Among other findings, provided that patients carrying apolipoprotein (ApoE) ε4 allele(s) linked to increased sporadic AD risk, enhanced Aβ aggregation, neurodegeneration, and neuroinflammation (Parhizkar and Holtzman, 2022), Ulrich and colleagues found that in APPPS1ΔE9 and APPPS1-21 transgenic mice, fibrillar Aβ deposition and also inflammatory microgliosis was dramatically reduced in the absence of ApoE, indicating that this may be an important inflammatory mediator of Aβ (Ulrich et al., 2018). Here, APOE is linked to Alzheimer disease.