||Tau filaments and development of positron emission tomography (PET) tracers
Goedert, Michel ,
Yamaguchi, Yoshiki ,
K. Mishra, Sushi ,
higuchi, MakotoSahara, Naruhiko
Neurofibrillary lesions strongly correlate with cognitive deficits, making them an important therapeutictarget for Alzheimer’s disease (AD) (1, 2). Dominantly inherited mutations in MAPT, the Taugene, cause a form of frontotemporal dementia that can be associated with parkinsonism (FTDP-17T), showing that dysfunction of Tau protein is sufficient to cause neurodegeneration and dementia(3). In FTDP-17T, abundant filamentous Tau inclusions are present in either nerve cells or in bothnerve cells and glial cells. Aβ deposits, a defining feature of AD, are not characteristic of FTDP-17T.However, there are many similarities between cases of FTDP-17T and other pure Tauopathies, suchas sporadic progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilicgrain disease (AGD), and Pick’s disease, especially with regard to the isoform composition of Taufilaments.