NGINFAD

Targeting Inflammation and Neurogenesis using cannabinoids to delay the onset of Alzheimer’s disease

Coordinatore	UNIVERSITE D'AIX MARSEILLE    more  Organization address address: Boulevard Charles Livon 58 city: Marseille postcode: 13284 contact info Titolo: Ms. Nome: Céline Cognome: Damon Email: send email Telefono: +33 4 91 31 97 97
Nazionalità Coordinatore	France [FR]
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-2009-RG
Funding Scheme	MC-IRG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-04-01   -   2014-03-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE D'AIX MARSEILLE  Organization address address: Boulevard Charles Livon 58 city: Marseille postcode: 13284 contact info Titolo: Ms. Nome: Céline Cognome: Damon Email: send email Telefono: +33 4 91 31 97 97	FR (Marseille)	coordinator	100˙000.00
2	UNIVERSITE DE LA MEDITERRANEE D'AIX-MARSEILLE II  Organization address address: Boulevard Charles Livon, Jardin du Pharo 58 city: MARSEILLE postcode: 13284 contact info Titolo: Ms. Nome: Céline Cognome: Damon Email: send email Telefono: 33491319797 Fax: 33491317177	FR (MARSEILLE)	participant	0.00

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 Obiettivo del progetto (Objective)

'Alzheimer’s disease (AD) is the most common neurodegenerative disease and accounts for the majority of diagnosed dementia after age 60. It is estimated to currently affect between 20 and 30 million people worldwide, with 4 millions in the U.S. alone. As life expectancy increases in developed countries, the prevalence of AD, and its burden on healthcare, is very likely to increase dramatically in the next few decades. While waiting for a cure for AD as its prevalence will increase drastically over the years, a medication approach that would delay the onset of the disease would have a major impact of the disease incidence and prevalence, and thus on its burden on the economy of industrialized countries. Our main hypothesis is that excessive inflammatory processes (and its subsequent effect on protein function like MMPs and neurogenesis) are part of the early events triggering deleterious processes observed in AD later on. We do hypothesize that a diminution (but not complete inhibition) of those inflammatory processes, notably using the EC system, could benefit brain functions (neurogenesis, memory processes, APP processing to non-toxic amyloid forms…) and thus decrease the incidence of AD by delaying/reducing the appearance of hallmarks of AD. This proposal will then clarify the possible influence in vivo of chronic inflammation and its pharmacological modulation (and inflammatory-related proteases as MMPS), as well as neurogenic processes and behavior in a well-established transgenic model of AD. This study will thus provide valuable mechanistic information underlying the possible modulating role of the inflammation, MMPs and EC in the development of the AD pathology. Overall, those experiments could pave the way to a possible active treatment aiming at lowering the incidence of AD.'

Introduzione (Teaser)

Alzheimer's disease is the most prevalent form of age-related neurodegeneration. With increased life expectancy, disease incidence is anticipated to rise, necessitating new medications that would delay disease onset.