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        <title>Advances in Drug and Alcohol Research | New and Recent Articles</title>
        <link>https://www.frontierspartnerships.org/journals/advances-in-drug-and-alcohol-research</link>
        <description>RSS Feed for Advances in Drug and Alcohol Research | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-04T09:32:07.665+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2026.16094</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2026.16094</link>
        <title><![CDATA[A two-factor structure for cannabis use disorder identification test and its associations with demographic factors and cannabis use motives]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nadine Heckel</author><author>Carlos Nordt</author><author>Etna J. E. Engeli</author><author>Patricia Dürler</author><author>Marcus Herdener</author>
        <description><![CDATA[IntroductionCannabis use is linked to the risk of developing a Cannabis Use Disorder (CUD), which can often be chronic. Early identification of problematic cannabis use is crucial to lower the risk of CUD and associated adverse effects. However, the factor structure of the widely used Cannabis Use Disorder Identification Test (CUDIT) remains ambiguous. Furthermore, the impact of age and gender on CUD assessed with CUDIT is unknown. Exploring cannabis use motives has been proposed to better understand susceptibility to CUD. This study aims to clarify the CUDIT’s factor structure, its links to cannabis use motives, and the influence of age and gender on CUD.Materials and MethodsWe analyzed data from 3454 people who use cannabis (20.5% women; mean age = 30.31 years), collected from a Swiss online survey. Participants were categorized into four groups: younger men, younger women, older men, older women. Principal Component Analysis and Confirmatory Factor Analysis tested the factor structure of the revised CUDIT version (CUDIT-R). Structural Equation Modeling explored whether the influence of use motives on the CUDIT-R factors differs between demographic groups.ResultsThe results suggest that the CUDIT-R scale is best represented by two factors: Use Intensity (Cronbach’s α = 0.71) and Awareness of Problematic Use (Cronbach’s α = 0.72). Use Intensity was lowest for younger women, and younger participants were more aware of negative effects. Gender, age, and use motives uniquely relate with both CUDIT-R factors, highlighting the CUDIT-R’s potential to guide early identification and treatment of individuals at risk for CUD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2026.15431</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2026.15431</link>
        <title><![CDATA[Molecular and biochemical correlates of frontal lobe white matter degeneration in humans with alcohol use disorder]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Suzanne M. de la Monte</author><author>Ming Tong</author><author>Greg Sutherland</author>
        <description><![CDATA[BackgroundAlcohol-related brain damage caused by heavy alcohol misuse is associated with cognitive-motor impairment and white matter (WM) degeneration. Oligodendrocytes and myelin are major targets, but the underlying mechanisms remain incompletely characterized, particularly in humans.PurposeThis study investigates the nature of oligodendrocyte dysfunction in anterior frontal lobe tissue from humans with alcohol use disorder (AUD), focusing on molecular and biochemical pathologies that may underlie WM ARBD.MethodsCores of fresh frozen human postmortem frontal lobe WM from adults with AUD or no history of substance use disorder (N = 6/group) were analyzed with duplex enzyme-linked immunosorbent assays, multiplex immunoassays, and multiplex RNA hybridization panels.ResultsAUD anterior frontal lobe WM tissue exhibited myelin loss with significant changes in oligodendrocyte/myelin glycoprotein immunoreactivity and mRNA expression, increased glial fibrillary acidic protein, and reduced expression of mRNA transcripts encoding upstream components of the insulin and insulin-like growth factor networks, aspartyl-asparaginyl-β-hydroxylase, and the Notch signaling pathway. In contrast, neuroinflammatory mediators and Alzheimer’s disease (AD) biomarkers were largely unaffected.ConclusionHuman AUD anterior frontal lobe WM pathology is accompanied by significant alterations in oligodendrocyte and astrocyte function, with alterations in Notch and insulin/IGF signaling. The findings provide new information on the mechanisms of AUD-mediated WM degeneration as well as potential strategies for diagnosing ARBD in humans.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.15477</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.15477</link>
