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MITOPOMPE SIGNED

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

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 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.

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

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.

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

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