Fig.5.

Aβ₄₂ internalization is enhanced by anti-α7nAChR autoantibodies. Differentiated cell treated with 100 nM FITC-labeled (green) Aβ₄₂ for 72 h in medium containing antibody directed against the α7nAChR and visualized using Cy3 (red) secondary antibodies. FITC-Aβ₄₂ internalization was enhanced over that in cells treated with FITC-Aβ₄₂ alone, and nearly all was co-localized with α7nAChR (yellow) either in small dispersed granules or uniform clusters of these granules. A) Cell treated for 72 h in medium containing both FITC-Aβ₄₂ and serum from an AD patient showing extensive FITC-Aβ₄₂ internalization and co-localization with α7nAChR. B) Quantification showing increased Aβ₄₂ internalization in cells treated with anti-α7nAChR antibody over those exposed to FITC-Aβ₄₂ alone. Cells treated with IgG purified from AD serum showed a higher level of FITC-Aβ₄₂ internalization than those treated with anti-α7nAChR. Removal of IgG from AD serum caused a dramatic reduction in Aβ₄₂ internalization. Scale bar = 10 μm. *p < 0.05, ***p < 0.001. AD, Alzheimer’s disease serum.