The neurotoxicity of environmental aluminum is still an issue.
Evidence for the neurotoxicity of extended exposure to low levels of aluminum salts is described using an animal model treated with aluminum at low levels reflecting those found in some water supplies. Emphasis is given to the potential role of aluminum in acceleration and promotion of some indices characteristic of brain aging. These hallmarks include the appearance of excess levels of inflammation in specific brain areas. Aluminum salts can increase levels of glial activation, inflammatory cytokines and amyloid precursor protein within the brain. Both normal brain aging and to a greater extent, Alzheimer's disease are associated with elevated basal levels of markers for inflammation. These are not attributable to obvious exogenous stimuli and may reflect the lifespan history of the organism's immune responses. It is possible that aluminum salts can act as a subtle promoter of such apparently unprovoked responses.
Bondy
Stephen C
SC
Program in Environmental Toxicology, Division Occupational and Environmental Health, Department of Medicine, University of California, Irvine, CA 92697-1825, USA. scbondy@uci.edu
D000535:Aluminum / Q000633:toxicity*; D000544:Alzheimer Disease / Q000139:chemically induced / Q000453:epidemiology; D000818:Animals; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology; D004781:Environmental Exposure; D006801:Humans; D020258:Neurotoxicity Syndromes / Q000453:epidemiology / Q000209:etiology*
D000535:Aluminum