        <title><![CDATA[HALT: Relapse prevention to resilience]]></title>
        <pubdate>2026-01-09T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Daniel Kretchman</author>
        <description><![CDATA[The impact of compulsive behaviors (aka addictions), whether substance- or behavioral-based, is substantial. The acronym HALT (Hungry, Angry, Lonely, Tired) has long been used in recovery. This paper provides a discussion of the history and basic concept, with application for relapse prevention and increasing resilience for mental health. It further offers a rationale for expanding this skill set with new and easily applied contextual domains. Using a familiar tool as a building block provides a framework for helping individuals with current or past compulsive behaviors, and for those assisting them. This may decrease relapse incidents which impact the individual and society.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14591</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14591</link>
        <title><![CDATA[Sex differences in reward network activation are linked to problematic substance use among high-risk adolescents]]></title>
        <pubdate>2025-12-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Olivia K. Murray</author><author>Paola P. Mattey-Mora</author><author>Joseph Aloi</author><author>Sydney Lovins</author><author>Michael P. Smoker</author><author>Leslie A. Hulvershorn</author>
        <description><![CDATA[BackgroundAdolescents with externalizing (EXT) disorders, such as attention-deficit/hyperactivity disorder and conduct disorder—characterized by impulsivity and rule-breaking, are at elevated risk for substance use disorders (SUDs), partly due to deficits in risky decision-making. Sex differences in this association are understudied. Neuroimaging research shows females and males with EXT disorders exhibit different brain activation patterns during risky decisions. This study will explore how these sex differences relate to the development of problematic substance use in youth with EXT disorders.MethodA total of 115 (78 males, 37 females) drug-naive adolescents with EXT psychopathology performed the Balloon Analogue Risk Task (BART) during magnetic resonance imaging to assess risky decision-making brain activation. Then, participants and their guardians completed questionnaires at 6-month intervals to assess problematic substance use. Statistical analyses evaluated sex differences in brain activation—both parametrically modulated and unmodulated—within a priori-selected regions associated with risky decision-making and problematic substance use, using Cox proportional hazards models.ResultsHigher modulated brain activation (as explosion probability increased) during the choice phase contrast, Choose Inflate—Choose Win, was associated with a lower hazard of problematic substance use in the right nucleus accumbens (Hazard Ratio (HR) = 0.68, 95% CI [0.49, 0.94], p = 0.01). This association was significant for females, but not for males, with the hazard ratios being significantly different between sexes. In the right nucleus accumbens, higher unmodulated choice phase activation in males was associated with lower hazard of problematic substance use (HR = 0.60, 95% CI [0.37, 0.97], p = 0.03); and in the right subgenual anterior cingulate cortex, higher unmodulated activation in this same contrast in females was associated with a lower hazard of problematic substance use [HR = 0.49, 95% CI (0.24, 0.97), p = 0.03].ConclusionThis study offers insight into sex differences in risky decision-making neural mechanisms and SUD risk among youth with EXT disorders. Our findings suggest typical risk signaling in the reward-processing network (nucleus accumbens and subgenual anterior cingulate cortex) may protect against substance use, particularly in females with EXT disorders. These findings emphasize the need for further sex-specific research and interventions for youth with EXT disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.15342</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.15342</link>
        <title><![CDATA[Molecular and biochemical pathologies in human alcohol-related cerebellar white matter degeneration]]></title>
        <pubdate>2025-11-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Suzanne M. de la Monte</author><author>Ming Tong</author>
