期刊
ANTIOXIDANTS
卷 11, 期 10, 页码 -出版社
MDPI
DOI: 10.3390/antiox11102078
关键词
oxidative stress; alcohol withdrawal; alcohol use disorder; alcohol brain damage; Wernicke encephalopathy; cognitive impairment; thiamine; diathesis
Chronic and excessive alcohol use can lead to alcohol-related neurocognitive disorders, and inadequate management of alcohol withdrawal reactions may result in severe consequences such as seizures or delirium tremens, with oxidative stress playing a key role in these conditions. Therefore, conducting research and developing neuroprotective strategies are crucial for preventing severe alcohol-related brain damage and cognitive impairments.
Alcohol use is a leading cause of mortality, brain morbidity, neurological complications and minor to major neurocognitive disorders. Alcohol-related neurocognitive disorders are consecutive to the direct effect of chronic and excessive alcohol use, but not only. Indeed, patients with severe alcohol use disorders (AUD) associated with pharmacological dependence suffer from repetitive events of alcohol withdrawal (AW). If those AW are not managed by adequate medical and pharmacological treatment, they may evolve into severe AW, or be complicated by epileptic seizure or delirium tremens (DT). In addition, we suggest that AW favors the occurrence of Wernicke's encephalopathy (WE) in patients with known or unknown thiamine depletion. We reviewed the literature on oxidative stress as a core mechanism in brain suffering linked with those conditions: AW, epileptic seizure, DT and WE. Thus, we propose perspectives to further develop research projects aiming at better identifying oxidative stress brain damage related to AW, assessing the effect of repetitive episodes of AW, and their long-term cognitive consequences. This research field should develop neuroprotective strategies during AW itself or during the periwithdrawal period. This could contribute to the prevention of severe alcohol-related brain damage and cognitive impairments.
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