Less accepte distheevidence that aluminum can beacausal factor
inpromotingAlzheimer’s disease.Thisareahasbeenhandicappedby
earlier erroneous reports of heightened levels of aluminum in
amyloid plaques. Tissue aluminumlevels are notoriously difficult to
determine and later more reliable findings leading to similar
conclusions have been overshadowed by these original reports.
Themain objective of our more recent studies has been to study the
effects of extended exposure of experimental animals to levels of
aluminum that have relevance for the human population. Demonstration
that these can provoke cerebral inflammatory responses
resembling those that are foundwith brainsenescence, canprovide a
mechanistic link to epidemiological reports.