IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-05-31 DOI: 10.1016/j.alcohol.2025.05.005

David M. Lovinger

Much of the behavioral repertoire of humans and other vertebrates is learned and controlled through the function of brain circuits involving the cortex, thalamus and Basal Ganglia (for simplicity we will refer to this as the Cortico-Thalamo-Basal Ganglia, or CTBG, circuitry). As the name implies, these circuits include the different regions of cortex and thalamus, as well as BG subregions including the striatum, globus pallidus (GP), substantia nigra (SN)/ventral tegmental area (VTA), and the subthalamic nucleus (STN). This circuitry has developed evolutionarily to provide overarching control of actions following discrete environmental events as well as self-initiated actions. Several parallel CTBG circuits have been identified and linked to different aspects of action control under different circumstances. Research in experimental psychology and Neuroscience has established how different CTBG circuits contribute to control of actions based on environmental circumstances and past learning history. There is also a large and growing body of evidence that misused substances, including alcohol, act on cells within these circuits. These actions promote acute intoxication and drug seeking and contribute to changes in behavior induced by chronic alcohol exposure, withdrawal and relapse. Alcohol exposure also influences which of the different CTBG circuits has the strongest influence on behavior. This review will cover the relevant circuitry and describe the current state of knowledge as to how alcohol alters CTBG circuit function and control of behavior. Studies in rodents, non-human primates and humans will be discussed. Finally, ideas for future research directions in this area will be considered.

人类和其他脊椎动物的许多行为都是通过大脑回路的功能来学习和控制的，这些回路涉及皮层、丘脑和基底神经节（为简单起见，我们将其称为皮质-丘脑-基底神经节，或CTBG回路）。顾名思义，这些回路包括皮层和丘脑的不同区域，以及包括纹状体、白球（GP）、黑质(SN)/腹侧被盖区（VTA）和丘脑下核（STN）在内的BG亚区。这种电路已经进化发展到提供对离散环境事件以及自我启动行为的总体控制。已经确定了几个平行的CTBG电路，并将其与不同情况下动作控制的不同方面联系起来。实验心理学和神经科学的研究已经确定了不同的CTBG回路是如何根据环境和过去的学习历史来控制行为的。越来越多的证据表明，包括酒精在内的滥用物质会对这些神经回路中的细胞起作用。这些行为促进急性中毒和药物寻求，并有助于慢性酒精暴露、戒断和复发引起的行为改变。酒精暴露也会影响不同CTBG回路中哪一个对行为的影响最大。这篇综述将涵盖相关的电路，并描述当前关于酒精如何改变CTBG电路功能和行为控制的知识状态。将讨论啮齿动物、非人类灵长类动物和人类的研究。最后，对该领域未来的研究方向进行了展望。

{"title":"Alcohol effects on associative and sensorimotor cortico-thalamo-basal ganglia circuits alter decision making and alcohol intake","authors":"David M. Lovinger","doi":"10.1016/j.alcohol.2025.05.005","DOIUrl":"10.1016/j.alcohol.2025.05.005","url":null,"abstract":"<div><div>Much of the behavioral repertoire of humans and other vertebrates is learned and controlled through the function of brain circuits involving the cortex, thalamus and Basal Ganglia (for simplicity we will refer to this as the Cortico-Thalamo-Basal Ganglia, or CTBG, circuitry). As the name implies, these circuits include the different regions of cortex and thalamus, as well as BG subregions including the striatum, globus pallidus (GP), substantia nigra (SN)/ventral tegmental area (VTA), and the subthalamic nucleus (STN). This circuitry has developed evolutionarily to provide overarching control of actions following discrete environmental events as well as self-initiated actions. Several parallel CTBG circuits have been identified and linked to different aspects of action control under different circumstances. Research in experimental psychology and Neuroscience has established how different CTBG circuits contribute to control of actions based on environmental circumstances and past learning history. There is also a large and growing body of evidence that misused substances, including alcohol, act on cells within these circuits. These actions promote acute intoxication and drug seeking and contribute to changes in behavior induced by chronic alcohol exposure, withdrawal and relapse. Alcohol exposure also influences which of the different CTBG circuits has the strongest influence on behavior. This review will cover the relevant circuitry and describe the current state of knowledge as to how alcohol alters CTBG circuit function and control of behavior. Studies in rodents, non-human primates and humans will be discussed. Finally, ideas for future research directions in this area will be considered.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 21-46"},"PeriodicalIF":2.5,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pain in comorbid alcohol use disorder and HIV: A network meta-analysis study 伴随酒精使用障碍和HIV的疼痛：一项网络荟萃分析研究

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-05-27 DOI: 10.1016/j.alcohol.2025.05.003

