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. 2009 Apr;16(4):267–272. doi: 10.1101/lm.1310209

Figure 2.

Figure 2.

Memory impairment produced by the depletion of endogenous Aβ(1−42) is rescued by exogenous oligomeric human Aβ(1−42). (A) Oligo/monomeric preparation of Aβ42 was examined by 4%–12% tris-tricine nondenaturing PAGE Western blotting (Garcia-Osta et al. 2006) using the anti-Aβ monoclonal antibody 6E10 (Covance Research 1:1000) (Tomiyama et al. 2008). Bands corresponding to tetramers, trimers, and monomers were detected. (B) Memory acquisition (Acq) and retention are expressed as mean latency ± SEM (in seconds, s). Rats received intrahippocampal injections of either anti-Aβ or control mAb antibody combined with either scrambled (sc) peptide or Aβ(1–42) 15 min before IA training. *P < 0.05, ** P < 0.01, *** P < 0.001. Test 1, 24 h after training; Test 2, 5 d after training. (C) Memory acquisition (Acq) and retention expressed as mean latency ± SEM (s) of rats that received intrahippocampal injections of PBS, sc peptide, or Aβ(1–42) immediately after IA training. Administration of Aβ(1–42) immediately after IA training enhances memory retention 24 h after training. * P < 0.05, ** P < 0.01.