Tau protein fibrillation has been implicated in Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD) subtypes and related disorders, which are collectively referred to as tauopathies.1 FTLD tauopathies, including PSP and corticobasal degeneration (CBD), are characterized by the deposition of four‐repeat tau isoforms in neurons, astrocytes, and oligodendrocytes.2 Distinct tau isoforms cause ultrastructural and conformational diversity of the pathological fibrils, represented by paired helical filaments in AD and straight filaments in PSP and CBD.3 This evidence concerns the gene MAPT and tauopathy.