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NGINFAD

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Targeting Inflammation and Neurogenesis using cannabinoids to delay the onset of...

Targeting Inflammation and Neurogenesis using cannabinoids to delay the onset of Alzheimer s disease 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 million... ver más

31/03/2014

AMU

100K€

Presupuesto del proyecto: 100K€

Líder del proyecto

UNIVERSITE DAIX MARSEILLE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Ver 2 Participantes

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2014-03-31 No tenemos la información de la convocatoria

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

2 Participantes

AMU

0.00€ | Lider

UnivMed

N.D. | Participante

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Líder del proyecto

UNIVERSITE DAIX MARSEILLE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 100K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto 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.

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