        <description><![CDATA[BackgroundAlcohol use disorder (AUD) marked by heavy chronic or binge alcohol consumption, causes cerebellar and white matter (WM) atrophy with cognitive-motor impairments. Major pathological features of alcohol-related brain damage (ARBD) include alterations in WM integrity with myelin loss, and cerebellar degeneration with neuronal loss.PurposeThis study characterizes molecular and biochemical oligodendrocyte-related pathology in cerebellar tissue from donors with AUD to better understand the mechanisms of ARBD in humans.MethodsCores of cerebellar vermis, including cortex and underlying WM from adult human postmortem AUD and control brains, were processed for RNA and protein analyses using duplex and multiplex panels.ResultsAUD cerebellar WM had significant alterations in immature and mature oligodendrocyte protein and mRNA expression, and reduced expression of hepatocyte growth factor, Akt and GSK-3β signaling molecules, and Notch pathway activation. Moreover, the only significant AUD-related alteration in cerebellar cytokine/chemokine expression was reduced IL-16 immunoreactivity.ConclusionHuman AUD WM degeneration is associated with oligodendrocyte dysfunction, which mechanistically could be mediated by impairments in insulin/IGF signaling through Akt/GSK-3β or Notch pathway activation. Future studies should focus on the non-invasive detection and monitoring of AUD-related oligodendrocyte pathology through the analysis of cell-type-specific exosomes isolated from peripheral blood.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14858</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14858</link>
        <title><![CDATA[Prenatal environmental exposures and brain development: studies with baboons and other nonhuman primates]]></title>
        <pubdate>2025-08-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Igor Y. Iskusnykh</author><author>Shiwani Thapa</author><author>Victor V. Chizhikov</author><author>Anna N. Bukiya</author>
        <description><![CDATA[During pregnancy, the fetal brain undergoes rapid development and is highly sensitive to environmental influences. Understanding the intricate processes that underlie fetal brain development will be critical for advancing maternal-fetal health and mitigating the risks associated with developmental brain disorders. Nonhuman primate (NHP) animal models provide a unique and highly translational platform for studying brain development during pregnancy due to the close anatomical, physiological, and behavioral resemblance of these animals to humans. Our review explores the use of NHP models in elucidating key milestones of prenatal brain maturation and the mechanisms that govern typical and atypical development. We further examine the impact of environmental insults on fetal brain development, including air pollution, infection, ionizing radiation, and exposure to toxicants, and highlight the ways in which these factors can disrupt brain development and neural circuitry, leading to long-term cognitive and behavioral deficits. Recent studies demonstrate that the baboon (Papio hamadryas) animal model provides a fruitful yet underused translational model for research related to environmental adverse effects on pregnancy. Lastly, we review the effects of drugs of abuse on the developing fetal brain, highlighting the underlying biological mechanisms identified through clinical and laboratory studies. A combined approach offers a comprehensive understanding of the vulnerabilities of the developing nervous system, informing new strategies for the treatment and prevention of neurodevelopmental disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14199</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14199</link>
        <title><![CDATA[Chronic alcohol withdrawal-associated increases in VTA Hcrtr1 expression are associated with heightened nociception and anxiety-like behavior in female rats]]></title>
        <pubdate>2025-04-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shealan Cruise</author><author>Maria E. Secci</author><author>Leslie K. Kelley</author><author>Nathan M. Sharfman</author><author>Keishla Rodriguez-Graciani</author><author>Tiffany A. Wills</author><author>Nicholas W. Gilpin</author><author>Elizabeth M. Avegno</author>
        <description><![CDATA[Alcohol withdrawal is characterized by various symptoms that include pain and negative affect in the absence of the drug. The neural underpinnings of these behaviors are not entirely understood, but orexin has emerged as a candidate target for the treatment of substance use disorders. Here, we explored changes in orexin system-related gene expression in brain regions important for mediating reward and stress, including the ventral tegmental area (VTA) and extended amygdala (including the central amygdala, nucleus accumbens shell, and bed nucleus of the stria terminalis), in adolescent and adult female Wistar rats following chronic alcohol exposure. We observed higher numbers of Hcrtr1- (orexin receptor 1)-expressing neurons in the VTA of adolescent and adult female rats during withdrawal from chronic alcohol exposure. The number of Hcrt1+ VTA neurons was negatively correlated with thermal sensitivity in adolescent female rats and anxiety-like behavior in adult female rats. These data suggest that chronic alcohol effects on orexin receptor expression in the VTA are related to specific behaviors that manifest during withdrawal, highlighting potential avenues for targeting alcohol withdrawal-associated behaviors across development.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14149</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.14149</link>
