title: Is aluminium an etiologic contributor to alcoholic amnesia and dementia?
abstract: Neurotoxicity from excess brain exposure to aluminium (Al) is well-documented, from both clinical observations and animal experiments, to impair learning, memory and cognition. The etiology of the cognitive impairment in chronic abusers of ethanol--alcoholic amnesia or dementia--is not known, but it is likely to be multifactorial. We hypothesize that a slowly-progressive accumulation of Al in the brain, so as to reach functionally-toxic levels, may be one such factor. This could occur because of an increased permeability of intestinal mucosa to entry of Al, arising from sustained exposure of the gastrointestinal tract to alcoholic beverages, plus a trend for more frequent ingestion of antacids based on Al salts for treating gastritis or ulcers caused by such exposure. If this be true, use of Al-containing medications, as well as all avoidable exposures to Al, should be contra-indicated for chronic heavy drinkers.
authors.forename: W M
authors.initials: WM
authors.lastname: Davis
mesh_terms: D000425:Alcohol Amnestic Disorder / Q000209:etiology*; D000535:Aluminum / Q000009:adverse effects* / Q000493:pharmacokinetics; D000818:Animals; D004347:Drug Interactions; D000431:Ethanol / Q000009:adverse effects; D006801:Humans; D007408:Intestinal Absorption; D008959:Models, Neurological; D011604:Psychoses, Alcoholic / Q000209:etiology*
chemical_list: D000431:Ethanol; D000535:Aluminum