Muhammed Bishir, Mohamed Sheik Tharik Abdul Azeeze, Sulie L. Chang

Alcohol use is prevalent among people with HIV (PWH). PWH often experience pain (said discomfort) and use alcohol to combat pain. We reported that short-term alcohol exposure exerts analgesic effect. Prolonged exposure is known to result in chronic pain. We hypothesize that alcohol exposure, either in-vivo for macaques or in-silico simulation exposure onto differentially expressed genes (DEGs) from HIV-1Tg rats and HIV patients, exacerbates discomfort in PWH. To substantiate this hypothesis, we analyzed genomic data collected from three brain datasets including the hippocampus of alcohol-exposed Macaca mulatta (GSE69685), HIV-1Tg rats (GSE47474), and post-mortem brain tissue of HIV-positive patients (GSE28160). Ingenuity Pathway Analysis (IPA)-Core Analysis revealed activation of neuroinflammation, neuropathic pain signaling pathways, and the inhibition of opioid signaling as well as in the increase of neuromuscular disease with neuropathy in Macaca mulatta exposed to binge EtOH and SIV infection. IPA-Core Analysis of the DEGs from HIV-1Tg rats, a rat model that mimics HIV patients on cART, possessing 7 of 9 HIV viral proteins, showed activation of neuroinflammation, neuropathic pain signaling pathways. IPA-Core Analysis of the DEGs from HIV patients showed activation of neuroinflammation and inhibition of neuropathic pain and increase in neuromuscular disease with neuropathy. To study the impact of alcohol exposure in HIV-1Tg rats and HIV patients, in-silico simulation of ethanol (EtOH) treatment mimicking exposure of alcohol onto the DEGs in response to HIV viral proteins in HIV-1Tg rats and HIV infection in HIV patients enhanced discomfort and increased neuromuscular diseases. These molecules showed significant modulation by simulated alcohol exposure, further supporting the link between alcohol use and heightened pain in PWH. Taking together, our findings suggest that alcohol consumption and HIV promote pain via modulating signaling pathways including neuroinflammation, and neuropathic pain signaling pathways and by disease like neuromuscular disease with neuropathy.

酒精使用在艾滋病毒感染者（PWH）中很普遍。PWH经常感到疼痛（不适），并使用酒精来对抗疼痛。我们报道了短期酒精暴露有镇痛作用。已知长时间接触会导致慢性疼痛。我们假设酒精暴露，无论是猕猴体内暴露，还是在计算机模拟中暴露于来自HIV- 1tg大鼠和HIV患者的差异表达基因（DEGs），都会加剧PWH的不适。为了证实这一假设，我们分析了从三个大脑数据集收集的基因组数据，包括酒精暴露的猕猴（GSE69685）的海马、HIV-1Tg大鼠（GSE47474）和hiv阳性患者（GSE28160）的死后脑组织。独创性途径分析(IPA)-核心分析显示，暴露于暴食EtOH和SIV感染的猕猴的神经炎症、神经性疼痛信号通路的激活和阿片信号的抑制，以及神经肌肉疾病伴神经病变的增加。HIV- 1tg大鼠是一种在cART上模仿HIV患者的大鼠模型，拥有9种HIV病毒蛋白中的7种，其deg的IPA-Core分析显示，神经炎症、神经性疼痛信号通路被激活。HIV患者deg的IPA-Core分析显示，神经炎症激活，神经性疼痛抑制，神经肌肉疾病伴神经病增加。为了研究酒精暴露对HIV- 1tg大鼠和HIV患者的影响，硅模拟乙醇（EtOH）治疗模拟酒精暴露于HIV- 1tg大鼠的deg对HIV病毒蛋白的反应，以及HIV患者的HIV感染会增加不适和增加神经肌肉疾病。这些分子通过模拟酒精暴露表现出显著的调节，进一步支持酒精使用与PWH疼痛加剧之间的联系。综上所述，我们的研究结果表明，饮酒和艾滋病毒通过调节信号通路（包括神经炎症、神经性疼痛信号通路）和神经肌肉疾病（如神经病变）等疾病来促进疼痛。

{"title":"Pain in comorbid alcohol use disorder and HIV: A network meta-analysis study","authors":"Muhammed Bishir, Mohamed Sheik Tharik Abdul Azeeze, Sulie L. Chang","doi":"10.1016/j.alcohol.2025.05.003","DOIUrl":"10.1016/j.alcohol.2025.05.003","url":null,"abstract":"<div><div>Alcohol use is prevalent among people with HIV (PWH). PWH often experience pain (said discomfort) and use alcohol to combat pain. We reported that short-term alcohol exposure exerts analgesic effect. Prolonged exposure is known to result in chronic pain. We hypothesize that alcohol exposure, either <em>in-vivo</em> for <em>macaques</em> or <em>in-silico</em> simulation exposure onto differentially expressed genes (DEGs) from HIV-1Tg rats and HIV patients, exacerbates discomfort in PWH. To substantiate this hypothesis, we analyzed genomic data collected from three brain datasets including the hippocampus of alcohol-exposed <em>Macaca mulatta</em> (GSE69685), HIV-1Tg rats (GSE47474), and post-mortem brain tissue of HIV-positive patients (GSE28160). Ingenuity Pathway Analysis (IPA)-Core Analysis revealed activation of neuroinflammation, neuropathic pain signaling pathways, and the inhibition of opioid signaling as well as in the increase of neuromuscular disease with neuropathy in <em>Macaca mulatta</em> exposed to binge EtOH and SIV infection. IPA-Core Analysis of the DEGs from HIV-1Tg rats, a rat model that mimics HIV patients on cART, possessing 7 of 9 HIV viral proteins, showed activation of neuroinflammation, neuropathic pain signaling pathways. IPA-Core Analysis of the DEGs from HIV patients showed activation of neuroinflammation and inhibition of neuropathic pain and increase in neuromuscular disease with neuropathy. To study the impact of alcohol exposure in HIV-1Tg rats and HIV patients, <em>in-silico</em> simulation of ethanol (EtOH) treatment mimicking exposure of alcohol onto the DEGs in response to HIV viral proteins in HIV-1Tg rats and HIV infection in HIV patients enhanced discomfort and increased neuromuscular diseases. These molecules showed significant modulation by simulated alcohol exposure, further supporting the link between alcohol use and heightened pain in PWH. Taking together, our findings suggest that alcohol consumption and HIV promote pain via modulating signaling pathways including neuroinflammation, and neuropathic pain signaling pathways and by disease like neuromuscular disease with neuropathy.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 43-53"},"PeriodicalIF":2.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Alcohol consumption during early adulthood increases the vulnerability of locus coeruleus neurons and amyloid beta pathology in female APP/PS1 mice 成年早期饮酒增加雌性APP/PS1小鼠蓝斑神经元的易感性和淀粉样蛋白病理。

