Firstly, murine tau does not naturally form fibrils with age, and only a few mouse models show accumulation of endogenous murine Aβ.[100] Even the most aggressive models, such as the 5xFAD mouse, which rapidly accumulates Aβ and develops early plaques, do not exhibit secondary tau tangle formation or significant neuronal loss as seen in human AD.[101] Consequently, most commonly used transgenic mouse models rely on the expression of mutant human tau protein, such as P301L and P301S,[102] which are associated to rare, early‐onset forms of tauopathies. This evidence concerns the gene MAPT and Alzheimer disease.