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NEVULA SIGNED

Understanding selective neuronal vulnerability in Alzheimer’s disease

Total Cost €

0

EC-Contrib. €

0

Partnership

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Project "NEVULA" data sheet

The following table provides information about the project.

Coordinator
KAROLINSKA INSTITUTET 

Organization address
address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177
website: www.ki.se

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 Sweden [SE]
 Total cost 247˙059 €
 EC max contribution 247˙059 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-GF
 Starting year 2018
 Duration (year-month-day) from 2018-09-01   to  2021-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET SE (STOCKHOLM) coordinator 247˙059.00
2    THE ROCKEFELLER UNIVERSITY NOT FOR PROFIT CORPORATION US (NEW YORK) partner 0.00

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 Project objective

The aim of this action is to understand the mechanisms behind the susceptibility of enthorinal cortex II (ECII) neurons to neurofibrillary tangle (NFT) formation in Alzheimer´s disease. To do so we will modulate the expression of the genes that according to NetWAS (Network-wide Association Study) are more directly involved in NFT formation in ECII neurons.

Understanding why the pathological lesions that lead to neurodegeneration appear earlier in some specific neurons of the human brain is one of the major challenges in the neuroscience field.

Prof. Greengard´s lab has generated a transgenic mouse that allows the immunoprecipitation of ribosome-bound mRNAs specifically from ECII neurons (ECII-bacTRAP mice). We will perform AAV stereotaxic injections in the enthorinal cortex of these mice followed by RNA-seq to determine how the modulation of our target genes affects ECII neurons expression profile. We will also explore whether our intervention can influence ECII neurons susceptibility to NFT in P301S AD mice. The results obtained in mice will be validated by immunofluorescence and in situ hybridization studies in human samples from control and AD patients at different Braak stages.

Our results could add extremely relevant information on the mechanisms underlying AD pathogenesis and reveal these genes as new therapeutic targets for the disease.

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The information about "NEVULA" are provided by the European Opendata Portal: CORDIS opendata.

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