        <title><![CDATA[Missed opportunities: the detection and management of at-risk drinking and illicit drug use in acutely hospitalized patients]]></title>
        <pubdate>2025-03-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Danil Gamboa</author><author>Saranda Kabashi</author><author>Benedicte Jørgenrud</author><author>Anners Lerdal</author><author>Gudmund Nordby</author><author>Stig Tore Bogstrand</author>
        <description><![CDATA[At-risk alcohol and illicit drug use are risk factors for disease and in-hospital complications. This study investigated whether clinicians document substance use in the electronic records of acutely hospitalized internal medicine patients. Alcohol and illicit drug positive patients were identified using prospectively gathered substance use data from a study sample comprising 2,872 patients included from November 2016 to December 2017 at an internal medicine hospital in Oslo, Norway. These data were unknown to hospital staff. Whether physicians recorded quantitative substance use assessments and interventions was examined in patients with study-verified alcohol use in excess of low-risk guidelines (Alcohol Use Disorder Identification Test-4 scores [AUDIT-4] of ≥5 for women and ≥7 for men) and/or illicit drug use (one or more illicit drug detected by liquid chromatography-mass spectrometry [LC-MS] analysis). Among 548 study-verified alcohol-positive patients, physicians documented quantity and frequency (QF) of use in 43.2% (n = 237) and interventions in 22.0% (n = 121). Alcohol interventions were associated with harmful drinking (AUDIT-4 ≥9 points; adjusted odds ratio [AOR] = 4.87; 95% CI: 2.54–9.31; p < 0.001) and QF assessments (AOR = 3.66; 95% CI: 1.13–11.84; p = 0.02). Among 157 illicit-positive patients, drug use was described quantitatively in 34.4% (n = 54) and interventions in 26.0% (n = 40). The rate of quantitative alcohol and illicit drug use assessment by hospital physicians is poor, with a correspondingly low intervention rate. Important opportunities for attenuating or intervening in at-risk alcohol and illicit drug use are missed.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2025.13969</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2025.13969</link>
        <title><![CDATA[Perceptions of the term “abstinence” among adolescents and young adults: a qualitative study on alcohol non-consumption in Switzerland]]></title>
        <pubdate>2025-02-17T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Diana Fernandes Palhares</author><author>Lorraine Chok</author><author>Joan-Carles Suris</author><author>Yara Barrense-Dias</author>
        <description><![CDATA[As part of a broader qualitative study aimed at understanding the experiences and opinions of adolescents and young adults (AYA) who do not drink alcohol in Switzerland, participants were questioned about their perceptions of the term “abstinence” in the context of alcohol non-consumption. Twelve focus groups were conducted with 63 participants (36 females, 27 males), aged between 14 years and 20 years. Participants were grouped by gender, age (based on Swiss alcohol laws), and drinking status (non-drinker or drinker). The discussions were recorded and transcribed, and thematic content analysis was used to identify and categorize key themes. The terms “abstinence,” “abstainer,” and “abstention” were generally considered unsuitable when describing young people who do not consume alcohol regardless of the drinking status of the participants. The connotation carried by the terms was mostly perceived as religious, sexual, negative and stigmatizing. “Abstinence” was considered more appropriate for adults who have stopped drinking due to alcohol-related issues. When referring to youths, terms such as “non-drinking,” “non-drinkers” or “alcohol non-consumption” were preferred, especially to better integrate non-drinking youths and positively highlight their choices in preventive and educational initiatives.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.13706</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.13706</link>
        <title><![CDATA[Editorial: 8th biennial international drug and alcohol research society conference 2022]]></title>