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-05-21 DOI: 10.1016/j.alcohol.2025.05.004

Shaydel Engel, Madison Dillerud, Matthew Scalf, Ruth Dobbelmann, Yijuan Du, Anna M. Lee, Steven M. Graves

Alcohol use disorder is the most common substance misuse disorder and Alzheimer's disease (AD) is the most common neurodegenerative disease. Evidence suggests that alcohol consumption may increase the risk for developing dementia and AD. The locus coeruleus (LC) is a region wherein the impact of alcohol and AD may converge. The LC is a noradrenergic nucleus that is highly vulnerable to degeneration in AD, and loss of LC neurons is associated with increased amyloid beta (Abeta) pathology. The present study examined whether alcohol consumption during early adulthood impacts LC degeneration and Abeta using the APP/PS1 mouse model. Female APP/PS1 mice underwent an eight-week chronic intermittent access (IA) alcohol consumption paradigm followed by twenty-three weeks of abstinence; water-consuming control subjects were run in parallel. APP/PS1 mice that had IA to alcohol showed a 21.9% decrease in the number of LC neurons and a decrease in the length of noradrenergic axons innervating the primary motor cortex. Furthermore, this alcohol induced LC deficit was associated with an increase in Abeta pathology in the primary motor cortex. In contrast to results from female APP/PS1 mice, there were no deficits in axon length and only a 9.4% decrease in the number of LC neurons in non-transgenic female subjects after abstinence from IA to alcohol. Our results demonstrate that alcohol consumption during early adulthood increases the vulnerability of LC neurons to degeneration and exacerbates Abeta pathology in female APP/PS1 mice, providing evidence that a history of alcohol abuse may impact the trajectory and severity of AD.

酒精使用障碍是最常见的物质滥用障碍，阿尔茨海默病（AD）是最常见的神经退行性疾病。有证据表明，饮酒可能会增加患痴呆症和阿尔茨海默病的风险。蓝斑（LC）是酒精和AD的影响可能汇合的区域。LC是一种去肾上腺素能核，在AD中极易变性，LC神经元的丧失与淀粉样蛋白（Abeta）病理增加有关。本研究通过APP/PS1小鼠模型研究了成年早期饮酒是否会影响LC变性和β。雌性APP/PS1小鼠进行了为期8周的慢性间歇获取（IA）酒精消费范式，随后进行了23周的禁欲；饮水对照受试者平行进行实验。APP/PS1小鼠酒精浓度为IA后，LC神经元数量减少21.9%，支配初级运动皮质的去甲肾上腺素能轴突长度减少。此外，这种酒精诱导的LC缺陷与初级运动皮层中Abeta病理的增加有关。与雌性APP/PS1小鼠的结果相反，非转基因雌性受试者在戒酒后，轴突长度没有缺陷，LC神经元数量仅减少9.4%。我们的研究结果表明，成年早期饮酒增加了雌性APP/PS1小鼠LC神经元对变性的易感性，并加剧了Abeta病理，这为酗酒史可能影响AD的发展轨迹和严重程度提供了证据。

{"title":"Alcohol consumption during early adulthood increases the vulnerability of locus coeruleus neurons and amyloid beta pathology in female APP/PS1 mice","authors":"Shaydel Engel, Madison Dillerud, Matthew Scalf, Ruth Dobbelmann, Yijuan Du, Anna M. Lee, Steven M. Graves","doi":"10.1016/j.alcohol.2025.05.004","DOIUrl":"10.1016/j.alcohol.2025.05.004","url":null,"abstract":"<div><div>Alcohol use disorder is the most common substance misuse disorder and Alzheimer's disease (AD) is the most common neurodegenerative disease. Evidence suggests that alcohol consumption may increase the risk for developing dementia and AD. The locus coeruleus (LC) is a region wherein the impact of alcohol and AD may converge. The LC is a noradrenergic nucleus that is highly vulnerable to degeneration in AD, and loss of LC neurons is associated with increased amyloid beta (Abeta) pathology. The present study examined whether alcohol consumption during early adulthood impacts LC degeneration and Abeta using the APP/PS1 mouse model. Female APP/PS1 mice underwent an eight-week chronic intermittent access (IA) alcohol consumption paradigm followed by twenty-three weeks of abstinence; water-consuming control subjects were run in parallel. APP/PS1 mice that had IA to alcohol showed a 21.9% decrease in the number of LC neurons and a decrease in the length of noradrenergic axons innervating the primary motor cortex. Furthermore, this alcohol induced LC deficit was associated with an increase in Abeta pathology in the primary motor cortex. In contrast to results from female APP/PS1 mice, there were no deficits in axon length and only a 9.4% decrease in the number of LC neurons in non-transgenic female subjects after abstinence from IA to alcohol. Our results demonstrate that alcohol consumption during early adulthood increases the vulnerability of LC neurons to degeneration and exacerbates Abeta pathology in female APP/PS1 mice, providing evidence that a history of alcohol abuse may impact the trajectory and severity of AD.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 1-9"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ethanol exposure promotes tumor cell migration and angiogenesis in a mouse model of glioblastoma 在胶质母细胞瘤小鼠模型中，乙醇暴露促进肿瘤细胞迁移和血管生成。

