The aim of the current study was to explore how genetic predispositions (AD PRS, AD PRSINFL, and sum PRSIMMUNE) might manifest as observable traits in the form of innate immune activation (three anti‐inflammatory markers: soluble triggering receptor expressed on myeloid cell 2 (sTREM2), clusterin and fractalkine and one inflammatory marker: chitinase‐3‐like protein 1 (YKL‐40)) in the presence of neurodegeneration measured as CSF total tau (t‐tau) and neurofilament light chain (NfL), two neurodegeneration markers representing different neuropathological processes.19 The gene discussed is MAPT; the disease is Alzheimer disease.