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T2DM and AD SIGNED

Study of the interaction between metabolic stress and a specific genetic background on the contribution of sporadic Alzheimer's Disease

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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Project "T2DM and AD" data sheet

The following table provides information about the project.

Coordinator
AGENCIA ESTATAL CONSEJO SUPERIOR DEINVESTIGACIONES CIENTIFICAS 

Organization address
address: CALLE SERRANO 117
city: MADRID
postcode: 28006
website: http://www.csic.es

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Project website http://embomolmed.embopress.org/content/10/1/7.long
 Total cost 170˙121 €
 EC max contribution 170˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-04-01   to  2019-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    AGENCIA ESTATAL CONSEJO SUPERIOR DEINVESTIGACIONES CIENTIFICAS ES (MADRID) coordinator 170˙121.00

Mappa

 Project objective

Different from the familial forms, late onset Alzheimer’s disease (LOAD) is not the consequence of a single cause: neither aging, nor genetic polymorphisms nor an environmental disturbance do, per se, suffice to produce this disease. It is currently thought that instead disease is the consequence of an interaction of all the above circumstances. With that perception in mind, I here propose to study i) the effect of type 2 diabetes mellitus (T2DM), a metabolic disturbance strongly associated with propensity to LOAD, on the appearance of AD-associated features (biochemical, electrophysiological and behavioral) ii) in the brains of aged mice iii) bearing a genetic insufficiency in either the gene SORL1 or in CD2AP, both of which have been linked to higher risk of late onset AD in recent familial genome wide association studies (GWAS). Once the phenotypic analysis is completed, I will perform genome wide epigenetic analysis of T2DM on specific neuronal populations of wild type and the genetically deficient mice. All in all, my studies should help to determine the mechanisms by which environment, age and disease-predisposing genetic weaknesses link together to produce this disease.

 Work performed, outcomes and results:  advancements report(s) 

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The information about "T2DM AND AD" are provided by the European Opendata Portal: CORDIS opendata.

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