VD&NVD

"Vascular Dementia: revealing the detrimental synergy between hypertension, micro-strokes and Neuro-Vascular Decoupling"

 Coordinatore TEL AVIV UNIVERSITY 

 Organization address address: RAMAT AVIV
city: TEL AVIV
postcode: 69978

contact info
Titolo: Ms.
Nome: Lea
Cognome: Pais
Email: send email
Telefono: 97236408774
Fax: 97236409697

 Nazionalità Coordinatore Israel [IL]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2013-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-09-01   -   2017-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    TEL AVIV UNIVERSITY

 Organization address address: RAMAT AVIV
city: TEL AVIV
postcode: 69978

contact info
Titolo: Ms.
Nome: Lea
Cognome: Pais
Email: send email
Telefono: 97236408774
Fax: 97236409697

IL (TEL AVIV) coordinator 100˙000.00

Mappa

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 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

parenchyma    neuronal    hypoperfusion    alzheimer    barrier    brain    hypertension    ad   

 Obiettivo del progetto (Objective)

'Research in recent years has started to provide an alternative view to Alzheimer's etiology emphasizing the role of other factors such as inflammation and brain vascular alterations in the development of Alzheimer. Of major interest is the link between AD and hypertension, another global epidemic affecting millions of people worldwide. Hypertension results in increased stiffness of the brain vasculature leading, among others, to chronic cerebral hypoperfusion. Little is known about the short and long-term consequences of such hypoperfusion on neuronal dynamics. Hypoperfusion alters the function of the blood brain barrier; a cellular ensemble that actively keeps at bay pathogens and alike from entering the brain parenchyma. Amyloid and its products are under strict control across this barrier. Hence, damage to the barrier results in their accumulation in the brain parenchyma, which likely contributes to neuronal dysfunction and dementia. This recently recognized tight association between AD and hypertension opens new venues for both basic and translational research with the promise to better understand and likely treat these two maladies together.'

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