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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Prog Brain Res. 2009;175:83. doi: 10.1016/S0079-6123(09)17506-4

Fig. 2.

Fig. 2

Neuropathological and biochemical analysis of R-2xAβ1-15 (B, D) or 2x-Aβ1-15 (C, E) immunized animals compared to their corresponding group of adjuvant-treated control hAPPFAD animals (A, D, E). (A–C) Sections representing the median Aβ plaque load are shown for each group (A, B, C). (D and E) Quantitative image analysis of Aβ42- and Aβ40-specific immunoreactive and thioflavin S-positive plaque load. Aβ42-, Aβ40-, and thioflavin S-positive areas were significantly reduced in the hippocampus after immunization with R-2xAβ1-15+LT(R192G) (D, p < 0.05, MWU). 2xAβ1-15+LT(R192G)-immunized mice showed a significant reduction of Aβ42-specific immunoreactivity (E, p < 0.05, MWU) compared to vehicle-treated controls. (F and G) Insoluble (guanidinium-soluble) brain Aβ, TBS-soluble brain Aβ, and plasma Aβ levels were analyzed by capture ELISA [absolute values of controls in R-2xAβ1-15 immunization experiment (F) were plasma Aβx–tot 0.03±0.01 pmol/ml, Aβ42 insoluble 2052±417 pmol/g, Aβ40 insoluble 485±100 pmol/g, Aβ42 TBS soluble 1.6±0.1 pmol/g, and Aβ40 TBS soluble 0.3±0.1 pmol/g; and in the 2xAβ1-15 immunization experiment (G, measured in a different ELISA run), Aβ40 plasma 0.9±0.6 pmol/ml, Aβ42 plasma 0.3±0.1 pmol/ml, Aβ42 insoluble 3590±800 pmol/g, Aβ40 insoluble 132±32.5 pmol/g, Aβ42 TBS soluble 2.1±0.8 pmol/g, and Aβ40 TBS soluble 4.6±0.5 pmol/g]. Asterisk indicates a significant difference (MWU, p < 0.05). Adapted from Maier et al. (2006) with permission from the Society for Neuroscience.