Although tau has long been recognized as the principle component of neurofibrillary tangles (NFTs) in FTD (Joachim et al., 1987) and mutations in the microtubule associated protein tau (MAPT) are responsible for a subset of FTD cases (Hutton et al., 1998; Spillantini et al., 1998; D’Souza et al., 1999), investment in tau therapies has traditionally lagged somewhat due to the focus on proteotoxicity of other aggregated proteins such as amyloid-beta (Aβ) in Alzheimer’s disease (AD; Schneider et al., 2014). This evidence concerns the gene MAPT and Alzheimer disease.