Furthermore, only 15–25% of the synaptosomes were positive for intact C-terminal tau or fully functional MTBR, suggesting that a combination of release of different tau peptides from AD synapses and the phosphorylation of those C-terminal truncated fragments exacerbate tau aggregation and synaptic dysfunction Cleavage and propagation of tau may be due to high tau localization in synaptic terminals in the cortex (Sokolow et al., 2015). Here, MAPT is linked to Alzheimer disease.