Therefore, in vitro work that showed dose-dependent disaggregation of pre-formed tau fibrils but the inability to prevent aggregation even at high concentrations of 5000 μM in contrast to in vivo and ex vivo work that reported a significant reduction in tau hyperphosphorylation even after the establishment of tauopathy (Table 2) may simply reflect the absence of ATP that can modulate hydrophobic interactions from hydrogen-bonding activities. This evidence concerns the gene MAPT and tauopathy.