Alcohol最新文献

{"title":"Integrating TWAS and GWAS identifies gut microbiota–immune interactions to alcohol dependence genetics in European sample","authors":"Haohao Xu ,&nbsp;Peng Shen ,&nbsp;Zhenglin Zhao ,&nbsp;Yushuang Xing ,&nbsp;Tonghui Yi ,&nbsp;Chao Yang ,&nbsp;Han Gao ,&nbsp;Hongyan Guo ,&nbsp;Mingqian Zhao ,&nbsp;Shanbo Zhang ,&nbsp;Di Jia ,&nbsp;Weiming Zhao","doi":"10.1016/j.alcohol.2025.05.006","DOIUrl":"10.1016/j.alcohol.2025.05.006","url":null,"abstract":"<div><h3>Objective</h3><div>Alcohol dependence (AD) is a global public health concern with strong genetic characteristics. The purpose of this study was to explore the underlying pathogenic genes and mechanisms associated with AD.</div></div><div><h3>Methods</h3><div>This study employed a multi-omics Mendelian randomization approach to identify potential disease-causing genes for AD. Specifically, we integrated transcriptome-wide association studies (TWAS) with summary-data-based Mendelian randomization (SMR) to pinpoint candidate genes associated with AD. Additionally, mediating Mendelian randomization was utilized to investigate the mediating role of the gut microbiota in the relationship between immune cell phenotypes and AD.</div></div><div><h3>Results</h3><div>Two susceptibility genes associated with AD, ADH1C and POLI, were identified a joint analysis of SMR and integrated cross-tissue and single tissue TWAS in European population. A new genetic locus associated with AD, rs62307318, was uncovered through cross-organism TWAS. This finding was further validated using Mendelian randomization and Phenome-wide association analysis. Additionally, Mendelian randomization identified Paceibacteria as a possible mediator between Myeloid DC AC and AD.</div></div><div><h3>Conclusion</h3><div>This study identified two genes closely related to AD and explored the possible pathogenesis of AD, which provides a new insight into the treatment and pathogenesis of AD.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"127 ","pages":"Pages 11-20"},"PeriodicalIF":2.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227931","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}

{"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}

{"title":"Pain in comorbid alcohol use disorder and HIV: A network meta-analysis study","authors":"Muhammed Bishir,&nbsp;Mohamed Sheik Tharik Abdul Azeeze,&nbsp;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}

{"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,&nbsp;Madison Dillerud,&nbsp;Matthew Scalf,&nbsp;Ruth Dobbelmann,&nbsp;Yijuan Du,&nbsp;Anna M. Lee,&nbsp;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}

{"title":"Ethanol exposure promotes tumor cell migration and angiogenesis in a mouse model of glioblastoma","authors":"Bianca L. Myers ,&nbsp;C. Fernando Valenzuela ,&nbsp;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}

{"title":"An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers","authors":"Mariann R. Piano ,&nbsp;Shane A. Phillips ,&nbsp;Chueh-Lung Hwang ,&nbsp;Keng-Yu Chang ,&nbsp;Kevin M. Najarro ,&nbsp;Rachel H. McMahan ,&nbsp;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 &lt;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}

{"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,&nbsp;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}

{"title":"Corrigendum to “Time-course concentration of ethanol, acetaldehyde and acetate in rat brain dialysate following alcohol self-administration” [Alcohol 123 (2025) 69–76]","authors":"Tse-Ang Lee ,&nbsp;Hongjoo J. Lee ,&nbsp;Regina A. Mangieri ,&nbsp;Rueben Gonzales ,&nbsp;Heba Ajmal ,&nbsp;Tanya Hutter","doi":"10.1016/j.alcohol.2025.03.004","DOIUrl":"10.1016/j.alcohol.2025.03.004","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"125 ","pages":"Pages 53-54"},"PeriodicalIF":2.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143858996","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}

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

{"title":"Analysis of the synergy between prenatal ethanol and postnatal adolescent ethanol exposure","authors":"Leonardo Marengo ,&nbsp;Rodrigo García Virgolini ,&nbsp;Victoria Mujica ,&nbsp;María Carolina Fabio ,&nbsp;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, 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.</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}