Chronic alcohol exposure induces complex pathophysiological changes in the central nervous system (CNS), contributing to the onset and progression of neurodegenerative disorders. This review integrates recent findings on ethanol-induced neurotoxicity, focusing on key mechanisms including oxidative stress, protein misfolding, mitochondrial dysfunction, calcium dysregulation, neuroinflammation, and epigenetic alterations. We further discuss the detrimental impact of ethanol metabolism particularly its neurotoxic intermediates such as acetaldehyde and salsolinol on neuronal integrity. Special emphasis is placed on glial cell activation, blood–brain barrier disruption, and dysregulation of survival pathways such as PI3K/Akt/mTOR. Finally, we highlight promising therapeutic strategies targeting these molecular and cellular disruptions. A comprehensive understanding of these processes is critical for the development of neuroprotective interventions aimed at mitigating alcohol-related cognitive and functional decline.

Background: Thyroid dysfunction is a prevalent endocrine disorder with significant cardiovascular consequences, particularly through its effects on cardiac electrophysiology. Electrocardiography (ECG), as a widely available and cost-effective diagnostic tool, provides valuable insight into these alterations. This systematic review and meta-analysis aimed to evaluate the relationship between thyroid hormone imbalance and ECG parameters. Methods: A comprehensive search of PubMed, ScienceDirect, and Google Scholar identified 1099 studies, of which 121 underwent full-text analysis. Ultimately, 37 studies with complete datasets were included in the quantitative synthesis, encompassing 167,074 participants across overt hyperthyroidism, subclinical and overt hypothyroidism, and euthyroid control groups. Results: Meta-analysis revealed significant alterations in key electrophysiological markers. Overt hyperthyroidism was associated with QTc and Tp-e prolongation, consistent with increased repolarization heterogeneity and arrhythmic risk. In overt hypothyroidism, QTc and Tp-e intervals were also prolonged, accompanied by reduced heart rate variability, reflecting autonomic imbalance. Subclinical forms demonstrated more variable results, though trends toward conduction and repolarization disturbances were observed. Importantly, several studies indicated that levothyroxine therapy or surgical treatment normalized abnormal ECG findings, underscoring their reversible nature. Conclusions: These results highlight the strong association between thyroid hormone abnormalities and ECG alterations, which may serve as early markers of arrhythmic risk and sudden cardiac death. Incorporating ECG screening into thyroid disease management could improve early detection, risk stratification, and cardiovascular prevention strategies.