Ethanol consumption triggers oxidative stress by generating reactive oxygen species (ROS) through its metabolites. This process leads to steatosis and liver inflammation, which are critical for the development of alcoholic liver disease (ALD). Autophagy is a regulated dynamic process that sequesters damaged and excess cytoplasmic organelles for lysosomal degradation and may counteract the harmful effects of ROS-induced oxidative stress. These effects include hepatotoxicity, mitochondrial damage, steatosis, endoplasmic reticulum stress, inflammation, and iron overload. In liver diseases, particularly ALD, macroautophagy has been implicated as a protective mechanism in hepatocytes, although it does not appear to play the same role in stellate cells. Beyond the liver, autophagy may also mitigate the harmful effects of alcohol on other organs, thereby providing an additional layer of protection against ALD. This protective potential is further supported by studies showing that drugs that interact with autophagy, such as rapamycin, can prevent ALD development in animal models. This systematic review presents a comprehensive analysis of the literature, focusing on the role of autophagy in oxidative stress regulation, its involvement in organ–organ crosstalk relevant to ALD, and the potential of autophagy-targeting therapeutic strategies.

Introduction: The aim of this study was to characterize the epidemiology, risk factors, and clinical presentation of Wernicke encephalopathy (WE) and analyze differences between cases with and without excessive alcohol consumption. Methods: A systematic search was conducted in PubMed, Scopus, and Web of Science up to April 1, 2025. The included studies provided data on prevalence, risk factors, clinical and radiological findings, mortality, and prognosis in patients with WE. Pooled proportions and weighted means were calculated using random-effect models with Freeman-Tukey transformation. Heterogeneity was assessed using the I2 statistic. Subgroup comparisons were performed based on the presence or absence of excessive alcohol consumption. Results: A total of 12 studies comprising 5,510 patients were analyzed. Overall, 65.4% (95% CI: 56.0–74.2) were male, with a weighted mean age of 60.7 years. Among cases related to excessive alcohol consumption, 78.7% were male (mean age 55.2); in cases not related to such consumption, 52.6% were male (mean age 63.5). The classic triad was present in 32.7% of cases (95% CI: 19.2–47.7). Among patients evaluated by magnetic resonance imaging, typical lesions were identified in 82.0%, and atypical lesions were identified in 44.8%. Overall mortality was 5.1% (95% CI: 2.3–8.8%) and higher in non-alcohol-related cases (8.8%). Alcohol consumption was the main risk factor (90.7%); among non-alcohol-related cases, the most frequent clinical settings were malnutrition (30.2%), infections (25.1%), and psychiatric disorders (15.4%). Conclusion: WE is a multifactorial syndrome that extends beyond alcohol misuse, with wide clinical and pathophysiological variability. These findings underscore the importance of early recognition and prompt thiamine replacement, particularly in non-alcohol-related cases.

Background/Objectives: Wernicke encephalopathy (WE) is an acute neurological syndrome caused by severe thiamine deficiency. Early detection is challenging due to the low sensitivity of the classic triad. Methods: This retrospective observational study used the Spanish Minimum Basic Data Set, including hospital admissions with a primary diagnosis of WE (2016–2022). Demographic, clinical, and economic variables were also analyzed. Severity of illness (SOI) and risk of mortality (ROM) were assessed using the All Patient Refined Diagnosis-Related Groups (APR–DRG) system. Results: A total of 2477 WE episodes were included (1864 men; mean age, 58.2 years; standard deviation [SD], 11.0). The hospital admission rate increased by an average of 16% per year (incidence rate ratio [IRR], 1.16; p < 0.001). The proportion of foreign-born patients increased significantly over the study period. Most patients were discharged home (1868; 75.4%), whereas transfers to residential care facilities increased over time. The mean hospital stay was 19.0 days (SD 36.5). In-hospital mortality was 3.7%. In multivariable analysis, malnutrition (odds ratio [OR] 1.64), cancer (OR 2.11), and active infection (OR 5.79) were independently associated with mortality. The incorporation of ROM into the mortality model markedly improved discrimination, and mortality increased progressively with higher ROM categories: moderate (OR 3.45), major (OR 11.76), and extreme (OR 38.76) (all p < 0.001). Conclusions: WE is an increasingly frequent cause of neurological hospitalization in Spain, associated with a substantial clinical and economic burden. In-hospital mortality is driven mainly by overall clinical complexity and comorbidity burden rather than by WE in isolation.

Glycolysis is primarily involved in ATP production but also modulates oxidative stress. Chronic alcohol consumption is correlated with an increased incidence of multiple diseases, including cancer and neurodegenerative diseases (NDDs), though the underlying mechanisms remain unclear. Guided by a literature review and bioinformatics analysis, we evaluated the expression of 22 genes encoding various isoforms of seven glycolytic enzymes (GEs) in the peripheral blood of patients with alcohol use disorder (AUD), individuals with acute alcohol consumption (AAC), and their respective control groups using qPCR. In parallel, we evaluated the expression of selected genes coding for GEs linked to NDDs, as well as astrocytic markers in primary mouse astrocyte cultures exposed to ethanol. Thirteen GE-related genes, including non-canonical isoforms, were significantly dysregulated in AUD patients; notably, eight of these genes showed similar alterations in individuals with AAC. Several enzymes encoded by these genes are known to be regulated by oxidative stress. Ethanol-exposed astrocytes also showed altered expression of glycolytic genes associated with NDDs and astrocyte function. These findings indicate that glycolytic dysregulation is driven by ethanol intake, regardless of exposure duration or organic damage, highlighting a link between ethanol-driven redox imbalance and glycolytic remodeling, which could contribute to organ damage.