Infusion of Fe2+, Aβ42, and buthionine-sulfoximine (FAB), but not Aβ42 alone or in combination with Fe2+, into the left cerebral ventricle of Long-Evans rats for 4 weeks induced memory impairment that was accompanied by increased hyperphosphorylated Tau protein levels in the CSF. FAB-infused animals displayed thioflavin-S-positive amyloid deposits, hyperphosphorylated Tau protein, neuronal loss, and gliosis. Animals treated with Aβ42, Fe2+, or buthionine-sulfoximine alone or in combination failed to show the histological modifications seen with FAB. This data suggests that Aβ42 is not sufficient to induce an Alzheimer’s disease-like symptomatology, and it supports a model whereby a decrease in the brain’s antioxidant defense system leads to the Aβ42-independent oxidative stress necessary for the peptide to induce histopathological changes and memory loss.

Keywords:
Alzheimer, Amyloid deposit, Oxidative stress, Cerebrospinal fluid, Protein Tau, Neurodegenerative disease
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© 2006 S. Karger AG, Basel
2005
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