        <pubdate>2025-02-14T00:00:00Z</pubdate>
        <category>Special Issue Editorial</category>
        <author>Emmanuel S. Onaivi</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.13449</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.13449</link>
        <title><![CDATA[K-nearest neighbor algorithm for imputing missing longitudinal prenatal alcohol data]]></title>
        <pubdate>2025-01-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ayesha Sania</author><author>Nicolò Pini</author><author>Morgan E. Nelson</author><author>Michael M. Myers</author><author>Lauren C. Shuffrey</author><author>Maristella Lucchini</author><author>Amy J. Elliott</author><author>Hein J. Odendaal</author><author>William P. Fifer</author>
        <description><![CDATA[AimsThe objective of this study is to illustrate the application of a machine learning algorithm, K Nearest Neighbor (k-NN) to impute missing alcohol data in a prospective study among pregnant women.MethodsWe used data from the Safe Passage study (n = 11,083). Daily alcohol consumption for the last reported drinking day and 30 days prior was recorded using the Timeline Follow back method, which generated a variable amount of missing data per participants. Of the 3.2 million person-days of observation, data were missing for 0.36 million (11.4%). Using the k-NN imputed values were weighted for the distances and matched for the day of the week. Since participants with no missing days were not comparable to those with missing data, segments of non-missing data from all participants were included as a reference. Validation was done after randomly deleting data for 5–15 consecutive days from the first trimester.ResultsWe found that data from 5 nearest neighbors (i.e., K = 5) and segments of 55 days provided imputed values with least imputation error. After deleting data segments from the first trimester data set with no missing days, there was no difference between actual and predicted values for 64% of deleted segments. For 31% of the segments, imputed data were within +/−1 drink/day of the actual. Imputation accuracy varied by study site because of the differences in the magnitude of drinking and proportion of missing data.Conclusionk-NN can be used to impute missing data from longitudinal studies of alcohol during pregnancy with high accuracy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12197</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12197</link>
        <title><![CDATA[Using health belief model constructs to understand the role of perceived disease threat and resilience in responding to COVID-19 among people who use drugs: a cluster analysis]]></title>
        <pubdate>2024-07-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kirsten Paulus</author><author>Sarah Bauerle Bass</author><author>Patrick J. A. Kelly</author><author>Jenine Pilla</author><author>AnnaMarie Otor</author><author>Madison Scialanca</author><author>Anamarys Arroyo</author><author>Namaijah Faison</author>
        <description><![CDATA[IntroductionThe Health Belief Model (HBM) has been successfully applied to understanding adherence to COVID-19 prevention practices. It has not, however, been used to understand behavior in people who use drugs (PWUD). The aim of this study was to use the HBM to better understand COVID-19 perceptions among PWUD and understand how resiliency affects those perceptions.Materials and methodsA cross-sectional survey was completed from September to December 2021 with PWUD (n = 75) who utilize services at a large harm reduction organization in Philadelphia. Segmentation analysis was done using a k-means clustering approach. Two clusters emerged based on perceived COVID-19 personal impact and resiliency (Less COVID impact/High resilience (NoCOV/HR) and High COVID impact/Low resilience (COV/LR). Differences in responses by cluster to perceptions of COVID-19 and individual pandemic response grouped by HBM constructs were assessed using Student’s t-test and chi squares.ResultsSignificant differences in HBM constructs were seen between clusters. Those in the COV/LR cluster were more likely to think they were susceptible to getting COVID-19 and less likely to believe they knew how to protect themselves. The NoCOV/HR cluster believed they were able to protect themselves from COVID-19 and that they were able to easily understand messages about protecting themselves.ConclusionUnderstanding how PWUD conceptualize disease threat and using HBM can better inform interventions to improve future pandemic response. Findings suggest that resilience is key to protecting PWUD from future infectious disease outbreaks. Interventions aimed at increasing resiliency among PWUD may improve preventative behavior and decrease disease burden in this vulnerable population.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.11791</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.11791</link>
