DIABLO

Mechanisms of Developmental and Injury-related Axon Branch Loss

 Coordinatore TECHNISCHE UNIVERSITAET MUENCHEN 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙995˙000 €
 EC contributo 1˙995˙000 €
 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-2013-CoG
 Funding Scheme ERC-CG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-06-01   -   2019-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    TECHNISCHE UNIVERSITAET MUENCHEN

 Organization address address: Arcisstrasse 21
city: MUENCHEN
postcode: 80333

contact info
Titolo: Ms.
Nome: Ulrike
Cognome: Ronchetti
Email: send email
Telefono: +4989 28922616

DE (MUENCHEN) hostInstitution 1˙995˙000.00
2    TECHNISCHE UNIVERSITAET MUENCHEN

 Organization address address: Arcisstrasse 21
city: MUENCHEN
postcode: 80333

contact info
Titolo: Prof.
Nome: Thomas
Cognome: Misgeld
Email: send email
Telefono: +4989 41403512
Fax: +4989 41403352

DE (MUENCHEN) hostInstitution 1˙995˙000.00

Mappa


 Word cloud

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wallerian    forms    molecular    diseases    subcellular    mammalian    degeneration    nervous    past    loss    studying    motor    mechanisms    form    branch    years    cell    disease    aberrant    cns    axon    neurological   

 Obiettivo del progetto (Objective)

'My aim is to explore the subcellular (i.e. cell biological and molecular) mechanisms of axon loss in the developing and diseased mammalian nervous system. Axon loss not only sculpts neuronal networks in development, but also occurs early in numerous neurological diseases. Indeed, the life-time risk for diseases with an “axonopathic” component approaches 50%. Pathological axon loss likely involves aberrant activation of developmental programs – just as cell death in disease often takes the form of apoptosis, another prominent regressive event in neural development. Over the past few years, the first molecular pathways have emerged for one form of axon loss, Wallerian degeneration, which removes entire axon arbors after severing. However, Wallerian degeneration is of limited clinical significance – because the axon is cut and hence incapacitated before it is lost – and appears to play only minor roles in development. In contrast, “non-Wallerian” forms of axon loss that selectively remove individual “aberrant” branches dominate during development (“axon branch loss”). Due to the technical challenge of studying axon loss in the complex environment of the developing mammalian nervous system, the subcellular events that precede such non-Wallerian forms of axon branch loss are poorly understood, even though this phenomenon – when pathologically reactivated – likely contributes to axonal pathology in many neurological disorders. Over the past years, in parallel work on axon development and disease, my laboratory has devised functional imaging techniques that allow studying axon loss in vivo in the mammalian peripheral (PNS) and central nervous system (CNS) with subcellular resolution and molecular read-outs. Using these unique tools, I will address the following aims:

1 - Axon-intrinsic mechanisms of motor axon branch loss. 2 - Axon-glial mechanisms of motor axon branch loss. 3 - Axon branch loss during CNS development. 4 - Axon branch loss after CNS injury.'

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