@article{oai:repo.qst.go.jp:00049046,
 author = {Goedert, Michel and Yamaguchi, Yoshiki and K., Mishra Sushi and higuchi, Makoto and Sahara, Naruhiko and 樋口 真人 and 佐原 成彦},
 journal = {Frontiers in Neurology},
 month = {Feb},
 note = {Neurofibrillary lesions strongly correlate with cognitive deficits, making them an important therapeutic
target for Alzheimer’s disease (AD) (1, 2). Dominantly inherited mutations in MAPT, the Tau
gene, 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 both
nerve 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, such
as sporadic progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic
grain disease (AGD), and Pick’s disease, especially with regard to the isoform composition of Tau
filaments.},
 title = {Tau filaments and development of positron emission tomography (PET) tracers},
 volume = {9},
 year = {2018}
}