Deficits in hippocampus-dependent memory are an early feature of AD, and substantial research has focused on the hypothesis that toxic soluble forms of Aβ and tau disrupt hippocampal synaptic memory mechanisms, including long-term potentiation (LTP) (Spires-Jones and Hyman, 2014, Sweatt, 2016). This evidence concerns the gene MAPT and Alzheimer disease.