MAPT and Alzheimer disease: In addition, although a potential extracellular physiopathological role of full length tau has been highlighted, consistent with the recent findings that secreted tau is per se toxic on synaptic function [22, 23], no study has yet investigated whether one of the biologically relevant NH2-truncated forms of protein -which are largely detected in diseased CSF and released in vivo from AD nerve endings [9, 10, 11]- could affect the neurotransmission at the pre-synaptic level.