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-05-10 DOI: 10.1016/j.alcohol.2025.05.002

Bianca L. Myers , C. Fernando Valenzuela , Tou Yia Vue

Rapid progression of high-grade gliomas contributes to the poor survival rates of patients, particularly those with aggressive and heterogeneous brain tumors such as glioblastomas (GBMs). Before the onset of tumor symptoms, there exists a vulnerable period during which exposure to environmental factors could exacerbate glioma tumorigenicity. Alcohol (EtOH) is one such factor that has been shown to increase tumor size and vascularization of melanomas in xenograft mouse models and invasion of breast cancer cells in vitro. Currently, whether EtOH exposure promotes glioma progression in vivo is unknown. Here, we induced fluorescently labeled gliomas in immune-competent mice by injecting and electroporating Cre + CRISPR plasmids to delete tumor suppressor genes in neural progenitors lining the right lateral ventricle. Asymptomatic tumor mice were exposed to EtOH or Air vapors via inhalation chambers for five days, followed by two days of rest, then another five days of exposure. This paradigm produced blood ethanol concentrations (BECs) similar to episodic binge drinking, averaging ∼200 mg/dL on the final day of exposure. We found that EtOH exposure acutely increased tumor vascularization and invasion to the contralateral hemisphere. Notably, EtOH-exposed male mice exhibited a significant decrease in survival compared to Air-exposed controls and EtOH-exposed female mice. Overall, our study is the first to demonstrate that developing primary gliomas are susceptible to the tumorigenic effects of EtOH, with males being more vulnerable to increased mortality.

高级别胶质瘤的快速进展导致患者的生存率较低，特别是那些侵袭性和异质性脑肿瘤，如胶质母细胞瘤（GBMs）。在胶质瘤出现症状之前，存在一段易感期，暴露于环境因素会加剧胶质瘤的致瘤性。酒精（EtOH）就是这样一个因素，在异种移植小鼠模型中显示，它可以增加肿瘤大小和黑色素瘤的血管化，并在体外显示乳腺癌细胞的侵袭。目前，EtOH暴露是否促进胶质瘤在体内的进展尚不清楚。在这里，我们通过注射和电穿孔Cre + CRISPR质粒，在免疫功能正常的小鼠中诱导荧光标记的胶质瘤，以删除右侧侧脑室内衬神经祖细胞中的肿瘤抑制基因。无症状肿瘤小鼠通过吸入室暴露于EtOH或空气中5天，然后休息2天，然后再暴露5天。这种模式产生的血液乙醇浓度（BECs）与间歇性狂饮相似，在暴露的最后一天平均为~ 200 mg/dL。我们发现EtOH暴露会急剧增加肿瘤血管化，并促进肿瘤向对侧半球的侵袭。值得注意的是，与暴露于空气中的对照组和暴露于etoh的雌性小鼠相比，暴露于etoh的雄性小鼠的存活率显著降低。总的来说，我们的研究首次证明了发展中的原发性胶质瘤易受EtOH致瘤作用的影响，男性更容易受到死亡率增加的影响。

{"title":"Ethanol exposure promotes tumor cell migration and angiogenesis in a mouse model of glioblastoma","authors":"Bianca L. Myers , C. Fernando Valenzuela , Tou Yia Vue","doi":"10.1016/j.alcohol.2025.05.002","DOIUrl":"10.1016/j.alcohol.2025.05.002","url":null,"abstract":"<div><div>Rapid progression of high-grade gliomas contributes to the poor survival rates of patients, particularly those with aggressive and heterogeneous brain tumors such as glioblastomas (GBMs). Before the onset of tumor symptoms, there exists a vulnerable period during which exposure to environmental factors could exacerbate glioma tumorigenicity. Alcohol (EtOH) is one such factor that has been shown to increase tumor size and vascularization of melanomas in xenograft mouse models and invasion of breast cancer cells in vitro. Currently, whether EtOH exposure promotes glioma progression in vivo is unknown. Here, we induced fluorescently labeled gliomas in immune-competent mice by injecting and electroporating <em>Cre</em> + CRISPR plasmids to delete tumor suppressor genes in neural progenitors lining the right lateral ventricle. Asymptomatic tumor mice were exposed to EtOH or Air vapors via inhalation chambers for five days, followed by two days of rest, then another five days of exposure. This paradigm produced blood ethanol concentrations (BECs) similar to episodic binge drinking, averaging ∼200 mg/dL on the final day of exposure. We found that EtOH exposure acutely increased tumor vascularization and invasion to the contralateral hemisphere. Notably, EtOH-exposed male mice exhibited a significant decrease in survival compared to Air-exposed controls and EtOH-exposed female mice. Overall, our study is the first to demonstrate that developing primary gliomas are susceptible to the tumorigenic effects of EtOH, with males being more vulnerable to increased mortality.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 11-21"},"PeriodicalIF":2.5,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144048658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers 年轻成人低风险和高危饮酒者之间细胞因子和炎症特征的探索性研究。

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-05-07 DOI: 10.1016/j.alcohol.2025.05.001

Mariann R. Piano , Shane A. Phillips , Chueh-Lung Hwang , Keng-Yu Chang , Kevin M. Najarro , Rachel H. McMahan , Elizabeth J. Kovacs

Background

This exploratory study examined plasma levels of pro-inflammatory cytokines, chemokines and growth factors as well as intestinal fatty acid-binding protein (iFABP) and zonulin levels between young adult male and female low-risk and at-risk drinkers.

