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HUNTINFISH SIGNED

Generation of new zebrafish models for the study of the pathogenesis of Huntington´s disease and for the identification of new therapeutic targets.

Total Cost €

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EC-Contrib. €

0

Partnership

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 HUNTINFISH project word cloud

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

incurable    recapitulates    played    transgenic    neurodegenerative    genome    hd    cells    dominant    expansions    abnormally    proteasome    acute    unfortunately    autosomal    trinucleotide    lines    host    organism    date    encode    kinetics    slow    uas    photoconvertible    model    body    nd    polyq    disorder    inhibition    first    tissues    aggregation    examine    diseases    full    modeling    misfolding    glial    me    stimulation    polyglutamine    pathogenesis    clearance    neurons    life    mutant    toxic    gal4    prevent    relevance    straightforward    vitro    shared    expressing    wild    lab    generate    cag    construct    ubiquitin    inflammasome    previously    fish    length    huntingtin    treatments    models    protein    context    exon1    tools    nine    fluorescent    mentioned    complicated    caused    autophagy    disease    deeper    therapeutic    therapies    advantage    drugs    accelerate    fused    neuroinflammation    gain    integration    dendra    tracts    cycles    huntington    htt    vivo    proteins    human    forms    tract    strategies    validate    zebrafish   

Project "HUNTINFISH" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.ac.uk

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 United Kingdom [UK]
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-05-01   to  2020-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 183˙454.00

Map

 Project objective

Huntington´s disease (HD) is one of the nine neurodegenerative diseases (ND) caused by (CAG)n trinucleotide tract expansions that encode abnormally long polyglutamine (polyQ) tracts. The common features shared by many ND are the misfolding and aggregation of toxic proteins. Thus, HD recapitulates features of other, more complicated ND. As HD is an autosomal dominant disorder, modeling this disease in vitro and in vivo is straightforward. Unfortunately, HD is, to date, incurable and there are no drugs or therapies that are known to slow or prevent the disease. Thus, the strategies proposed in this project, taking advantage of the unique characteristics of the zebrafish as model organism to study human diseases, will allow me to gain a deeper understanding of its pathogenesis, and to generate tools to accelerate the development of new therapies. Moreover, my findings may have relevance to other ND. First, I propose to generate new zebrafish transgenic lines expressing different forms of human huntingtin (htt) (wild-type/mutant, full-length/exon1) fused to the photoconvertible fluorescent protein Dendra in whole body, neurons or glial cells using the UAS-GAL4 system. Next, I will validate the construct integration in the fish genome and characterize the transgenic lines. After that, I will use these new generated models to study the life cycles of the previously mentioned forms of htt in vivo, and I will examine their clearance kinetics in vivo in different tissues in the context of inhibition/stimulation of autophagy or ubiquitin-proteasome pathways. Moreover, I will assess the role played by the inflammasome in the context of the neuroinflammation present in HD. Finally, I will use these new zebrafish lines to test novel therapeutic targets recently identified in the host lab, in order to develop new treatments for HD.

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

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