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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Fatal attractions: abnormal protein aggregation and neuron death in Parkinson's disease and Lewy body dementia.
TL;DR: Increased understanding of the protein composition and pathological significance of LBs may provide insight into mechanisms of neuron dysfunction and death in other neurodegenerative disorders characterized by brain lesions containing massive deposits of proteinacious fibrils.
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Heparin-induced tau filaments are polymorphic and differ from those in Alzheimer's and Pick's diseases.
Wenjuan Zhang,Benjamin Falcon,Alexey G. Murzin,Juan Fan,R.A. Crowther,Michel Goedert,Sjors H.W. Scheres +6 more
TL;DR: Cryo- and immuno- electron microscopy is used to characterise tau filaments that were assembled from recombinant full-length human tau with four or three microtubule-binding repeats in the presence of heparin, illustrating the structural versatility of amyloid filaments and raising questions about the relevance of in vitro assembly.
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p42 map kinase phosphorylation sites in microtubule-associated protein tau are dephosphorylated by protein phosphatase 2A1 Implications for Alzheimer's disease
TL;DR: It is shown that p42 MAP kinase phosphorylates recombinant tau and converts it to a form which is similar to PHF tau, with PP2A1 being the most effective form of the enzyme.
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Filamentous nerve cell inclusions in neurodegenerative diseases.
Michel Goedert,Michel Goedert,Maria Grazia Spillantini,Maria Grazia Spillantini,Stephen W Davies,Stephen W Davies +5 more
TL;DR: The discovery last year of neuronal intranuclear inclusions in Huntington's disease and other disorders with expanded glutamine repeats has suggested a unifying mechanism underlying the pathogenesis of this class of neurodegenerative diseases.
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Nerve growth factor counteracts the neurophysiological and neurochemical effects of chronic sciatic nerve section
TL;DR: Radioimmunoassay of substance P revealed that chronic NGF treatment of a cut sciatic nerve does partially reverse the central changes that normally follow deafferentation.