        <title><![CDATA[Risk factors for poor treatment outcomes among opioid-dependent clients taking methadone in Mombasa, Kenya]]></title>
        <pubdate>2024-06-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nassoro Mwanyalu</author><author>Maria Nunga</author><author>Raphael Mwanyamawi</author><author>Saade Abdallah</author><author>Maurice Owiny</author>
        <description><![CDATA[Background: The Methadone Maintenance Treatment (MMT) program has been proven to be beneficial in reducing illicit opioid use, increasing access to and retention of HIV treatment and other therapies, and reducing HIV transmission, and other drug-related morbidities and mortalities. However, determinants of treatment retention and outcomes for opioid-dependent persons accessing MMT in Kenya are limited. We sought to identify factors contributing to poor treatment outcomes among opioid-dependent persons enrolled in the Mombasa MMT program, between 2017 and 2019.Method: We conducted a retrospective records review for opioid-dependent persons receiving Methadone treatment in the Kisauni MAT clinic enrolled during 2017–2019. We defined poor clinical or health-related treatment outcome as any client Lost-To-Follow-Up (LTFU), turned HIV or Viral hepatitis positive, and/or missed two or more antiretroviral therapy (ART) appointments intake during MMT. Variables abstracted from clinical and pharmacological MMT service delivery tools included socio-demographic characteristics, clinical history, risk factors, and MMT outcomes. Data were analyzed using Epi Info7. We calculated Prevalence Odds Ratios (POR) and 95% Confidence Intervals (CI) to identify factors associated with adverse health outcomes.Results: Of the total 443 eligible records, the mean age was 37 years (SD ± 7.2) and males comprised 90.7%. The majority of females clients, 79.1% (34/43), were aged ≤35 years, 7.0% (3/43) had no education, 32.6% (14/43) were employed, 39.5% (17/43) were HIV positive and 18.6% (8/43) were HCV-positive. Overall, adverse treatment outcomes were at 27.5% (122/443), namely: LTFU at 22.8% (101/443), new HIV cases at 1.0% (4/391), HCV at 1.2% (5/405), and Hepatitis B Virus (HBV) at 1.2% (5/411), and 1.1% (5/443) died. Of HIV-infected clients linked to Comprehensive Care Clinic (CCC), 3.6% (2/56) defaulted from ART, and 25% (2/8) had detectable Viral Load of those retested. Lack of formal education (POR: 2.7, 95% CI: 1.3–5.7), unemployment (POR: 2.4, 95% CI: 1.4–4.0), and being a Non-Injector (POR: 1.7, 95% CI: 1.0–2.9) were negatively associated with treatment retention.Conclusion: Females were younger, and more educated with higher HIV and HCV prevalence. Being a Non-injector, unemployment, and lack of formal education may increase the likelihood of poor treatment outcomes among MMT clients. Closer monitoring of MMT clients with these characteristics is recommended with the integration of CCC into MMT services.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12693</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12693</link>
        <title><![CDATA[Rethinking agrarian livelihoods affected by narcotic drug abuse on China’s Southeast Asian borders: a typological perspective]]></title>
        <pubdate>2024-05-09T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Xiaobo Hua</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12528</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12528</link>
        <title><![CDATA[Effects of repeated alcohol abstinence on within-subject prefrontal cortical gene expression in rhesus macaques]]></title>
        <pubdate>2024-04-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Robert Hitzemann</author><author>Lina Gao</author><author>Suzanne S. Fei</author><author>Karina Ray</author><author>Katinka A. Vigh-Conrad</author><author>Tamara J. Phillips</author><author>Robert Searles</author><author>Rita P. Cervera-Juanes</author><author>Rupak Khadka</author><author>Timothy L. Carlson</author><author>Steven W. Gonzales</author><author>Natali Newman</author><author>Kathleen A. Grant</author>