Methods

A total of 33 low-risk (phosphatidylethanol levels <20 ng/ml; 19 female) and 44 at-risk drinkers (phosphatidylethanol levels ≥20 ng/ml; 30 female) were included in this study. Fasting blood samples were obtained in all participants. A multiplex assay was used to measure 48 chemokines and growth factors. An enzyme-linked immunoassay was used to measure plasma levels of human iFABP and zonulin.

Results

We found that in young female, at-risk drinkers had a lower level of granulocyte-macrophage colony-stimulating factor (p = 0.04) and platelet-derived growth factor BB (P = 0.04) than low-risk drinkers, while in males, an elevated level of interferon-gamma was found in at-risk drinkers compared to low-risk drinkers (P = 0.04). Intestinal fatty acid-binding protein levels were significantly higher and zonulin levels were significantly lower in at-risk-risk drinkers compared to low-risk drinkers (P = 0.001 and P = 0.02, respectively).

Conclusions

These findings suggest that at-risk drinking in young adults is associated with alterations in specific cytokines and proteins involved in intestinal barrier function.

背景：本探索性研究检测了血浆中促炎细胞因子、趋化因子和生长因子水平以及肠道脂肪酸结合蛋白（iFABP）和zonulin水平在年轻成年男性和女性低危和高危饮酒者之间。结果：我们发现在年轻女性中，高危饮酒者的粒细胞-巨噬细胞集落刺激因子（p=0.04）和血小板衍生生长因子BB （p=0.04）水平低于低危饮酒者，而在男性中，与低危饮酒者相比，高危饮酒者的干扰素γ水平升高（p=0.04）。与低风险饮酒者相比，高危饮酒者肠道脂肪酸结合蛋白水平显著升高，zonulin水平显著降低（P分别=0.001和P=0.02）。结论：这些研究结果表明，年轻人的高危饮酒与肠道屏障功能相关的特定细胞因子和蛋白质的改变有关。

{"title":"An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers","authors":"Mariann R. Piano , Shane A. Phillips , Chueh-Lung Hwang , Keng-Yu Chang , Kevin M. Najarro , Rachel H. McMahan , Elizabeth J. Kovacs","doi":"10.1016/j.alcohol.2025.05.001","DOIUrl":"10.1016/j.alcohol.2025.05.001","url":null,"abstract":"<div><h3>Background</h3><div>This exploratory study examined plasma levels of pro-inflammatory cytokines, chemokines and growth factors as well as intestinal fatty acid-binding protein (iFABP) and zonulin levels between young adult male and female low-risk and at-risk drinkers.</div></div><div><h3>Methods</h3><div>A total of 33 low-risk (phosphatidylethanol levels <20 ng/ml; 19 female) and 44 at-risk drinkers (phosphatidylethanol levels ≥20 ng/ml; 30 female) were included in this study. Fasting blood samples were obtained in all participants. A multiplex assay was used to measure 48 chemokines and growth factors. An enzyme-linked immunoassay was used to measure plasma levels of human iFABP and zonulin.</div></div><div><h3>Results</h3><div>We found that in young female, at-risk drinkers had a lower level of granulocyte-macrophage colony-stimulating factor (p = 0.04) and platelet-derived growth factor BB (P = 0.04) than low-risk drinkers, while in males, an elevated level of interferon-gamma was found in at-risk drinkers compared to low-risk drinkers (P = 0.04). Intestinal fatty acid-binding protein levels were significantly higher and zonulin levels were significantly lower in at-risk-risk drinkers compared to low-risk drinkers (P = 0.001 and P = 0.02, respectively).</div></div><div><h3>Conclusions</h3><div>These findings suggest that at-risk drinking in young adults is associated with alterations in specific cytokines and proteins involved in intestinal barrier function.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 23-29"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Resilience building discourse in online spaces: A comparative analysis of user statements following the disclosure of a break in alcohol abstinence 网络空间中的弹性建构话语：对戒酒中断披露后用户陈述的比较分析。

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-04-29 DOI: 10.1016/j.alcohol.2025.04.003

Lynda K. Maxfield, Tara M. Emmers-Sommer

This study investigates statements made by individuals who either disclose having experienced a break in alcohol abstinence or provide a first-level response to such disclosures. An average month of public Reddit data were examined, resulting in 193 posts and 1238 responses. Post statements were binarily considered according to eight a priori categories, primarily guided by the communication resilience process scale (CRPS; Wilson et al., 2021). Coded response posts were collapsed into sets corresponding to initial posts, facilitating the saturation comparison of resilience building statements between initial and response posts. Results indicate that responses were more resilience-heavy than initial posts, suggesting users looking to disclose an abstinence break have a good chance of experiencing resilience building responses. Notably, the top three resilience building categories identified in this study were identical for initial and response posts. Discussion, implications, and future research directions regarding communicating resilience and resilience building discourse follow.

