MIRNA_AD

Role of microRNA dysregulation in Alzheimers Disease

 Coordinatore VIB 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Belgium [BE]
 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-2010-AdG_20100317
 Funding Scheme ERC-AG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-05-01   -   2016-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    VIB

 Organization address address: Rijvisschestraat 120
city: ZWIJNAARDE - GENT
postcode: 9052

contact info
Titolo: Mr.
Nome: Rik
Cognome: Audenaert
Email: send email
Telefono: +32 9 2446611
Fax: +32 9 2446610

BE (ZWIJNAARDE - GENT) hostInstitution 2˙500˙000.00
2    VIB

 Organization address address: Rijvisschestraat 120
city: ZWIJNAARDE - GENT
postcode: 9052

contact info
Titolo: Prof.
Nome: Bart Geert Alfons Paul
Cognome: De Strooper
Email: send email
Telefono: +32 16 346227

BE (ZWIJNAARDE - GENT) hostInstitution 2˙500˙000.00

Mappa


 Word cloud

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integrity    functioning    genetic    brain    mirna    expression    disease    relevance    ad    normal    sporadic    alterations    brains    mirnas    functional    gt   

 Obiettivo del progetto (Objective)

'Alzheimer's Disease (AD) is a major health problem in aging societies. Remarkable progress in the study of the rare genetic forms of the disease has lead to the identification of several key players like APP and the secretases, but the molecular basis of sporadic AD remains largely unresolved. The convergence of several factors (multicausality) has to be considered. miRNAs are crucially involved in normal brain functioning and integrity. Evidence obtained from analyzing a limited number of brains indicates that miRNA expression is affected in sporadic AD. We propose the hypothesis that such changes can affect normal functioning of neurons increasing their susceptibility to AD. We will document in 3 brain regions in >100 sporadic AD patients and in >100 controls alterations in miRNA expression and explore whether similar alterations can be detected in cerebrospinal fluid. This part of the study will firmly establish which miRNAs are altered in AD. We will then investigate the functional relevance of those miRNAs by gain and loss of function experiments in brains of zebra fish and mice. We will determine the target genes of the miRNA with genetic and proteomic approaches, and establish the functional networks controlled by those miRNA. We anticipate that this will lead to complete novel insights in the role of miRNAs in AD and in maintenance of brain integrity. Our work is likely to have diagnostic relevance for AD and will identify novel drug targets for the disease.'

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