Long-term oral intake of aluminium or zinc does not accelerate Alzheimer pathology in AßPP and AßPP/tau transgenic mice

Whether or not the oral intake of metals such as aluminium (Al) and zinc (Zn) is a risk for Alzheimer's disease (AD) has been a matter of controversy. Lack of AD pathology in patients with Al encephalopathy indicates Al does not cause AD. On the other hand, some epidemiological studies have suggested high Al increases the occurrence of AD. Our purpose is to test if high Al in drinking water is a risk factor for AD. We administered Al and Zn in drinking water to Tg2576, a transgenic mouse model for amyloid beta-protein (A beta) deposition with the A beta precursor protein (A beta PP) mutations (K670N/M671L), and Tg2576/tau(P301L), a model for A beta and tau deposition. Deionized water was given to the control Tg2576 and Tg2576/tau. After administration for 410 months of approximately 100 mg/kg body weight Al or Zn per day, we were not able to find by quantitative immunohistochemical analyses differences in the deposition of A beta and tau between the treated and untreated groups. Nor did the Al or Zn treatment affect the amount of soluble A beta and A beta*56, an A beta oligomer, measured by ELISA or immunoblot. The oral intake of excess Al or Zn does not accelerate AD pathology in the transgenic mouse models for A beta and tau accumulation. Such results do not seem to support the notion that excessive oral intake of Al or Zn is a risk factor for AD.