As noted above, the two unexpected associations with plasma biomarkers (i.e., lower GFAP with URTIs and slower pTau-181 increases with miscellaneous bacterial infections) may be attributed to a variety of factors, including the antimicrobial properties of pathological proteins underlying ADRD [31, 32], as well as the pleiotropic and disease stage-dependent relationships between immune functioning and AD neuropathology [33–35]. This evidence concerns the gene GFAP and Alzheimer disease.