MAPT and Alzheimer disease: Our research group has extensively investigated a 20–22 kDa peptide generated from pathological truncation at the N-terminal domain of tau (aka NH2htau) which: (1) is detected in cellular and animal AD models [51]; (2) accumulates at human AD presynaptic terminals and is present in CSF from patients suffering from AD and other related tauopathies [52–54]; (3) negatively impacts on synaptic and cognitive functions, both in vitro and in vivo [55, 56].