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Prion Respiration SIGNED

The Role of Complex I Assembly Factors during Prion Diseases: Insights into Mitochondrial Neurobiology

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 Prion Respiration project word cloud

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

mitochondrial    broad    neurological    correct    neurons    prions    demonstrates    acad9    mitochondria    structural    found    biology    generate    assembly    denoted    oxidative    complexes    age    cellular    decrease    animal    drug    chain    cell    survival    diminish    proteins    insights    models    ndufaf1    disease    responsible    stresses    misassembly    helping    prion    diseases    energetic    aberrant    transport    prevent    respiratory    neuronal    nuclear    energy    cells    dysfunctions    biological    spectrum    exacerbated    defects    identification    altered    cryo    integrity    syndrome    interfering    respiration    electron    saxs    strategies    components    neurodegeneration    afs    alzheimer    encoded    apoptosis    structure    mechanisms    levels    em    mutations    functional    aging    subsequently    dieseas    function    characterization    disorders    constitute    leigh    ecsit    parkinson    childhood    declines    neurodegenerative    lived    underlying   

Project "Prion Respiration" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI TRENTO 

Organization address
address: VIA CALEPINA 14
city: TRENTO
postcode: 38122
website: www.unitn.it

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 Italy [IT]
 Total cost 171˙473 €
 EC max contribution 171˙473 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-10-01   to  2021-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI TRENTO IT (TRENTO) coordinator 171˙473.00

Map

 Project objective

Mitochondria have a crucial role in cell survival and apoptosis, in particular in long-lived cells such as neurons. Mitochondria generate energetic potential through respiratory complexes I to IV, which constitute the electron transport chain. A number of studies demonstrates that mitochondrial integrity declines as a function of aging and dysfunctions may be exacerbated by age-related neurodegenerative diseases. Altered levels of complex I proteins have been found to be directly responsible for a decrease in energy production in Alzheimer’s and Parkinson's disease. Recently, a number of nuclear encoded mitochondrial proteins, denoted as “assembly factors” (AFs), have been identified as crucial components helping the complex I assembly. Defects in AFs (due to mutations or aberrant AFs processing) may cause complex I misassembly and mitochondrial dysfunctions leading to a broad spectrum of diseases, including neurological disorders in childhood-related dieseas as Leigh syndrome. The functional role of AFs during neurodegeneration has not been investigated yet. With the “Prion Respiration” project I propose to develop a research approach aimed at the identification of the biological role of three crucial complex I AFs (namely ECSIT, NDUFAF1 and ACAD9) in cellular and animal models using prion diseases as robust system to study neurodegenerative diseases. Subsequently, the role of prions in interfering the with the correct assembly of the AFs will be investigated using structural biology approaches, as SAXS and cryo-EM methods. The structural and functional characterization of key proteins involved in mitochondrial respiration will provide insights into the underlying mechanisms involved in neuronal function and may represent novel targets for structure-based drug design strategies to prevent or diminish the oxidative stresses underlying neurodegeneration.

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