BBBARRIER

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

 Coordinatore UPPSALA UNIVERSITET 

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 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

Mappa


 Word cloud

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models    diseases    stroke    blood    permeability    molecular    drug    animal    trauma    mechanisms    cns    tissue    brain    transport    tools    demand    pericytes    vivo    bbb    neurodegenerative   

 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.'

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