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.

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

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.)

RipGEESE (2020)

Identifying the ripples of gene regulation evolution in the evolution of gene sequences to determine when animal nervous systems evolved

Read More  

5G-ACE (2019)

Beyond 5G: 3D Network Modelling for THz-based Ultra-Fast Small Cells

Read More  

MY MITOCOMPLEX (2021)

Functional relevance of mitochondrial supercomplex assembly in myeloid cells

Read More