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Understanding selective neuronal vulnerability in Alzheimer s disease

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... see more

01/10/2021

247K€

Project Budget: 247K€

Project leader

KAROLINSKA INSTITUTET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

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Financing granted El organismo H2020 notifico la concesión del proyecto The day 2021-10-01

MSCA-IF-2017: Individual Fellowships Objective:The goal of the Individual Fellowships is to enhance the creative and innovative potential...

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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

3 Participantes

247.06K€ | Leader

THE ROCKEFELLER UNIVERSITY N...

160.13K€ | participant

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Project duration: 42 months Date Start: 2018-03-07
End date: 2021-10-01

Project leader

KAROLINSKA INSTITUTET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 247K€

participation deadline Sin fecha límite de participación.

Project description 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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