这项研究调查了一些人的陈述，这些人要么透露自己经历了戒酒的中断，要么对这种披露提供了一级反应。研究人员检查了Reddit平均一个月的公开数据，共有193条帖子和1238条回复。后陈述根据八个先验类别进行二元考虑，主要以沟通弹性过程量表(CRPS；Wilson et al., 2021)。编码响应岗位被压缩成与初始岗位相对应的集合，便于初始岗位和响应岗位弹性建设陈述的饱和比较。结果表明，回应比最初的帖子更有弹性，这表明希望透露禁欲休息的用户很有可能经历弹性建设的回应。值得注意的是，本研究确定的前三个弹性建设类别对于初始和响应职位是相同的。最后，讨论了沟通弹性和弹性建设的相关问题，并提出了未来的研究方向。

{"title":"Resilience building discourse in online spaces: A comparative analysis of user statements following the disclosure of a break in alcohol abstinence","authors":"Lynda K. Maxfield, Tara M. Emmers-Sommer","doi":"10.1016/j.alcohol.2025.04.003","DOIUrl":"10.1016/j.alcohol.2025.04.003","url":null,"abstract":"<div><div>This study investigates statements made by individuals who either disclose having experienced a break in alcohol abstinence or provide a first-level response to such disclosures. An average month of public Reddit data were examined, resulting in 193 posts and 1238 responses. Post statements were binarily considered according to eight a priori categories, primarily guided by the communication resilience process scale (CRPS; Wilson et al., 2021). Coded response posts were collapsed into sets corresponding to initial posts, facilitating the saturation comparison of resilience building statements between initial and response posts. Results indicate that responses were more resilience-heavy than initial posts, suggesting users looking to disclose an abstinence break have a good chance of experiencing resilience building responses. Notably, the top three resilience building categories identified in this study were identical for initial and response posts. Discussion, implications, and future research directions regarding communicating resilience and resilience building discourse follow.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 31-41"},"PeriodicalIF":2.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “Time-course concentration of ethanol, acetaldehyde and acetate in rat brain dialysate following alcohol self-administration” [Alcohol 123 (2025) 69–76] “自我给药后大鼠脑透析液中乙醇、乙醛和醋酸盐的时间过程浓度”的勘误表[酒精123 (2025)69-76]

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-04-23 DOI: 10.1016/j.alcohol.2025.03.004

Tse-Ang Lee , Hongjoo J. Lee , Regina A. Mangieri , Rueben Gonzales , Heba Ajmal , Tanya Hutter

引用次数: 0

New developments on the effects of alcohol use on immunity, inflammation and organ function: A summary of the 2024 Alcohol and Immunology Research Interest Group (AIRIG) meeting 饮酒对免疫、炎症和器官功能影响的新进展：2024年酒精和免疫学研究兴趣小组（AIRIG）会议总结

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-04-21 DOI: 10.1016/j.alcohol.2025.04.002

Madison M. Tschann , Vidula Vachharajani , Eileen M. Redmond , Andrew Hoisington , Sarah E. Cohen , Moses New-Aaron , Cristina Llorente , Janos Paloczi , Claudia R. Keating , Wiramon Rungratanawanich , Ellen L. Burnham , John J. Callaci , Preeti Raju , Weizhe Zhong , Abhishek Mandal , Justine R. Zimmerly , Adriana S.P. Nuncio , Pranoti Mandrekar , Rebecca L. McCullough , Rachel H. McMahan , Mashkoor A. Choudhry

The 29th annual Alcohol and Immunology Research Interest Group (AIRIG) meeting was held on November 22nd, 2024, at Loyola University Chicago, Health Science Campus, Maywood, Illinois. The meeting was divided into three plenary sessions and a poster session. The overall focus of this year’s meeting was on alcohol and host immunity, alcohol and organ dysfunction, and alcohol, inflammation, and tissue injury. The presentations in each session shared the latest developments on the impact of alcohol in a wide variety of fields including trauma, emergency care and hospitalization, cardiovascular health, neurodegenerative disease, gut microbiome, and hepatology.

第29届年度酒精和免疫学研究兴趣小组（AIRIG）会议于2024年11月22日在伊利诺伊州梅伍德的芝加哥洛约拉大学健康科学校区举行。会议分为三次全体会议和一次海报会议。今年会议的总体重点是酒精与宿主免疫、酒精与器官功能障碍以及酒精、炎症和组织损伤。每次会议的报告都分享了酒精在各种领域的影响的最新进展，包括创伤、急诊护理和住院、心血管健康、神经退行性疾病、肠道微生物群和肝病学。

{"title":"New developments on the effects of alcohol use on immunity, inflammation and organ function: A summary of the 2024 Alcohol and Immunology Research Interest Group (AIRIG) meeting","authors":"Madison M. Tschann , Vidula Vachharajani , Eileen M. Redmond , Andrew Hoisington , Sarah E. Cohen , Moses New-Aaron , Cristina Llorente , Janos Paloczi , Claudia R. Keating , Wiramon Rungratanawanich , Ellen L. Burnham , John J. Callaci , Preeti Raju , Weizhe Zhong , Abhishek Mandal , Justine R. Zimmerly , Adriana S.P. Nuncio , Pranoti Mandrekar , Rebecca L. McCullough , Rachel H. McMahan , Mashkoor A. Choudhry","doi":"10.1016/j.alcohol.2025.04.002","DOIUrl":"10.1016/j.alcohol.2025.04.002","url":null,"abstract":"<div><div>The 29th annual Alcohol and Immunology Research Interest Group (AIRIG) meeting was held on November 22nd, 2024, at Loyola University Chicago, Health Science Campus, Maywood, Illinois. The meeting was divided into three plenary sessions and a poster session. The overall focus of this year’s meeting was on alcohol and host immunity, alcohol and organ dysfunction, and alcohol, inflammation, and tissue injury. The presentations in each session shared the latest developments on the impact of alcohol in a wide variety of fields including trauma, emergency care and hospitalization, cardiovascular health, neurodegenerative disease, gut microbiome, and hepatology.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"126 ","pages":"Pages 1-10"},"PeriodicalIF":2.5,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143912241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Analysis of the synergy between prenatal ethanol and postnatal adolescent ethanol exposure 产前乙醇和产后青少年乙醇暴露的协同作用分析

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-04-09 DOI: 10.1016/j.alcohol.2025.04.001

