Cells were treated for 24 h with the indicated concentrations of CNI-1493

Medium was changed and drug treatment was continued for an additional 4 h to allow Aβ secretion. Total secreted Aβ (total sAβ) was analyzed by immunoblot using 6E10 antibody (a). APP C-terminal fragments, C99 (b), and C83 (c) were analyzed using 6E10 and R1 antibodies, respectively. Full-length APP (d) was tested with antibodies LN27.<p><b>Copyright information:</b></p><p>Taken from "CNI-1493 inhibits Aβ production, plaque formation, and cognitive deterioration in an animal model of Alzheimer's disease"</p><p></p><p>The Journal of Experimental Medicine 2008;205(7):1593-1599.</p><p>Published online 7 Jul 2008</p><p>PMCID:PMC2442637.</p><p></p

60 μg protein were separated by precast NuPAGE Novex 4–12% Bis-Tris gels and transferred onto nitrocellulose membranes using the XCell II blot system

The activation of glial cells was assessed by staining for the macrophage activation with antibodies against the F4/80 antigen. Immunoblot analysis revealed a decline of F4/80 in all CNI-1493 animals. Equal protein loading was assessed by reprobing the membrane with monoclonal antibodies against GAPDH.<p><b>Copyright information:</b></p><p>Taken from "CNI-1493 inhibits Aβ production, plaque formation, and cognitive deterioration in an animal model of Alzheimer's disease"</p><p></p><p>The Journal of Experimental Medicine 2008;205(7):1593-1599.</p><p>Published online 7 Jul 2008</p><p>PMCID:PMC2442637.</p><p></p