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NEUROTUNN

Mechanisms of α-synuclein spreading, implications for synucleinopathies

Total Cost €

0

EC-Contrib. €

0

Partnership

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 NEUROTUNN project word cloud

Explore the words cloud of the NEUROTUNN project. It provides you a very rough idea of what is the project "NEUROTUNN" about.

interactions    questioning    cell    strategies    diseases    direct    mediated    beta    tau    striking    autonomous    misfolded    normal    contribution    tses    regions    molecular    mediate    recovery    prion    molecules    proteinaceous    mainly    proteins    engrafted    series    spreading    physiologically    neuronal    cells    neurons    exploring    vitro    pathological    encephalopathies    nanotubes    nervous    stages    protein    prions    spongiform    therapies    mortem    patients    disease    readily    glial    fundaments    hypothesize    misfolding    tnts    shown    neuron    brains    passage    embryonic    communication    tnt    therapeutic    valuable    intercellular    investigation    neurodegenerative    prevention    underlying    transplants    alzheimer    transfer    amyloidogenic    suggested    models    modifying    transmission    tunneling    transplanted    prevalent    alpha    poliq    accessible    mechanism    parkinson    huntingtin    amyloid    illnesses    cellular    synuclein    transport    aggregates    post    transmissible   

Project "NEUROTUNN" data sheet

The following table provides information about the project.

Coordinator
INSTITUT PASTEUR 

Organization address
address: RUE DU DOCTEUR ROUX 25-28
city: PARIS CEDEX 15
postcode: 75724
website: http://www.pasteur.fr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country France [FR]
 Project website https://research.pasteur.fr/fr/member/frida-loria-salinas/
 Total cost 185˙076 €
 EC max contribution 185˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-03-01   to  2018-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT PASTEUR FR (PARIS CEDEX 15) coordinator 185˙076.00

Map

 Project objective

A common feature of neurodegenerative diseases, including highly prevalent illnesses, is the presence of misfolded protein aggregates in affected regions of the nervous system. Aggregates result from the misfolding of one or more specific proteins, for example, amyloid-β in Alzheimer’s disease, α-synuclein in Parkinson’s disease, and the normal prion protein in transmissible spongiform encephalopathies (TSEs). Recently a series of exciting studies has suggested a prion-like mechanism underlying the pathological spreading of misfolded proteins (mainly tau, α-synuclein and huntingtin) involved in various neurodegenerative diseases. Particularly striking is the recovery of α-synuclein aggregates from engrafted embryonic neurons in post-mortem brains transplanted from Parkinson’s patients. Thus, while questioning the therapeutic use of transplants, the understanding of the molecular and cellular fundaments of cell-to-cell transmission of proteinaceous aggregates is clearly in the early stages of investigation and may represent a more readily accessible target for novel disease-modifying therapies, allowing the development of possible common therapeutic strategies. Tunneling nanotubes (TNTs) represent a novel mechanism of direct intercellular communication that has been shown to mediate both transfer of prions between neuronal cells and the passage of poliQ huntingtin between neurons. We hypothesize that TNT-mediated transfer of amyloidogenic protein aggregates represents one of the main pathways of communication between cells. Thus, molecules involved in TNT formation could represent valuable targets for the disease prevention. Here I will assess the underlying mechanism of cell-to cell transfer of α-synuclein, exploring whether its transport could be mediated by TNTs in physiologically relevant in vitro models, evaluating as well the possible contribution of non-cell autonomous processes, via neuron-glial interactions, to the pathological spreading of the protein.

 Publications

year authors and title journal last update
List of publications.
2017 Frida Loria, Jessica Y. Vargas, Luc Bousset, Sylvie Syan, Audrey Salles, Ronald Melki, Chiara Zurzolo
α-Synuclein transfer between neurons and astrocytes indicates that astrocytes play a role in degradation rather than in spreading
published pages: 789-808, ISSN: 0001-6322, DOI: 10.1007/s00401-017-1746-2
Acta Neuropathologica 134/5 2019-06-13
2016 Saïda Abounit, Luc Bousset, Frida Loria, Seng Zhu, Fabrice de Chaumont, Laura Pieri, Jean‐Christophe Olivo‐Marin, Ronald Melki, Chiara Zurzolo
Tunneling nanotubes spread fibrillar α‐synuclein by intercellular trafficking of lysosomes
published pages: 2120-2138, ISSN: 0261-4189, DOI: 10.15252/embj.201593411
The EMBO Journal 35/19 2019-06-13

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