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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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The novel MAPT mutation K298E: Mechanisms of mutant tau toxicity, brain pathology and tau expression in induced fibroblast-derived neurons

TL;DR: This is the first example of the successful generation of iNs from skin cells retrieved post-mortem, which affects both protein function and alternative mRNA splicing in frontotemporal dementia and parkinsonism linked to chromosome 17.
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The effects of chronic neuroleptic treatment on neurotensin-like immunoreactivity in the rat central nervous system.

TL;DR: The dopamine receptor antagonist fluphenazine decanoate, when administered for a total period of 10 months, produced a large increase in neurotensin-like immunoreactivity in dopamine-rich brain areas, such as the nucleus accumbens, the striatum and the frontal cortex, providing further evidence in favour of a functional interaction between neurotens in and dopamine in the central nervous system.
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Tau Filaments and the Development of Positron Emission Tomography Tracers.

TL;DR: An overview of Tau filaments and their positron emission tomography ligands is provided 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.
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Silver staining (Campbell-Switzer) of neuronal α-synuclein assemblies induced by multiple system atrophy and Parkinson's disease brain extracts in transgenic mice

TL;DR: In this article, the authors compared the abilities of brain extracts from multiple system atrophy (MSA) and Parkinson's disease (PD) patients to induce neuronal α-synuclein assembly and neurodegeneration following intracerebral injection in heterozygous mice transgenic for human mutant A53T.
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Immunosympathectomy: Lack of evidence for a complement-mediated cytotoxic mechanism

TL;DR: It is concluded that they involve a small population of neurons, sensitive to short-term NGF deprivation whereas the majority of the neurons can withstand deprivation for up to 48 h without sustaining irreversible damage.