Although our post hoc interaction models suggest a lack evidence for AD neuropathology interactions on this association with PAM in the caudate, diagnosis-stratified results suggest this is indeed an AD-relevant phenomenon—it may be that our analyses are picking up on a compensatory response of the TREM2 pathway in the caudate that is disease-stage specific (see TREM2 across Braak stages Supplementary Figure 8C, phospho-tau levels by amyloid status Supplementary Figure 6, and annual changes in global cognition stratified by diagnosis Supplementary Figure 11C). This evidence concerns the gene MAPT and Alzheimer disease.