Behavioral and electrophysiological studies of Alzheimer’s disease (AD) and other tauopathies have revealed that the onset of cognitive decline correlates better with synaptic dysfunctions than with hallmark pathologies such as the accumulation of extracellular amyloid-β plaques, intra-neuronal neurofibrillary tangles formed by aberrantly phosphorylated tau, degeneration of neurites or neuronal loss (Terry et al., 1991; Arriagada et al., 1992; Selkoe, 2002; Coleman and Yao, 2003; Giannakopoulos et al., 2003; Saul et al., 2013). This evidence concerns the gene MAPT and tauopathy.