ArticleAlcoholism, clinical and experimental research2019
A Pivotal Role for Thiamine Deficiency in the Expression of Neuroinflammation Markers in Models of Alcohol-Related Brain Damage.
Article in Alcoholism, clinical and experimental research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 33 citations in OpenAlex.
- Thiamine Deficiency and Neuroinflammation Are Important Contributors to Alcohol Use Disorder.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Promising strategies for the prevention of alcohol-related brain damage through optimised management of acute alcohol withdrawal: A focussed literature review.Journal of psychopharmacology (Oxford, England) · 2025Review
- Adolescent Alcohol and the Spectrum of Cognitive Dysfunction in Aging.Advances in experimental medicine and biology · 2025Review
- Chronic ethanol induces a pro-inflammatory switch in interleukin-1β regulation of GABAergic signaling in the medial prefrontal cortex of male mice.Brain, behavior, and immunity · 2023Article
- The neuroimmune system - Where aging and excess alcohol intersect.Alcohol (Fayetteville, N.Y.) · 2023Review
- Disinhibition-Like Behavior Correlates with Frontal Cortex Damage in an Animal Model of Chronic Alcohol Consumption and Thiamine Deficiency.Biomedicines · 2022Article
- Altered Global Signal Topography in Alcohol Use Disorders.Frontiers in aging neuroscience · 2022Article
- Upregulation of TLR4/MyD88 pathway in alcohol-induced Wernicke's encephalopathy: Findings in preclinical models and in a postmortem human case.Frontiers in pharmacology · 2022Article
- Midline Thalamic Damage Associated with Alcohol-Use Disorders: Disruption of Distinct Thalamocortical Pathways and Function.Neuropsychology review · 2021Review
- The Effect of Chronic Ethanol Exposure and Thiamine Deficiency on Myelin-related Genes in the Cortex and the Cerebellum.Alcoholism, clinical and experimental research · 2020Article
- Aging with alcohol-related brain damage: Critical brain circuits associated with cognitive dysfunction.International review of neurobiology · 2019Review
- From adolescence to late aging: A comprehensive review of social behavior, alcohol, and neuroinflammation across the lifespan.International review of neurobiology · 2019Review
- Preface: Setting the stage for understanding alcohol effects in late aging: A special issue including both human and rodent studies.International review of neurobiology · 2019Article
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4 authors at 1 institution in 1 country.
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Abstract
backgroundAlcohol-related brain damage (ARBD) is associated with neurotoxic effects of heavy alcohol use and nutritional deficiency, in particular thiamine deficiency (TD), both of which induce inflammatory responses in brain. Although neuroinflammation is a critical factor in the induction of ARBD, few studies have addressed the specific contribution(s) of ethanol (EtOH) versus TD.
methodsAdult rats were randomly divided into 6 conditions: chronic EtOH treatment (CET) where rats consumed a 20% v/v solution of EtOH for 6 months; CET with injections of thiamine (CET + T); severe pyrithiamine-induced TD (PTD); moderate PTD; moderate PTD during CET; and pair-fed controls. After the treatments, the rats were split into 3 recovery phase time points: the last day of treatment (time point 1), acute recovery (time point 2: 24 hours posttreatment), and delayed recovery (time point 3: 3 weeks posttreatment). At these time points, vulnerable brain regions (thalamus, hippocampus, frontal cortex) were collected and changes in neuroimmune markers were assessed using a combination of reverse transcription polymerase chain reaction and protein analysis.
resultsCET led to minor fluctuations in neuroimmune genes, regardless of the structure being examined. In contrast, PTD treatment led to a profound increase in neuroimmune genes and proteins within the thalamus. Cytokine changes in the thalamus ranged in magnitude from moderate (3-fold and 4-fold increase in interleukin-1β [IL-1β] and IκBα) to severe (8-fold and 26-fold increase in tumor necrosis factor-α and IL-6, respectively). Though a similar pattern was observed in the hippocampus and frontal cortex, overall fold increases were moderate relative to the thalamus. Importantly, neuroimmune gene induction varied significantly as a function of severity of TD, and most genes displayed a gradual recovery across time.
conclusionsThese data suggest an overt brain inflammatory response by TD and a subtle change by CET alone. Also, the prominent role of TD in the immune-related signaling pathways leads to unique regional and temporal profiles of induction of neuroimmune genes.
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