This evidence is biologically relevant to human pathology and important in terms of translational outcome, in view the fact that a population of NH2-terminal truncated fragments of tau protein -including our peptide [21, 27, 28]- is mainly present in CSF from human AD patients and secreted from cryopreserved synaptosomes following depolarizing stimulus [9, 28]. Here, MAPT is linked to Alzheimer disease.