Opendata, web and dolomites

MITOPOMPE SIGNED

Targeting mitochondrial defects and oxidative stress in Pompe Disease: from pathogenesis to therapy

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 MITOPOMPE project word cloud

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

avenues    mingozzi    synaptic    point    neuronal    phenotypes    oxidative    mouse    caused    transmission    complemented    treatment    mitoq    lsd    neuron    lysosomal    nrf2    brain    muscle    rna    disease    reversal    therapeutic    regulated    amounts    atp    tissues    antioxidants    mitochondrial    enzyme    apoptosis    full    everyday    functional    neuromuscular    motor    accordingly    fighting    competent    extensive    buffering    dependent    treat    dr    respiratory    gaa    mutations    cell    muscular    alpha    functionally    transcriptomic    defects    function    rescue    sequencing    expertise    little    pd    perform    storage    potentially    involvement    interacting    cardiomyopathy    nervous    therapy    neurological    phosphorylation    mtgsh    dysfunction    central    calcium    cellular    mitochondria    pathology    heavily    severity    depending    synapses    aav    organelle    tested    interventions    pharmaceutical    signaling    model    evident    disorders    lsds    ko    pathophysiology    gene    stress    boost    acid    missing    weakness    therapies    glucosidase    pompe    active    group    combined    mitocatalase   

Project "MITOPOMPE" data sheet

The following table provides information about the project.

Coordinator
ASSOCIATION GENETHON 

Organization address
address: RUE DE L INTERNATIONALE 1 BIS
city: EVRY
postcode: 91002
website: www.genethon.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 173˙076 €
 EC max contribution 173˙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-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-01-01   to  2020-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    ASSOCIATION GENETHON FR (EVRY) coordinator 173˙076.00

Map

 Project objective

The central role of ATP production by oxidative-phosphorylation, together with calcium buffering and apoptosis, makes mitochondria an organelle interacting with many processes within the cell. Neuronal and muscular tissues require high amounts of ATP to perform their everyday function, therefore are heavily dependent on mitochondrial function. Neuromuscular synapses are of particular importance since synaptic transmission is a highly regulated process which requires active and functionally competent mitochondria. Accordingly, mitochondrial involvement is becoming increasingly evident in is Lysosomal Storage Disorders (LSDs) along with neurological pathology. Over the past several years Dr. Mingozzi’s group has built extensive expertise in Pompe Disease (PD), an LSD which is caused by mutations in the enzyme acid α-glucosidase (GAA). Muscle weakness, cardiomyopathy, respiratory failure, central nervous system and more specifically motor-neuron defects are observed depending on the severity of the disease. Little is known about the role of mitochondria in the pathophysiology of PD and interventions aimed at addressing mitochondrial defects in PD is currently missing. The aim of this proposal is to characterize the mitochondrial dysfunction in the Gaa KO mouse model of PD. This to assess potential rescue of such phenotypes by AAV-based GAA gene therapy complemented with therapeutic interventions targeted to treat and boost mitochondrial function by fighting against oxidative stress. Two mitochondrial treatment approaches; (i) pharmaceutical antioxidants, e.g. mitoQ or mtGSH and (ii) AAV based approaches; AAV-Nrf2 and AAV-mitoCatalase will be tested. Combined therapies with the AAV-GAA treatment will aim to reach full rescue of the muscle and brain pathology and functional reversal of mitochondrial defects. Transcriptomic changes will also be analyzed by RNA sequencing to investigate cellular signaling changes which will potentially point to novel therapeutic avenues.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "MITOPOMPE" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.3.2.)

RAMBEA (2019)

Realistic Assessment of Historical Masonry Bridges under Extreme Environmental Actions

Read More  

IRF4 Degradation (2019)

Using a novel protein degradation approach to uncover IRF4-regulated genes in plasma cells

Read More  

PROSPER (2019)

Politics of Rulemaking, Orchestration of Standards, and Private Economic Regulations

Read More