Several epidemiological studies suggest the involvement of aluminum (AI) in the pathogenesis of Alzheimer's disease (AD). There is an increase in the levels of Aβ and ubiquitin in the pathological lesions of AD. Therefore, we have investigated whether aluminum (AI) treatment alters the levels of Aβ and ubiquitin in murine neuroblastoma (NBP2) and rat glioma (C-6) cell cultures. At a low concentration (10 μM), aluminum sulfate stimulated the level of immunoreactive Aβ and ubiquitin in NBP2 cells without changing the levels of the amyloid precursor protein (APP). However, at higher concentrations (100 and 500 μM), aluminum failed to elicit any significant effect on β-amylold, whereas ubiquitin levels continued to increase. No changes in the Aβ and ubiquitin content were found in the C-6 glioma cells following treatment with AI at any of the concentrations tested. Exposure of cells to aluminum salts did not alter the rate of proliferation in either of the two cell lines. These data suggest that one of the mechanisms by which AI may play a role in AD is by promoting the formation of Aβ and ubiquitin in neurons.
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