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.

Alcohol use disorder (AUD) is influenced by genetic factors that affect key neurobiological systems, including dopaminergic and GABAergic pathways, which regulate neurobehavioral functions and are modulated by brain-derived neurotrophic factor (BDNF). Variations in these genes contribute to individual vulnerability to AUD. In this study, we investigated single-nucleotide polymorphisms (SNPs) and haplotypic associations in GABRA1, GABRA2, and GABRA6, along with the dopaminergic pathway genes DRD2/ANKK1 and BDNF, in a Spanish cohort. Peripheral blood-derived genomic DNA was genotyped, and haplotype analyses were conducted. Individual SNPs in GABRA1, GABRA2, BDNF, and DRD2/ANKK1 showed no significant associations with AUD. In GABRA6, the rs3219151 T allele was more frequent in AUD patients than in controls (57.9% vs. 49.3%; p = 0.03), while the C allele appeared to show a potential protective association. In addition, the GAC haplotype of GABRA6 (rs2197414, rs1992647, rs3219151) was less frequent in AUD than in controls (0.071 vs. 0.122) and showed a protective association (OR = 0.58; 95% CI = 0.34–0.99; p = 0.045). Our findings provide exploratory evidence suggesting that specific genetic variants and haplotypes may contribute to AUD susceptibility and support the relevance of multigenic and haplotypic approaches for exploring the neurobiological mechanisms underlying AUD.

Background: MicroRNAs (miRNAs) are a subclass of small non-coding RNAs that regulate gene expression and play important roles in infectious diseases. Echinococcosis is a globally distributed disease caused by various species of Echinococcus . The disease can be asymptomatic in the early stages, but if left untreated, it can lead to severe complications. Like other helminths, Echinococcus spp. exhibit immunomodulatory capacities that favour infection establishment and progression. Currently, there is no fully accurate, non-invasive method for early detection of echinococcosis. This systematic review provides a comprehensive analysis of the existing literature and discusses recent advances in the study of miRNAs during host– Echinococcus spp. interactions, emphasizing their intriguing role in immunomodulation and their potential as biomarkers for detection, disease activity, prognosis, and therapeutic monitoring, as well as their possible relevance for future therapeutic research. Methods: This systematic review was conducted in accordance with the PRISMA 2020 guidelines. Searches were performed in PubMed, Web of Science, and Scopus without date restrictions to identify studies assessing the diagnostic potential of miRNAs in cystic echinococcosis (CE) and alveolar echinococcosis (AE). Fourteen original research articles were included in the final analysis. Results: Parasite-derived miRNAs have been detected in plasma, serum, and liver tissue, with egr-let-7-5p and egr-miR-71-5p emerging as candidates for CE detection and monitoring. In CE, dysregulation of host miRNAs was observed, displaying cyst activity-dependent patterns associated with inflammation, immunomodulation, and fibrosis, including a consistent upregulation of hsa-miR-146a-5p in plasma and serum samples. In AE, several host miRNAs exhibited altered expression in liver tissue and plasma, with hsa-miR-483-3p consistently upregulated. Comparative analyses revealed partially distinct but overlapping miRNA profiles in CE and AE, reflecting host-driven regulatory responses related to immunomodulation and tissue remodeling with stage-dependent patterns. Most included studies were based on case–control designs, with small sample sizes and limited validation, suggesting high overall risk of bias. Conclusions: Current evidence suggests that miRNAs have translational potential as complementary biomarkers for diagnosis, patient stratification, prognostic assessment, and disease monitoring in echinococcosis and may support future therapeutic research. Nonetheless, methodological heterogeneity and limited validation may contribute to overestimating diagnostic performance and hinder clinical translation.

Alcohol exposure affects immune regulation and tissue homeostasis. Antimicrobial peptides (AMPs) are essential components of innate immunity, not only defending against pathogens but also modulating processes such as inflammation. However, their tissue-specific regulation in response to alcohol remains poorly characterized, particularly in humans after acute intoxication. We evaluated the expression of AMPs in the peripheral blood of patients with alcohol use disorder (AUD, n = 9), individuals with acute alcohol consumption (AAC, n = 9), and controls using quantitative polymerase chain reaction (qPCR). Additionally, we analyzed AMP expression in selected tissues of mice exposed to chronic ethanol feeding (National Institute on Alcohol Abuse and Alcoholism model for 5 days) and performed a systematic review of AMP regulation in alcohol-related disorders (2005–2025; n = 36 studies, reflecting a limited and heterogeneous body of available evidence). Human cathelicidin antimicrobial peptide (LL-37), lipopolysaccharide-binding protein (LBP), and bactericidal/permeability-increasing protein (BPI) were significantly upregulated in patients with AUD, whereas LL-37 and LBP were significantly upregulated in AAC. In the livers of ethanol-fed mice, LEP2, LCN2, and LBP levels were markedly increased, whereas LL-37 and LEP1 were downregulated. Duodenal tissue exhibited upregulation of DEFB1. In adipose tissue, DEFA2 was significantly increased in peripheral depots, whereas only LCN2 was upregulated in brain tissue. The systematic review demonstrated complex, heterogeneous, and organ-dependent AMP regulation and also highlighted the paucity of human data on AAC, a gap that our study partially addresses. Our results are consistent with the hypothesis that selected AMPs may serve as candidate markers of organ damage or microbial translocation and as possible therapeutic targets, a hypothesis that requires confirmation in larger, adequately powered studies.