Tau pathology in triple knock‐in mouse model of Alzheimer's Disease expressing APOE3 and APOE4

The results of this project demonstrate that tau pathology markers appear to increase as a function of age, APOE4 and the ability to accumulate insoluble Abeta and plaques^. These results agree with the notion that amyloid and APOE4 can increase tau markers even in less aggressive animal models without tau overexpression or mutations. Our findings also suggest that there are no genotype-dependent differences in learning and memory in the PAL task at early ages, despite these mice presenting other cognitive deficits at that stage.