BBBARRIER

Mechanisms of regulation of the blood-brain barrier; towards opening and closing the barrier on demand

Coordinatore	UPPSALA UNIVERSITET    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Sweden [SE]
Totale costo	2˙499˙427 €
EC contributo	2˙499˙427 €
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-2011-ADG_20110310
Funding Scheme	ERC-AG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-08-01   -   2017-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	KAROLINSKA INSTITUTET  Organization address address: Nobels Vag 5 city: STOCKHOLM postcode: 17177 contact info Nome: Jill Cognome: Blomstrand Email: send email Telefono: +46 8 52487687	SE (STOCKHOLM)	beneficiary	64˙100.00
2	UPPSALA UNIVERSITET  Organization address address: SANKT OLOFSGATAN 10 B city: UPPSALA postcode: 751 05 contact info Titolo: Mrs. Nome: Birgitta Cognome: Gustafsson Email: send email Telefono: +46 18 4715029 Fax: +46 18 4715077	SE (UPPSALA)	hostInstitution	2˙435˙327.00
3	UPPSALA UNIVERSITET  Organization address address: SANKT OLOFSGATAN 10 B city: UPPSALA postcode: 751 05 contact info Titolo: Prof. Nome: Björn Christer Cognome: Betsholtz Email: send email Telefono: +46 18 4714363 Fax: +46 18 4715077	SE (UPPSALA)	hostInstitution	2˙435˙327.00

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 Obiettivo del progetto (Objective)

'In the bone-enclosed CNS, increased vascular permeability may cause life-threatening tissue swelling, and/or ischemia and inflammation which compromise tissue repair after trauma or stroke. The brain vasculature possesses several unique features collectively named the blood-brain barrier (BBB) in which passive permeability is almost completely abolished and replaced by a complex of specific transport mechanisms. The BBB is necessary to uphold the specific milieu necessary for neuronal function. Whereas breakdown of the BBB is part of many CNS diseases, including stroke, neuroinflammation, trauma and neurodegenerative disorders, its molecular mechanisms and consequences are unclear and debated. Conversely, the intact BBB is a huge obstacle for drug delivery to the brain. Research on the BBB therefore has two seemingly opposing aims: 1) to seal a damaged BBB and protect the brain from toxic blood products, and 2) to open the BBB “on demand” for drug delivery. A major problem in the BBB field has been the lack of in vivo animal models for molecular and functional studies. So far, available in vitro models are not recapitulating the in vivo BBB. Our recent work on mouse models lacking pericytes, a BBB-associated cell type, demonstrates a specific role for pericytes in the development and regulation of the mammalian BBB. These animal models are the first ones showing a general and significant BBB impairment in adulthood, and as such they provide a unique opportunity to address molecular mechanisms of BBB disruption in disease and in drug transport across the BBB. Importantly, the new models and tools that we have developed allow us to search for relevant druggable mechanisms and molecular targets in the BBB. The long-term goals of this proposal are to develop molecular strategies and tools to open and close the BBB “on demand” for drug delivery to the CNS, and to explore the importance and mechanisms of BBB dysfunction in neurodegenerative diseases and stroke.'