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Mechanisms of α-synuclein spreading, implications for synucleinopathies

Total Cost €


EC-Contrib. €






 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.

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

Project "NEUROTUNN" data sheet

The following table provides information about the project.


Organization address
address: RUE DU DOCTEUR ROUX 25-28
city: PARIS CEDEX 15
postcode: 75724

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
 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


Take a look of project's partnership.

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


 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.


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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