        <description><![CDATA[Male rhesus monkeys (n = 24) had a biopsy of prefrontal cortical area 46 prior to chronic ethanol self-administration (n = 17) or caloric control (n = 7). Fourteen months of daily self-administration (water vs. 4% alcohol, 22 h access/day termed “open-access”) was followed by two cycles of prolonged abstinence (5 weeks) each followed by 3 months of open-access alcohol and a final abstinence followed by necropsy. At necropsy, a biopsy of Area 46, contralateral to the original biopsy, was obtained. Gene expression data (RNA-Seq) were collected comparing biopsy/necropsy samples. Monkeys were categorized by drinking status during the final post-abstinent drinking phase as light (LD), binge (BD), heavy (HD) and very heavy (VHD drinkers). Comparing pre-ethanol to post-abstinent biopsies, four animals that converted from HD to VHD status had significant ontology enrichments in downregulated genes (necropsy minus biopsy n = 286) that included immune response (FDR < 9 × 10−7) and plasma membrane changes (FDR < 1 × 10−7). Genes in the immune response category included IL16 and 18, CCR1, B2M, TLR3, 6 and 7, SP2 and CX3CR1. Upregulated genes (N = 388) were particularly enriched in genes associated with the negative regulation of MAP kinase activity (FDR < 3 × 10−5), including DUSP 1, 4, 5, 6 and 18, SPRY 2, 3, and 4, SPRED2, BMP4 and RGS2. Overall, these data illustrate the power of the NHP model and the within-subject design of genomic changes due to alcohol and suggest new targets for treating severe escalated drinking following repeated alcohol abstinence attempts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12793</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12793</link>
        <title><![CDATA[Book Review: Research ethics in the life sciences]]></title>
        <pubdate>2024-04-22T00:00:00Z</pubdate>
        <category>Book Review</category>
        <author>Stephanie J. Bird</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12094</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12094</link>
        <title><![CDATA[Epigenetic regulation of microglia and neurons by proinflammatory signaling following adolescent intermittent ethanol (AIE) exposure and in human AUD]]></title>
        <pubdate>2024-03-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fulton T. Crews</author><author>Victoria Macht</author><author>Ryan P. Vetreno</author>
        <description><![CDATA[Adolescent alcohol drinking is linked to high rates of adult alcohol problems and alcohol use disorder (AUD). The Neurobiology of Alcohol Drinking in Adulthood (NADIA) consortium adolescent intermittent ethanol (AIE) models adolescent binge drinking, followed by abstinent maturation to adulthood to determine the persistent AIE changes in neurobiology and behavior. AIE increases adult alcohol drinking and preference, increases anxiety and reward seeking, and disrupts sleep and cognition, all risks for AUD. In addition, AIE induces changes in neuroimmune gene expression in neurons and glia that alter neurocircuitry and behavior. HMGB1 is a unique neuroimmune signal released from neurons and glia by ethanol that activates multiple proinflammatory receptors, including Toll-like receptors (TLRs), that spread proinflammatory gene induction. HMGB1 expression is increased by AIE in rat brain and in post-mortem human AUD brain, where it correlates with lifetime alcohol consumption. HMGB1 activation of TLR increase TLR expression. Human AUD brain and rat brain following AIE show increases in multiple TLRs. Brain regional differences in neurotransmitters and cell types impact ethanol responses and neuroimmune gene induction. Microglia are monocyte-like cells that provide trophic and synaptic functions, that ethanol proinflammatory signals sensitize or “prime” during repeated drinking cycles, impacting neurocircuitry. Neurocircuits are differently impacted dependent upon neuronal-glial signaling. Acetylcholine is an anti-inflammatory neurotransmitter. AIE increases HMGB1-TLR4 signaling in forebrain, reducing cholinergic neurons by silencing multiple cholinergic defining genes through upregulation of RE-1 silencing factor (REST), a transcription inhibitor known to regulate neuronal differentiation. HMGB1 REST induction reduces cholinergic neurons in basal forebrain and cholinergic innervation of hippocampus. Adult brain hippocampal neurogenesis is regulated by a neurogenic niche formed from multiple cells. In vivo AIE and in vitro studies find ethanol increases HMGB1-TLR4 signaling and other proinflammatory signaling as well as reducing trophic factors, NGF, and BDNF, coincident with loss of the cholinergic synapse marker vChAT. These changes in gene expression-transcriptomes result in reduced adult neurogenesis. Excitingly, HMGB1 antagonists, anti-inflammatories, and epigenetic modifiers like histone deacetylase inhibitors restore trophic the neurogenesis. These findings suggest anti-inflammatory and epigenetic drugs should be considered for AUD therapy and may provide long-lasting reversal of psychopathology.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12734</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12734</link>
        <title><![CDATA[Editorial: Substance abuse and the microbiome]]></title>
        <pubdate>2024-03-06T00:00:00Z</pubdate>
