This corroborates with recent studies showing a correlation of plasma pTau181, and not Aβ42/40, with cognitive impairment in DLB.21,22 It is also consistent with AD staging models positing that amyloid changes are early events, whereas later-stage tau deposition is correlated best with neurodegeneration and its subsequent clinical phenotype.60 Our findings might suggest potential for pTau181 as an exploratory end point in clinical trials, although this would require further validation on larger samples and longitudinal data. This evidence concerns the gene MAPT and Lewy body dementia.