Fig. 4

Impaired NCAM1–MHC-I interaction in AD pathology. A, B Co-immunoprecipitation analysis of interactions between endogenous MHC-I and NCAM1 in the brains of normal subjects (NM) and patients with AD (A, B; n = 4). The levels of co-immunoprecipitated NCAM1 were normalized to total NCAM1 levels (B). The data are presented as the mean ± SEM (**P < 0.001; unpaired two-tailed Student’s t-test). C–E Co-localization of MHC-I with NCAM1 on primary neurons. Scale bar: 10 µm (C). Relative fluorescence intensity of either MHC1 or NCAM1 (D) and colocalization of MHC1 and NCAM1 (F, G). Coimmunoprecipitation analysis of interactions between endogenous MHC-I and NCAM1 in oligomeric Aβ-treated primary neurons (F, n = 4). The levels of coimmunoprecipitated NCAM1 and MHC-I were normalized to the levels of total NCAM1 and MHC-I, respectively (G). (H, I) Oligomeric Aβ-mediated downregulation of NCAM1 signaling detected by CREB phosphorylation (H, n = 4). The levels of NCAM1, MHC-I, and phosphorylated CREB were normalized to the levels of total NCAM1, MHC-I, and CREB, respectively (I). All data are presented as the mean ± SEM (*P < 0.05, **P < 0.001, ***P < 0.005 by unpaired two-tailed Student’s t-test)