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LySyT SIGNED

Understanding the role of lysosomes in the intercellular TNT-mediated spreading of α-synuclein and the impact of lysosomal dysfunction

Total Cost €

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EC-Contrib. €

0

Partnership

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 LySyT project word cloud

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

shed    incurable    became    nds    microtubules    suggested    function    brain    showed    severe    mediating    spreading    understand    defective    caused    global    rare    linked    regions    pathology    soluble    thin    zurzolo    causes    group    cells    etiopathogenesis    monomers    materials    death    unravel    insights    inherited    spread    fibrils    tunneling    valuable    dysfunction    trait    lysosomal    lysosomes    nd    alpha    correlation    transferred    cargos    synuclein    aggregates    light    misfolded    accumulates    hallmark    move    pathogenesis    neurodegeneration    host    storage    physiopathology    degraded    disorders    expertise    loaded    escape    few    last    transport    enzyme    perspective    deep    tnts    diseases    skills    accumulation    over    nanotubes    actin    protein    lsds    neurodegenerative    membrane    mechanism    parkinson    neuronal    cytosolic    syn    generally    intercellular    acceptor    decades    metabolic    protrusions    disease    fate    induce    lysosome    progression    shared    combining    pd    inside    demonstrated    lab    aggregation    receiving    forms    implications    combat    prion   

Project "LySyT" 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]
 Total cost 184˙707 €
 EC max contribution 184˙707 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-12-01   to  2022-11-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT PASTEUR FR (PARIS CEDEX 15) coordinator 184˙707.00

Map

 Project objective

Over the last few decades, neurodegenerative diseases (NDs) became one of the top 10 global causes of death. The accumulation of misfolded protein aggregates in affected brain regions is a common hallmark shared by several NDs. Misfolded alpha-synuclein (α-syn) accumulates in Parkinson’s disease (PD), the second most common ND, and recently a “prion-like” mechanism linked to the spreading of α-syn has been suggested for the pathology progression. The Zurzolo group demonstrated that α-syn fibrils spread between neuronal cells inside lysosomes through tunneling nanotubes (TNTs), thin actin-based membrane protrusions mediating intercellular transport of various cargos. As known, lysosomes move along microtubules therefore this research aims to understand how lysosomes can move inside and through actin-based TNTs. The host lab also showed that the transferred α-syn fibrils induce the aggregation of soluble cytosolic α-syn in receiving cells and this project will unravel the mechanism by which α-syn fibrils escape from lysosomes to induce the aggregation of monomers in acceptor cells. In addition, since lysosomal dysfunction is a common feature of NDs, this research will shed light on the functionality and fate of α-syn-loaded lysosomes. Lysosomal dysfunction is also a trait of Lysosomal Storage Diseases (LSDs), a group of about 50 rare inherited metabolic disorders generally caused by the defective function of a specific lysosomal enzyme leading to the lysosomal accumulation of non-degraded materials and neurodegeneration in the forms most severe. This project will investigate the correlation between LSDs and NDs and the possible implications of TNTs in LSDs that represent a new perspective for LSDs etiopathogenesis. By combining my skills in lysosome physiopathology and the host lab expertise in TNTs and PD pathogenesis, this project will provide a deep understanding of the role of lysosomes in NDs pathogenesis and valuable insights to combat these incurable diseases.

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