        <category>Special Issue Editorial</category>
        <author>Prakash Nagarkatti</author><author>Mitzi Nagarkatti</author><author>Shilpa Buch</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12005</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.12005</link>
        <title><![CDATA[Alcohol use and the pain system]]></title>
        <pubdate>2024-01-24T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Michael Vigorito</author><author>Sulie L. Chang</author>
        <description><![CDATA[The World Health Organization’s epidemiological data from 2016 revealed that while 57% of the global population aged 15 years or older had abstained from drinking alcohol in the previous year, more than half of the population in the Americas, Europe, and Western Pacific consumed alcohol. The spectrum of alcohol use behavior is broad: low-risk use (sensible and in moderation), at-risk use (e.g., binge drinking), harmful use (misuse) and dependence (alcoholism; addiction; alcohol use disorder). The at-risk use and misuse of alcohol is associated with the transition to dependence, as well as many damaging health outcomes and preventable causes of premature death. Recent conceptualizations of alcohol dependence posit that the subjective experience of pain may be a significant contributing factor in the transition across the spectrum of alcohol use behavior. This narrative review summarizes the effects of alcohol at all levels of the pain system. The pain system includes nociceptors as sensory indicators of potentially dangerous stimuli and tissue damage (nociception), spinal circuits mediating defensive reflexes, and most importantly, the supraspinal circuits mediating nocifensive behaviors and the perception of pain. Although the functional importance of pain is to protect from injury and further or future damage, chronic pain may emerge despite the recovery from, and absence of, biological damage (i.e., in the absence of nociception). Like other biological perceptual systems, pain is a construction contingent on sensory information and a history of individual experiences (i.e., learning and memory). Neuroadaptations and brain plasticity underlying learning and memory and other basic physiological functions can also result in pathological conditions such as chronic pain and addiction. Moreover, the negative affective/emotional aspect of pain perception provides embodied and motivational components that may play a substantial role in the transition from alcohol use to dependence.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/adar.2024.11881</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/adar.2024.11881</link>
        <title><![CDATA[Adolescent alcohol drinking interaction with the gut microbiome: implications for adult alcohol use disorder]]></title>
        <pubdate>2024-01-15T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Bruk Getachew</author><author>Sheketha R. Hauser</author><author>Samia Bennani</author><author>Nacer El Kouhen</author><author>Youssef Sari</author><author>Yousef Tizabi</author>
        <description><![CDATA[Reciprocal communication between the gut microbiota and the brain, commonly referred to as the “gut-brain-axis” is crucial in maintaining overall physiological homeostasis. Gut microbiota development and brain maturation (neuronal connectivity and plasticity) appear to be synchronized and to follow the same timeline during childhood (immature), adolescence (expansion) and adulthood (completion). It is important to note that the mesolimbic reward circuitry develops early on, whereas the maturation of the inhibitory frontal cortical neurons is delayed. This imbalance can lead to increased acquirement of reward-seeking and risk-taking behaviors during adolescence, and consequently eventuate in heightened risk for substance abuse. Thus, there is high initiation of alcohol drinking in early adolescence that significantly increases the risk of alcohol use disorder (AUD) in adulthood. The underlying causes for heightened AUD risk are not well understood. It is suggested that alcohol-associated gut microbiota impairment during adolescence plays a key role in AUD neurodevelopment in adulthood. Furthermore, alcohol-induced dysregulation of microglia, either directly or indirectly through interaction with gut microbiota, may be a critical neuroinflammatory pathway leading to neurodevelopmental impairments and AUD. In this review article, we highlight the influence of adolescent alcohol drinking on gut microbiota, gut-brain axis and microglia, and eventual manifestation of AUD. Furthermore, novel therapeutic interventions via gut microbiota manipulations are discussed briefly.]]></description>
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