Latent Cortical Neurodegeneration in Moderate Alcohol Use: Silent Neurotoxicity Syndrome as a New Subtype of Chronic Alcohol-Induced Encephalopathy Without Clinical Dependence

Background. For a long time, clinical neuroscience has primarily focused on severe forms of alcohol-related encephalopathy, which are typically associated with pronounced dependency and macroscopic brain changes. However, recent interdisciplinary studies demonstrate that even regular moderate alcohol consumption without signs of dependence can initiate chronic morphofunctional changes in cortical brain structures. This has led to the identification of a new phenotype: Silent Neurotoxicity Syndrome (SNS), characterized by subclinical neuropsychological shifts, neuroinflammation, impaired neuroplasticity, and dysfunction in neuro-glio-capillary interaction. Purpose – of this study is to examine the clinical-functional, neuropsychological, and macromorphophysiological manifestations of latent cortical neurodegeneration in socially adapted patients with regular moderate alcohol consumption and no diagnosis of alcohol dependence, as well as to substantiate SNS as a distinct subtype of chronic alcohol-induced encephalopathy. Materials and Methods. A qualitative interdisciplinary study was conducted using in-depth semi-structured interviews (n=24, of which 20 met inclusion criteria), neuropsychological screenings (MMSE), and a systematic literature review across PubMed, Scopus, and Web of Science databases using relevant keywords. Special attention was paid to the phenomenon of compensatory alcohol use, the presence of subclinical complaints, and the formation of alcohol-modulated behavior. Results. Cognitive changes (such as reduced executive functioning, concentration, and attention) were found in 40% of participants, emotional-motivational disturbances in 30%, and visuospatial deficits in 25%. Neurophysiological mechanisms of SNS were described, including decreased BDNF levels, inhibition of synaptic plasticity, microglial activation, glio-capillary barrier dysfunction, and microatrophy in the prefrontal cortex and hippocampus. A staged model of SNS development was proposed: prodromal, latent, subclinical, and advanced latent stages. Transdisciplinary analysis confirmed that even low-dose regular alcohol consumption can lead to persistent neuromorphological changes in the absence of clinical dependence. Conclusions. Silent Neurotoxicity Syndrome is a newly identified subtype of alcoholinduced encephalopathy, marked by hidden but progressive damage to neuronalglial structures. It evades detection by standard diagnostic tools yet poses a significant threat to cognitive reserve and emotional regulation. The clinical implementation of SNS requires an update in the assessment of «safe» alcohol consumption, the inclusion of neuroplasticity screenings, and the development of early preventive strategies at preclinical stages.