The N-terminus extremity of tau, despite the lack of the microtubule binding domains which abnormally aggregate to form paired helical filaments, is prone to come into higher order of oligomerization (Feinstein et al., 2016) and is specifically released into the extracellular space in an in situ tauopathy model (Kim et al., 2010), suggesting a potential role for molecular ‘templating’ in the propagation of neurofibrillary lesions. This evidence concerns the gene MAPT and tauopathy.