IPLASTICITY
Induction of juvenile-like plasticity in the adult brain
| Coordinatore | HELSINGIN YLIOPISTO
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Finland [FI] |
| Totale costo | 2˙500˙000 € |
| EC contributo | 2˙500˙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-2012-ADG_20120314 |
| Funding Scheme | ERC-AG |
| Anno di inizio | 2013 |
| Periodo (anno-mese-giorno) | 2013-04-01 - 2018-03-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
HELSINGIN YLIOPISTO
Organization address
address: YLIOPISTONKATU 4 contact info |
FI (HELSINGIN YLIOPISTO) | hostInstitution | 2˙500˙000.00 |
| 2 |
HELSINGIN YLIOPISTO
Organization address
address: YLIOPISTONKATU 4 contact info |
FI (HELSINGIN YLIOPISTO) | hostInstitution | 2˙500˙000.00 |
Mappa
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Obiettivo del progetto (Objective)
'Neuronal networks are tuned to optimally represent external and internal milieu through neuronal plasticity during critical periods of juvenile life. After the closure of the critical periods, plasticity is considered to be much more limited. In a series of landmark studies, we have shown that critical period-like plasticity can be reactivated in the adult mammalian brain by pharmacological treatment with the antidepressant fluoxetine. These ground-breaking studies establish a new principle, induced juvenile-like plasticity (iPlasticity) and define a new class of drugs, iPlastic drugs. For optimal results, iPlastic drug must be combined with physical or psychological rehabilitation, which guide the plastic networks and together allow better adaptation towards changing environment. iPlasticity may facilitate functional recovery after brain injury and underlie the enhanced efficacy of combined antidepressant treatment and psychotherapy. We have uncovered iPlasticity as an exciting new concept and established experimental models to study the molecular, cellular and network level mechanisms underlying it. We will here focus on the role of neurotrophin BDNF, because our previous and unpublished work clearly shows that BDNF and its receptors TrkB and p75 are essential and sufficient for iPlasticity. We have found that a major developmental reorganization in TrkB signalling takes place coinciding with the end of critical periods, and its reversal may underlie iPlasticity. We will utilize our resources as a leading lab in BDNF effects in adult brain and through novel controlled transgenic models, genomics and proteomics, we will reveal the role of BDNF signalling through TrkB and p75 in brain maturation, iPlasticity and brain disorders. Understanding the neurobiological background of iPlasticity will be vital for iPlastic drug development and the numerous translational applications of iPlasticity clearly in sight.'