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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.

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

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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The information about "LYSYT" are provided by the European Opendata Portal: CORDIS opendata.

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