune Changes
- Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders
Showing 5 of 23 shared publications
- Pioglitazone Blocks Ethanol Induction of Microglial Activation and Immune Responses in the Hippocampus, Cerebellum, and Cerebral Cortex in a Mouse Model of Fetal Alcohol Spectrum Disorders
- Effects of Ethanol on Immune Response in the Brain: Region-Specific Changes in Adolescent Versus Adult Mice
- Protection of neurons and microglia against ethanol in a mouse model of fetal alcohol spectrum disorders by peroxisome proliferator-activated receptor-γ agonists
- Protection against alcohol-induced neuronal and cognitive damage by the PPARγ receptor agonist pioglitazone
- Effects of ethanol on immune response in the brain: region-specific changes in aged mice
Showing 5 of 13 shared publications
- Pioglitazone Blocks Ethanol Induction of Microglial Activation and Immune Responses in the Hippocampus, Cerebellum, and Cerebral Cortex in a Mouse Model of Fetal Alcohol Spectrum Disorders
- Effects of Ethanol on Immune Response in the Brain: Region-Specific Changes in Adolescent Versus Adult Mice
- Protection of neurons and microglia against ethanol in a mouse model of fetal alcohol spectrum disorders by peroxisome proliferator-activated receptor-γ agonists
- Effects of ethanol on immune response in the brain: region-specific changes in aged mice
- Neuroimmune mechanisms in fetal alcohol spectrum disorder
Showing 5 of 11 shared publications
- Ethanol Induces Neuroinflammation in a Chronic Plus Binge Mouse Model of Alcohol Use Disorder via TLR4 and MyD88-Dependent Signaling
- Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol effects on cerebellar myelination in a postnatal mouse model of fetal alcohol spectrum disorders
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
Showing 5 of 7 shared publications
- Pioglitazone Blocks Ethanol Induction of Microglial Activation and Immune Responses in the Hippocampus, Cerebellum, and Cerebral Cortex in a Mouse Model of Fetal Alcohol Spectrum Disorders
- Effects of Ethanol on Immune Response in the Brain: Region-Specific Changes in Adolescent Versus Adult Mice
- Effects of ethanol on immune response in the brain: region-specific changes in aged mice
- Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation
- Ethanol Induces Neuroinflammation in a Chronic Plus Binge Mouse Model of Alcohol Use Disorder via TLR4 and MyD88-Dependent Signaling
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation
- Ethanol-induced cerebellar transcriptomic changes in a postnatal model of fetal alcohol spectrum disorders: Focus on disease onset
- Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period
- Cerebellar Transcriptomic Analysis in a Chronic plus Binge Mouse Model of Alcohol Use Disorder Demonstrates Ethanol-Induced Neuroinflammation and Altered Glial Gene Expression
- Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders
- Ethanol effects on cerebellar myelination in a postnatal mouse model of fetal alcohol spectrum disorders
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation
- Ethanol modulation of hippocampal neuroinflammation, myelination, and neurodevelopment in a postnatal mouse model of fetal alcohol spectrum disorders
- Intragastric Intubation: Important Aspects of the Model for Administration of Ethanol to Rat Pups During the Postnatal Period
- Transforming growth factor-β2 both stimulates and inhibits neurogenesis of rat cerebellar granule cells in culture
- Transforming growth factor-β2 increases NMDA receptor-mediated excitotoxicity in rat cerebral cortical neurons independently of glia
- Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period
- Cerebellar Transcriptomic Analysis in a Chronic plus Binge Mouse Model of Alcohol Use Disorder Demonstrates Ethanol-Induced Neuroinflammation and Altered Glial Gene Expression
- Proceedings of the 2010 annual meeting of the Fetal Alcohol Spectrum Disorders Study Group
- Activated Macrophage/Microglial Cells Can Promote the Regeneration of Sensory Axons into the Injured Spinal Cord
- Axonal regeneration by chronically injured supraspinal neurons can be enhanced by exposure to insulin-like growth factor, basic fibroblast growth factor or transforming growth factor beta
- Methyl gallate, methyl-3,4,5-trihydroxybenzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. II. Antiviral activity of methyl gallate and its derivatives
- Methyl gallate, methyl-3,4,5-trihydroxy-benzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. I. Purification and characterization of methyl gallate from Sapium sebiferum
- Expression of fibrogenic cytokines in rat small intestine after fractionated irradiation
- Methyl gallate, methyl-3,4,5-trihydroxybenzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. II. Antiviral activity of methyl gallate and its derivatives
- Methyl gallate, methyl-3,4,5-trihydroxybenzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. II. Antiviral activity of methyl gallate and its derivatives
- Methyl gallate, methyl-3,4,5-trihydroxy-benzoate, is a potent and highly specific inhibitor of herpes simplex virus in vitro. I. Purification and characterization of methyl gallate from Sapium sebiferum
- Astrocytes in the aged rat spinal cord fail to increase GFAP mRNA following sciatic nerve axotomy
- Microglia, but not astrocytes, react to sciatic nerve injury in aging rats
- Proliferation of astroglia from the adult human cerebrum is inhibited by ethanol in vitro
- Active learning in the medical histology laboratory engages students and faculty, improving performance
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