ADAMNEURON

Study and Identification of ADAM10 as Neuronal α-secretase in relation to Alzheimer’s disease

 Coordinatore VIB 

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

contact info
Titolo: Dr.
Nome: Wim
Cognome: Goemaere
Email: send email
Telefono: 3292446611
Fax: 3292446699

 Nazionalità Coordinatore Belgium [BE]
 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-2007-4-3-IRG
 Funding Scheme MC-IRG
 Anno di inizio 2008
 Periodo (anno-mese-giorno) 2008-04-01   -   2012-03-31

 Partecipanti

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

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

contact info
Titolo: Dr.
Nome: Wim
Cognome: Goemaere
Email: send email
Telefono: 3292446611
Fax: 3292446699

BE (ZWIJNAARDE - GENT) coordinator 0.00

Mappa


 Word cloud

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

beta    brain    cures    ad    expectancy    determine    becoming    western    neuronal    disorder    alpha    secretase    cleaved    expression    amyloid    world    app    life    treatments    adam    progressive    disease    regulate    neurodegenerative    alzheimer    peptide   

 Obiettivo del progetto (Objective)

'With life expectancy increasing rapidly in our Western world, Alzheimer’s disease (AD), a progressive neurodegenerative disorder resulting in dementia, is becoming more common, however no cures or effective treatments are currently available. The neurotoxic amyloid-β (Aβ) peptide appears central to AD pathogenesis, and is generated by β- and γ-cleavage of the larger amyloid precursor protein (APP). APP can also be cleaved by α-secretase, which cleaves within the Aβ peptide region and hence precludes the generation of Aβ. To date, the exact nature of α-secretase in the brain remains unknown, although ADAM10 (A Disintegrin And Metalloproteinase) seems to be the most likely candidate. This proposal is designed to determine definitively whether ADAM10 comprises indeed neuronal α-secretase activity in vivo, and to determine which factors regulate its activity. Using human APP (hAPP) transgenic mice deficient in neuronal ADAM10 expression we will determine whether levels of α-cleaved APP are down- and Aβ upregulated, whether this results in increased Aβ deposition and neurodegeneration, and whether ADAM10 is involved in learning and memory. Using neuronal cell culture we will determine whether growth and neuroprotective factors induce ADAM10 expression. In addition we will set up a screening system that will be used to identify molecules that regulate ADAM10 expression. These experiments will further our understanding of α-secretase in the brain and will aid in the development of novel therapies for AD.'

Introduzione (Teaser)

Alzheimer's disease is becoming more common as life expectancy increases across the western world. There are currently no cures or effective treatments for this progressive neurodegenerative disorder.

Altri progetti dello stesso programma (FP7-PEOPLE)

NEURONAL POLARITY (2008)

Pyramidal neuron polarity decisions during migration and axonal outgrowth in the developing mammalian cerebral cortex

Read More  

TEMADEP (2011)

TEMPLATE-ASSISTED DEPOSITION OF FUNCTIONAL MATERIALS AND DEVICES

Read More  

COGNOVO (2013)

Cognitive Innovation

Read More