Leonardo Marengo , Rodrigo García Virgolini , Victoria Mujica , María Carolina Fabio , Ricardo Marcos Pautassi

Prenatal ethanol exposure (PEE) is associated with long-lasting neurodevelopmental alterations that increase susceptibility to adverse behavioral outcomes, including greater likelihood of binge drinking during adolescence. However, the interactive effects of these two developmental risk factors remain underexplored. The present study investigated the synergistic impact of PEE and adolescent binge-like ethanol exposure on behavioral and ethanol consumption patterns in Wistar rats. Pregnant dams received ethanol (2.0 g/kg/day) or vehicle from gestational days 17–20. Offspring were subjected to intermittent ethanol exposure (4.0 g/kg/day, two days on–two days off) or vehicle from postnatal days 23–36. Behavioral assessments included tests for anxiety-like behaviors (light–dark box test), anhedonia (sucrose preference test), exploratory behavior (multivariate concentric square field test), and voluntary ethanol consumption in early adulthood. PEE was associated with increased overall fluid consumption (p = 0.001, η²p = 0.17) and a sex-dependent increase in ethanol intake (p = 0.001, η²p = 0.05). PEE rats displayed reduced sucrose preference (p = 0.02, η²p = 0.07), suggesting an anhedonic-like phenotype independent of adolescent ethanol exposure. The latter exposure induced an anxious phenotype, characterized by reduced time in the illuminated compartment of the light–dark box test, which was attenuated in PEE-exposed rats (p = 0.03, η²p = 0.06). These findings suggest that PEE (a) facilitates ethanol consumption in offspring, potentially through tolerance mechanisms or altered chemosensory processing; and (b) modulates anxiety-like behaviors induced by adolescent ethanol exposure. Understanding these interactions is critical for elucidating the mechanisms underlying alcohol use disorders and designing targeted interventions for at-risk populations.

产前乙醇暴露（PEE）与长期的神经发育改变有关，增加了不良行为结果的易感性，包括青春期酗酒的可能性更大。然而，这两种发育风险因素的相互作用仍未得到充分探讨。本研究探讨了PEE和青少年酒精暴露对Wistar大鼠行为和酒精消费模式的协同影响。从妊娠第17-20天开始，孕鼠接受乙醇（2.0 g/kg/天）或载药。子代从出生后23-36天开始接受间歇乙醇暴露（4.0 g/kg/天，开两天，休息两天）或车辆。行为评估包括焦虑样行为（光-暗盒测试）、快感缺乏（蔗糖偏好测试）、探索性行为（多变量同心方场测试）和成年早期的自愿乙醇消费测试。PEE与总液体消耗量增加（p = 0.001, η2p = 0.17）和乙醇摄入量增加（p = 0.001, η2p = 0.05）相关。PEE大鼠表现出较低的蔗糖偏好（p = 0.02, η2p = 0.07），提示一种与青春期乙醇暴露无关的快感缺乏样表型。后一种暴露诱发了焦虑表型，其特征是在明暗箱试验的光照室中停留的时间减少，在pee暴露的大鼠中这种情况有所减弱（p = 0.03, η2p = 0.06）。这些发现表明，PEE (a)可能通过耐受性机制或改变化学感觉加工促进后代对乙醇的消耗；(b)调节青少年酒精暴露诱导的焦虑样行为。了解这些相互作用对于阐明酒精使用障碍的机制和为高危人群设计有针对性的干预措施至关重要。

{"title":"Analysis of the synergy between prenatal ethanol and postnatal adolescent ethanol exposure","authors":"Leonardo Marengo , Rodrigo García Virgolini , Victoria Mujica , María Carolina Fabio , Ricardo Marcos Pautassi","doi":"10.1016/j.alcohol.2025.04.001","DOIUrl":"10.1016/j.alcohol.2025.04.001","url":null,"abstract":"<div><div>Prenatal ethanol exposure (PEE) is associated with long-lasting neurodevelopmental alterations that increase susceptibility to adverse behavioral outcomes, including greater likelihood of binge drinking during adolescence. However, the interactive effects of these two developmental risk factors remain underexplored. The present study investigated the synergistic impact of PEE and adolescent binge-like ethanol exposure on behavioral and ethanol consumption patterns in Wistar rats. Pregnant dams received ethanol (2.0 g/kg/day) or vehicle from gestational days 17–20. Offspring were subjected to intermittent ethanol exposure (4.0 g/kg/day, two days on–two days off) or vehicle from postnatal days 23–36. Behavioral assessments included tests for anxiety-like behaviors (light–dark box test), anhedonia (sucrose preference test), exploratory behavior (multivariate concentric square field test), and voluntary ethanol consumption in early adulthood. PEE was associated with increased overall fluid consumption (p = 0.001, η<sup>2</sup>p = 0.17) and a sex-dependent increase in ethanol intake (p = 0.001, η<sup>2</sup>p = 0.05). PEE rats displayed reduced sucrose preference (p = 0.02, η<sup>2</sup>p = 0.07), suggesting an anhedonic-like phenotype independent of adolescent ethanol exposure. The latter exposure induced an anxious phenotype, characterized by reduced time in the illuminated compartment of the light–dark box test, which was attenuated in PEE-exposed rats (p = 0.03, η<sup>2</sup>p = 0.06). These findings suggest that PEE (a) facilitates ethanol consumption in offspring, potentially through tolerance mechanisms or altered chemosensory processing; and (b) modulates anxiety-like behaviors induced by adolescent ethanol exposure. Understanding these interactions is critical for elucidating the mechanisms underlying alcohol use disorders and designing targeted interventions for at-risk populations.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"125 ","pages":"Pages 25-33"},"PeriodicalIF":2.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Alcohol diminishes barrier integrity in human stem cell-derived brain microvascular endothelial cells: Role of reactive oxygen species 酒精降低人干细胞来源的脑微血管内皮细胞屏障完整性：活性氧的作用

