Excessive alcohol use is associated with a wide range of physical, psychological and social consequences, and is responsible for a significant proportion of the burden of disease globally. An area which has received increasing interest is alcohol-related brain damage, not just because of the cost to the individual and society through resource utilization, but also because of the potential for prevention and reversibility. This paper aims to review the current literature on this subject and seeks to explore issues around diagnosis and treatment of alcohol-related brain damage.
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http://dx.doi.org/10.2217/nmt-2016-0030 | DOI Listing |
EClinicalMedicine
December 2024
Nottingham Digestive Diseases Centre (NDDC), Translational Medical Sciences, School of Medicine, University of Nottingham, NG7 2UH, UK.
Background: Despite the availability of various pharmacological and behavioural interventions, alcohol-related mortality is rising. This systematic review aimed to critically evaluate the existing literature on the association between glucagon-like peptide-1 receptor agonists use (GLP-1 RAs) and alcohol consumption.
Methods: Electronic searches were conducted on Ovid Medline, EMBASE, PsycINFO, clintrials.
Addict Neurosci
June 2024
Bowles Center for Alcohol Studies, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Dysregulation of the dopamine (DA) system is a hallmark of substance use disorders, including alcohol use disorder (AUD). Of the DA receptor subtypes, the DA D2 receptors (D2Rs) play a key role in the reinforcing effects of alcohol. D2Rs are expressed in numerous brain regions associated with the regulation of appetitive behaviors.
View Article and Find Full Text PDFAlcohol Clin Exp Res (Hoboken)
December 2024
Integrated Program in Neuroscience, McGill University, Montreal, Quebec, Canada.
Background: Adolescent alcohol use is the norm, but only some develop a substance use disorder. The increased risk might reflect heightened mesocorticolimbic responses to reward-related cues but results published to date have been inconsistent.
Methods: Young social drinkers (age 18.
Neuropharmacology
December 2024
Department of Psychology, Center for Development and Behavioral Neuroscience, Binghamton University, Binghamton, NY, 13902, United States; Developmental Exposure Alcohol Research Center, Binghamton, NY, 13902, United States. Electronic address:
Individuals with prenatal alcohol exposure (PAE) are at a higher risk for developing alcohol use disorder (AUD). Using a rat model of moderate PAE (mPAE) on gestational day 12 (G12; ∼2nd trimesters in humans), a critical period for amygdala development, we have shown disruptions in medial central amygdala (CeM) function, an important brain region associated with the development of AUD. In addition to this, acute ethanol (EtOH) increases GABA transmission in the CeM of rodents in a sex-dependent manner, a mechanism that potentially contributes to alcohol misuse.
View Article and Find Full Text PDFJCI Insight
December 2024
Clinical Psychoneuroendocrinology and Neuropsychopharmacology Section, Translational Addiction Medicine Branch, National Institute on Drug Abuse (NIDA) Intramural Research Program, National Institute on Alcohol Abuse and Alcoholism (NIAAA) Division of Intramural Clinical and Biological Research, NIH, Baltimore and Bethesda, Maryland, USA.
BACKGROUNDStudies have demonstrated the role of ghrelin in alcohol-related behaviors and consumption. Blockade of the growth hormone secretagogue receptor (GHSR), which is the ghrelin receptor, has been shown to decrease alcohol drinking and reward-related behaviors across several animal models. We previously conducted a human study testing a GHSR inverse agonist/competitive antagonist, PF-5190457, in individuals who are heavy drinkers and showed its safety when coadministered with alcohol.
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