Conversely, hyperphosphorylated tau, as seen in tauopathies, is unable to stabilize microtubule assemblies and sequesters normal tau and other microtubule stabilizing protein such as MAP1A/MAP1B and MAP2, leading to disruption of microtubules and axonal transport, finally resulting in retrograde degeneration and cell death [17]. This evidence concerns the gene MAPT and tauopathy.