In line with these findings, the anti-inflammatory action of AFE was documented in previous studies of Alzheimer’s diseases animal models (reduces pro-inflammatory cytokines such as IL-1β, IL-2–6, IL-9,10, TNF-α, and eotaxin activity) [53] and renal ischemia animal models (reduces TNF-α and TGF-β) [28]. The gene discussed is CCL11; the disease is early-onset autosomal dominant Alzheimer disease.