The top predicted canonical pathways in the 30 ng/L treatment group were involved in S-methyl-5′-thioadenosine degradation II, cysteine biosynthesis/homocysteine degradation, neuroprotective role of THOP1 in Alzheimer’s disease, extrinsic prothrombin activation pathway, and coagulation system (Supplementary Figure S2). Here, F2 is linked to early-onset autosomal dominant Alzheimer disease.