In a study modeling AD using amyloid-β 42 (Aβ42)-activated MCM, treatment with the MCM resulted in the expected astrocyte polarization, as evidenced by increasing levels of inflammatory A1-associated C3 and decreasing levels of A2-like-associated transforming growth factor β (TGF-β) [135] (Fig. 2). This evidence concerns the gene C3 and Alzheimer disease.