Fractionation of transgenic mouse brain extracts.

<p>Fractions of mouse brain homogenate from AβPP_ArcSwe transgenic mice (n = 5) and non-transgenic littermates (n = 5) were analyzed with Aβ1–42 (A), Aβ1–40 (B) and Aβ protofibril specific (C) ELISAs. Horizontal lines indicate the mean value of each group. Immunoprecipitation of pooled material from fraction 2 of transgenic mouse brain homogenate with the conformation specific Aβ protofibril selective antibody mAb158 covalently coupled to Dynabeads (0 – non immunoprecipitated sample, IP – immunoprecipitated material, S – supernatant remaining after ip) (D). Error bars indicate the standard deviation.</p

Fractionation of human brain extracts.

<p>Fractions of human brain homogenate from temporal cortex of diseased AD patients (n = 7, including one AβPP_Swe and one AβPP_Arc mutation carrier) and non-AD subjects (n = 4, one control subject and three FTD patients) were analyzed with Aβx-42 (A), Aβx-40 (B), Aβ1–42 (C) and Aβ1–40 (D) ELISAs. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032014#s2" target="_blank">Results</a> from the individual carrying the Swedish mutation is marked ‘Swe’ in the Aβx-40 and Aβ1–40 graphs. Horizontal lines indicate the mean value of each group. The level of N-terminal truncation of Aβ42 was determined as a ratio between Aβ1–42 and Aβx-42 (1-[Aβ1–42]/[Aβx-42]) (E), with error bars indicating the standard deviation. Immunoprecipitation of pooled material from fraction 2 of AD brain and non-AD brain with the conformation specific Aβ protofibril selective antibody mAb158 covalently coupled to Dynabeads (0 – non immonuprecipitated sample, IP – immunoprecipitated material, S – supernatant remaining after ip) (F). Error bars indicate the standard deviation.</p

Summary of cases.

<p>Summary of cases.</p

Molecular sizes of fractionated synthetic Aβ42, determined with AFM.

<p>Molecular sizes of fractionated synthetic Aβ42, determined with AFM.</p