Why increased CSF t-tau and p-tau are specific to AD can be explained by considering that (1) the pattern of tau phosphorylation occurring in these disorders is disease-specific, (2) tangle pathology and neurodegeneration in AD may be consequent to Aβ accumulation, with disease-specific molecular cascades, such as kinases and proteases activation, (3) disease-specific tau truncation could prevent detection by currently available assays, and (4) specific pathological changes can be more severe in AD than in other tauopathies. Here, MAPT is linked to tauopathy.