Cis P-tau is aggregated more than trans P-tau because it is resistant to dephosphorylation and degradation, cannot reinforce microtubule assembly, and is more prone to aggregation [4]. Twenty hours after the onset of tauopathy, cis P-tau was dramatically aggregated in the cerebral cortex and remained high for up to 2 months, and was propagated from the cerebral cortex into the hippocampus 6 months later [11]. The gene discussed is MAPT; the disease is tauopathy.