CD86 and Alzheimer disease: In order to investigate whether MaR1 could alter the phenotype of d‐THP‐1 cells in the context of AD, cells were incubated for 2 hours with 5 μM Aβ42 alone or together with 5 μM MaR1, followed by analysis of the pro‐inflammatory (CD40 and CD86) and anti‐inflammatory (CD163 and CD200R) biomarkers using flow cytometry (Figure 7).