Premium
Zinc Deficiency and Corticosteroids in the Pathogenesis of Alcoholic Brain Dysfunction—A Review
Author(s) -
Menzano E.,
Carlen P. L.
Publication year - 1994
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1994.tb00057.x
Subject(s) - neurotoxicity , excitotoxicity , kindling , chronic alcoholism , atrophy , medicine , chronic alcoholic , nmda receptor , pathogenesis , brain damage , zinc deficiency (plant disorder) , abstinence , alcohol dependence , alcohol , epilepsy , toxicity , pathology , psychiatry , receptor , chemistry , micronutrient , biochemistry
Chronic alcoholism is associated with hypercortisolemia and low serum zinc (Zn). Hypercortisolernia could be responsible for alcoholic cerebral atrophy and is also associated with enhanced NMDA neurotoxicity. It is hypothesized that low brain Zn, noted in chronic alcoholics, enhances NMDA excitotoxicity and ethanol withdrawal seizure susceptibility. Also, Zn deficiency can produce neuronal damage through increased free radical formation. Clinically, Zn replacement therapy may be a rational approach to the treatment of alcohol withdrawal seizures and alcohol‐related brain dysfunction.