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. 2001 Jul 10;98(15):8838–8843. doi: 10.1073/pnas.151254698

Figure 1.

Figure 1

Carboxyl-terminal-truncated forms of apoE accumulate in AD brains and NFTs. (a and b) Immunostaining of AD brain sections with anti-amino-terminal apoE (a) or anti-carboxyl-terminal apoE (b). (c and d) Double immunofluorescence staining of AD brain sections with anti-p-tau (red) and anti-amino-terminal apoE (green) (c) or anti-p-tau (red) and anti-carboxyl-terminal apoE (green) (d). (e and f) Neuro-2a cells expressing apoE3 or apoE4 were incubated with or without synthetic Aβ1–42 (10 μM) for 24 h at 37°C. After incubation, cell lysates were immunoprecipitated with a monospecific polyclonal anti-apoE followed by Western blotting with polyclonal anti-apoE (e) or monoclonal anti-apoE (6C5) (f) that recognizes the first 15 amino acids of the amino terminus of apoE (45). (gk) Brain tissues from two nondemented normal individuals (N1 and N2) and three AD patients (AD1, AD2, and AD3) were homogenized. Both the supernatants (g and h) and the solubilized pellets (ik) were subjected to SDS/PAGE and analyzed by Western blotting with polyclonal antibodies against full-length apoE (g and i), the carboxyl terminus (amino acids 272–299) of apoE (h and j), or a mAb against p-tau (AT8) (k). E Std, apoE standard (200 ng protein). (Original magnifications: a and b, ×200; c and d, ×600.)