Skip to main content
. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Alzheimers Dement. 2017 Jul 26;14(2):243–252. doi: 10.1016/j.jalz.2017.04.015

Fig. 1. Complement activation by Aβ and Aβ/4G8 ICs.

Fig. 1

A) Aβ42 was incubated with equimolar Aβ antibody 4G8 to form Aβ/4G8 ICs, then reacted with NHS as a complement source. Significant dose-dependent complement activation (P < 0.001), as measured by C3a generated, was observed for Aβ ICs even at low nM concentrations. Aβ alone and 4G8 alone also dose-dependently activated complement (P < 0.001), but required μM concentrations to stimulate C3a production above background levels. EDTA abolished these effects, showing that they are specific to complement mechanisms. B) Complement activation by Aβ ICs could also be shown to be dose-dependent with respect to the amount of Aβ antibody available (P < 0.001). Here, a constant amount of Aβ (2215 nM) was incubated with varying concentrations of Aβ antibody 4G8, from low to equimolar concentrations relative to Aβ. Note that the X-axis is log-scaled in these graphs to include the wide range of concentrations. For both figures, each data point represents the mean of triplicate samples. Error bars denote standard error of the mean. Standard error for replicates is not shown when they are smaller than the symbols for a particular concentration.