A group of neurological disorders collectively referred to as tauopathies have aggregates of tau protein as a core neuropathologic feature (see Table 1) [3]. In Alzheimer’s disease (AD), the most common and best studied tauopathy, tau aggregation into neurofibrillary tangles (NFTs) is one of two pathological hallmarks of the disease, the other being beta amyloid (Aβ) plaques [4]. Tau aggregation in the brainstem and entorhinal cortex has been shown to be the earliest histopathological finding in the neuropathology of AD, which can spread to other brain regions as the disease progresses over time and increases in severity [5-7]. Recent advances in tau-sensitive PET imaging have demonstrated that tau aggregation correlates neuroanatomically with both symptoms and severity in AD [8]; these findings are consistent with Braak staging in clinicopathological studies that have demonstrated regional tau burden correlates with clinical phenotype and predicts cognitive status [9,10].
