HEP
"Epilepsies of the temporal lobe: emergence, basal state and paroxysmal transitions"
| Coordinatore | INSTITUT DU CERVEAU ET DE LA MOELLE EPINIERE FONDATION
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | France [FR] |
| Totale costo | 1˙985˙057 € |
| EC contributo | 1˙985˙057 € |
| 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) | 2013-10-01 - 2018-09-30 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
INSTITUT DU CERVEAU ET DE LA MOELLE EPINIERE FONDATION
Organization address
address: BOULEVARD DE L'HOPITAL 47 contact info |
FR (PARIS) | hostInstitution | 1˙985˙057.00 |
| 2 |
INSTITUT DU CERVEAU ET DE LA MOELLE EPINIERE FONDATION
Organization address
address: BOULEVARD DE L'HOPITAL 47 contact info |
FR (PARIS) | hostInstitution | 1˙985˙057.00 |
Mappa
Word cloud
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
Obiettivo del progetto (Objective)
'This proposal focuses on a human disease: epilepsy of the temporal lobe. This syndrome has a relatively stereotyped history. Focal seizures emerge, with a delay of several years in the human, after an initial insult that results in neuronal death. We will use physiology, imaging, anatomy and transcriptomic techniques to ask how an epileptic brain emerges, to define different neuronal cell types in the basal epileptic state and to examine factors associated with the paroxysmal transition to a seizure. Specifically we will ask whether a loss of cholesterol homeostasis is involved in the initial sclerotic neuronal death. We will ask whether proteoglycans deposited in the extracellular space as a generalised wound healing response force the establishment of aberrant synaptic contacts and so facilitate the slow process of epileptogenesis. We will then study the basal state of an epileptic brain. We will establish the physiology, anatomy, connectivity and transcriptome of functionally distinct neurons defined by different contributions to epileptiform activities in human epileptic brain slices. Finally we will seek to establish what sudden changes in field potential, ionic homeostasis, cellular firing and synaptic interactions are associated with the paroxysmal moment of transition to seizure.'