A major constituent of SP in the brains of Alzheimer's disease is 39-43 amino acid peptide called β-amyloid peptide (Aβ). Recent data have demonstrated that Aβ has a strong tendency to form insoluble aggregates and that toxic effects of Aβ is based on its aggregation. In the current study, 100 μg of human synthetic Aβ 1-42 (sAβ 1-42) was infused into the lateral ventricle of rat brain using a short-term infusion model. At 2 or 7 days following the infusion, sAβ 1-42 was found to form insoluble aggregates, scattering throughout the entire ventricular systems. The sAβ 1-42 aggregates were partially engulfed by phagocytic cells and deposited at the meningeal vessels or the choroid plexuses. However, these deposits mostly disappeared from the ventricles by 28 days post-infusion. Here, it is reported for the first time that considerable amounts of sAβ 1-42 are almost cleared from the rat ventricular system by the mononuclear phagocytic system.
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