Neuroprotection in Multiple Sclerosis: From Molecular Imaging to Screenable Models


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 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙487˙200 €
 EC contributo 1˙487˙200 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2012-StG_20111109
 Funding Scheme ERC-SG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-12-01   -   2017-11-30


# participant  country  role  EC contrib. [€] 

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
postcode: 80539

contact info
Titolo: Mr.
Nome: Danny
Cognome: Duhme
Email: send email
Telefono: +49 89 2180 3605
Fax: +49 89 2180 2985

DE (MUENCHEN) hostInstitution 1˙487˙200.00

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
postcode: 80539

contact info
Titolo: Prof.
Nome: Martin
Cognome: Kerschensteiner
Email: send email
Telefono: +49 89 218078282
Fax: +49 89 218078285

DE (MUENCHEN) hostInstitution 1˙487˙200.00


 Word cloud

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vivo    axons    want    mechanisms    imaging    damage    axon    us    strategies    neuroinflammatory    deficits    molecular    fad    sequence    ability    ms    experimental    functional    lesions    therapeutic    axonal    stages   

 Obiettivo del progetto (Objective)

'Multiple Sclerosis (MS) is an inflammatory CNS disease that affects more than 2.5 million individuals worldwide. Damage to axonal connections determines the functional deficits of MS patients. How axons are damaged in MS is only incompletely understood. Using in vivo multiphoton imaging we have discovered a novel axon loss process that underlies axonal damage in experimental and human neuroinflammatory lesions. We have termed this process Focal Axonal Degeneration (FAD). FAD is characterized by a sequence of morphologically defined stages that ultimately result in axonal fragmentation. Notably, intermediate stages of FAD can persist for several days in vivo and still recover spontaneously. In this proposal I want to explore the biological and medical significance of FAD by addressing its:

1. Functional Characteristics I want to analyze two key aspects of axonal function, the ability to transport cargoes and the ability to propagate action potentials, in experimental neuroinflammatory lesions to better understand the in vivo relation between structural and functional deficits during axon damage.

2. Molecular Mechanisms I want to deploy new molecular imaging approaches to directly monitor the redox potential, calcium and ATP levels of axons and their mitochondria in experimental neuroinflammatory lesions. This will allow us to reveal the key effector mechanisms of FAD and the sequence in which they are activated in vivo.

3.Therapeutic Opportunities I plan to make use of advances in automated imaging and microfluidics to develop new in vivo assays for high-throughput screening of therapeutic interventions. This will help us to identify novel strategies for limiting progression and improving recovery of axon damage.

The proposed project should provide new insights into the functional and molecular underpinnings of axon damage in vivo, establish new tools and models to study it and guide the development of therapeutic strategies that can prevent or reverse it.'

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