M
Michel Goedert
Researcher at Laboratory of Molecular Biology
Publications - 353
Citations - 72555
Michel Goedert is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Tau protein & Frontotemporal dementia and parkinsonism linked to chromosome 17. The author has an hindex of 125, co-authored 337 publications receiving 64671 citations. Previous affiliations of Michel Goedert include University of Pisa & Max Planck Society.
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Journal ArticleDOI
The cellular localization of preprotachykinin A messenger RNA in the bovine nervous system.
Michel Goedert,S.P. Hunt +1 more
TL;DR: The present findings allow an unambiguous identification of the cellular sites of synthesis of preprotachykinin A messenger RNA; in situ hybridization should also prove a useful technique for investigating the regulation of neuropeptide biosynthesis at the cellular level.
Book ChapterDOI
Tau proteinopathies and the prion concept.
TL;DR: The ordered assembly of a small number of proteins into amyloid filaments is central to age-related neurodegenerative diseases as discussed by the authors, and Tau is the most commonly affected of these proteins.
Journal ArticleDOI
α-Synuclein filaments from transgenic mouse and human synucleinopathy-containing brains are major seed-competent species.
Sophie A. Morgan,Isabelle Lavenir,Juan Fan,Masami Masuda-Suzukake,Daniela Passarella,Michael DeTure,Dennis W. Dickson,X. Bernardino Ghetti,Michel Goedert +8 more
TL;DR: It is concluded that α-synuclein filaments are the main driving force for amplification and propagation of pathology in synucleinopathies.
Journal ArticleDOI
Mutations in the tau gene (MAPT) in FTDP-17: the family with Multiple System Tauopathy with Presenile Dementia (MSTD).
Maria Grazia Spillantini,Jill R. Murrell,Michel Goedert,Martin R. Farlow,Aaron Klug,Bernardino Ghetti +5 more
TL;DR: In 1998, the relevance of tau dysfunction for the neurodegenerative process became clear, when mutations in the tau gene were found to cause the inherited "frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17)".
Journal ArticleDOI
Characterisation of an antibody relevant to the neuropathology of Alzheimer disease.
TL;DR: This work has used enzyme-linked immunosorbent assays, immunoblots, and immunohistochemistry, together with appropriate controls, to show that BR88 does not cross-react with τ, contradicting the claim in question and confirming the previous findings.