Tau filaments and the development of positron emission tomography tracers

Michel Goedert, Yoshiki Yamaguchi, Sushil K. Mishra, Makoto Higuchi, Naruhiko Sahara

Research output: Contribution to journalReview articlepeer-review

27 Citations (Scopus)

Abstract

A pathological pathway leading from soluble, monomeric to insoluble, filamentous Tau, is believed to underlie human Tauopathies. Cases of frontotemporal dementia are caused by dominantly inherited mutations in MAPT, the Tau gene. They show that dysfunction of Tau protein is sufficient to cause neurodegeneration and dementia. Extrapolation to the more common sporadic Tauopathies leads one to conclude that the pathological pathway is central to the development of all cases of disease, even if there are multiple reasons for Tau assembly. These findings are conceptually similar to those reported for beta-amyloid, alpha-synuclein and prion protein. Here, we provide an overview of Tau filaments and their positron emission tomography ligands.

Original languageEnglish
Article number70
JournalFrontiers in Neurology
Volume9
Issue numberFEB
DOIs
Publication statusPublished - 15-02-2018
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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