Figure 5. A schematic representation of Tau deregulation resulting in AD pathology. Under normal conditions, Tau stabilizes microtubules within neurons. Microtubules are essential for normal axonal transport. In AD and other tauopathies kinases hyperphosphorylate Tau impairing its normal functioning and reducing the Tau binding to microtubules thus followed by subsequent sequestering of hyperphosphorylated Tau into neurofibrillary tangles (NFTs). The reduction of available of Tau leads to microtubule instability and reduces cellular transport further attributing to neuropathology.