IF 2.5 4区医学 Q3 PHARMACOLOGY & PHARMACY

Alcohol

Pub Date : 2025-04-03 DOI: 10.1016/j.alcohol.2025.03.005

Kameron T. Bell , Jason M. Hughes , Wesley A. Borman , Ryan D. Stoffel , Scott G. Canfield

The World Health Organization has linked alcohol consumption to over 200 diseases including neurodegenerative diseases. A dysfunctional blood–brain barrier (BBB) has been found to be influential in a number of brain disorders. The BBB is critical in maintaining homeostasis between the brain vasculature and parenchyma and a loss in barrier integrity would enable otherwise impermeable immune cells, molecules, and inflammatory mediators to reach the brain parenchyma. A subset of studies demonstrated that alcohol could diminish BBB integrity, but it is unclear if this effect translates clinically. In this study, we utilize a human stem cell-derived BBB model with near in vivo properties to investigate the effects of alcohol on critical barrier properties. Barrier forming brain-like microvascular endothelial cells (BMECs) were derived from human induced pluripotent stem cells (iPSCs) and exposed to several alcohol concentrations. Alcohol decreased barrier integrity observed by a loss in trans-endothelial electrical resistance and an increase in sodium fluorescein permeability. Alcohol decreased expression and junctional localization of tight junction proteins, a critical component to barrier integrity. Additionally, alcohol did not affect efflux transporter activity or cell viability in BMECs. The detrimental effects of alcohol on BBB properties were due to in part elevated reactive oxygen species (ROS); as scavenging ROS improved barrier properties, including the restoration of tight junction expression and localization. These data suggest that excessive alcohol consumption could diminish the BBB and contribute to the development or exacerbation of brain disorders.

Clinical trial number and registry URL

Not applicable.

世界卫生组织将饮酒与200多种疾病联系起来，其中包括神经退行性疾病。血脑屏障功能障碍（BBB）已被发现对许多脑部疾病有影响。血脑屏障在维持脑血管和脑实质之间的稳态中起着至关重要的作用，屏障完整性的丧失将使原本不可渗透的免疫细胞、分子和炎症介质能够到达脑实质。一部分研究表明，酒精可以降低血脑屏障的完整性，但尚不清楚这种影响是否在临床上转化。在这项研究中，我们利用具有接近体内特性的人类干细胞衍生血脑屏障模型来研究酒精对关键屏障特性的影响。形成屏障的脑样微血管内皮细胞（BMECs）来源于人诱导多能干细胞（iPSCs），并暴露于几种浓度的酒精中。酒精降低屏障完整性，观察到跨内皮电阻的损失和荧光素钠通透性的增加。酒精降低了紧密连接蛋白的表达和连接定位，紧密连接蛋白是屏障完整性的关键组成部分。此外，酒精不影响bmec的外排转运蛋白活性或细胞活力。酒精对血脑屏障性能的有害影响部分是由于活性氧（ROS）的升高；清除活性氧可以改善屏障特性，包括恢复紧密连接的表达和定位。这些数据表明，过量饮酒可能会减少血脑屏障，导致大脑疾病的发展或恶化。临床试验编号和注册地址：不适用。

{"title":"Alcohol diminishes barrier integrity in human stem cell-derived brain microvascular endothelial cells: Role of reactive oxygen species","authors":"Kameron T. Bell , Jason M. Hughes , Wesley A. Borman , Ryan D. Stoffel , Scott G. Canfield","doi":"10.1016/j.alcohol.2025.03.005","DOIUrl":"10.1016/j.alcohol.2025.03.005","url":null,"abstract":"<div><div>The World Health Organization has linked alcohol consumption to over 200 diseases including neurodegenerative diseases. A dysfunctional blood–brain barrier (BBB) has been found to be influential in a number of brain disorders. The BBB is critical in maintaining homeostasis between the brain vasculature and parenchyma and a loss in barrier integrity would enable otherwise impermeable immune cells, molecules, and inflammatory mediators to reach the brain parenchyma. A subset of studies demonstrated that alcohol could diminish BBB integrity, but it is unclear if this effect translates clinically. In this study, we utilize a human stem cell-derived BBB model with near <em>in vivo</em> properties to investigate the effects of alcohol on critical barrier properties. Barrier forming brain-like microvascular endothelial cells (BMECs) were derived from human induced pluripotent stem cells (iPSCs) and exposed to several alcohol concentrations. Alcohol decreased barrier integrity observed by a loss in trans-endothelial electrical resistance and an increase in sodium fluorescein permeability. Alcohol decreased expression and junctional localization of tight junction proteins, a critical component to barrier integrity. Additionally, alcohol did not affect efflux transporter activity or cell viability in BMECs. The detrimental effects of alcohol on BBB properties were due to in part elevated reactive oxygen species (ROS); as scavenging ROS improved barrier properties, including the restoration of tight junction expression and localization. These data suggest that excessive alcohol consumption could diminish the BBB and contribute to the development or exacerbation of brain disorders.</div></div><div><h3>Clinical trial number and registry URL</h3><div>Not applicable.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"125 ","pages":"Pages 55-66"},"PeriodicalIF":2.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Alcohol最新文献

Background

Methods

Results

Conclusions

Clinical trial number and registry URL