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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.

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

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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