Amyloid β-protein (Aβ)1–40 protects neurons from damage induced by Aβ1–42 in culture and in rat brain

摘要: Previously, we found that amyloid β-protein (Aβ)1–42 exhibits neurotoxicity, while Aβ1–40 serves as an antioxidant molecule by quenching metal ions and inhibiting metal-mediated oxygen radical generation. Here, show another neuroprotective action of nonamyloidogenic against Aβ1–42-induced neurotoxicity in culture vivo. Neuronal death was induced Aβ1–42 at concentrations higher than 2 μm, which prevented concurrent treatment with a dose-dependent manner. However, chelators did not prevent neuronal death. Circular dichroism spectroscopy showed inhibited the β-sheet transformation Aβ1–42. Thioflavin-T assay electron microscopy analysis revealed fibril formation In contrast, Aβ1–16, Aβ25–35, Aβ40–1 inhibit nor injection into rat entorhinal cortex (EC) caused hyperphosphorylation tau on both sides EC hippocampus increased number glial fibrillary acidic protein (GFAP)-positive astrocytes ipsilateral EC, were Aβ1–40. These results indicate protects neurons from damage vitro vivo, sequestrating metals, but Our data suggest mechanism elevated Aβ1–42/Aβ1–40 ratio accelerates development Alzheimer's disease (AD) familial AD.