and other glial factors already maximally stimulate Aβ synthesis (Fig. 1D, S1H). Control experiments confirmed that our Aβ measurements monitored exclusively human neuronal Aβ synthesis, and were not contaminated by Aβ from other sources (Fig. S1I, S1J). Thus, ApoE secreted by cultured glia massively stimulates Aβ synthesis in human neurons, and ApoE2, ApoE3, and ApoE4 exhibit differential potency in stimulating Aβ-synthesis with a relative effect size that parallels the effect size of these risk factors on AD pathogenesis (Strittmatter et al., 1993).
