Although tau overexpression may not be the main mechanism for AD, it is well recognized that intraneuronal accumulation of the hyperphosphorylated tau is one of the two hallmarks in the AD brains,35 and mediates the synaptic toxicity of Aβ.26 Besides, there are over 20 kinds of tauopathies, including frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration, and so on, showing common abnormalities in tau accumulation in addition to AD. The gene discussed is MAPT; the disease is corticobasal degeneration disorder.