Increased release of tau after neuronal depolarisation has previously been shown in both wild-type rat primary cortical neurons11 and in vivo in wild-type mice.12 The reasons why KCl does not stimulate further tau release from 3xTg-AD slices are not yet identified, but may be a result of saturation of synaptic activity in 3xTg-AD slices as Aβ is known to cause increased cellular hyperexcitability.47, 48 Similarly, Aβ has been shown to accelerate the propagation of tau in vivo. This evidence concerns the gene MAPT and Alzheimer disease.