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The study reported in the present issue of the Journal of Alzheimer’s disease by Mizoroki et al. [8] concludes that the failure of treatment of transgenic mice with aluminum maltolate to induce Alzheimer’s-like neuropathological changes provides proof that aluminum is not a causative agent in the etiology of Alzheimer’s disease. In our opinion, this report by Mizoroki et al. fails to provide an incisive analysis of previous work on the possible role of aluminum as an initiator of neurodegeneration, both in experimental animals and in humans. Dietary aluminum has been shown to increase brain amyloidosis in APP transgenic mice [11]. Since neurofibrillary tangles and neuritic plaques appear to be seen in only a few animal species, including aged bears [1] and, of course, humans, it is not surprising that aluminum compounds in most species fails to reproduce the neuropathological and biochemical abnormalities seen in Alzheimer’s disease. Such a lack of an exact match in abnormal features does not rule out

Can Studies of Aluminum Toxicity In Vivo and In Vitro Provide Relevant Information on the Pathogenesis and Etiology of Alzheimer's Disease?