Accumulating evidence suggests that Aβ functions upstream of tau in AD pathogenesis, driving tau pathology through the modulation of protein kinases and phosphatases that regulate tau phosphorylation and the induction of tau misfolding, while tau in turn mediates the synaptic toxicity of Aβ at the postsynaptic compartment and dendritic spines [46,47,48]. This evidence concerns the gene WEE1 and Alzheimer disease.