Although the model for plasma p-tau181 accounted for 24% of the variability (Adj. R2 = 0.24), neither parietal cortex pT181 tau burden, parietal cortex amyloid-β burden, LATE-NC stage, nor Kalaria cerebrovascular disease score significantly contributed when modeled together (Fig. 3). This evidence concerns the gene MAPT and cerebrovascular disorder.