Transgenic dissection of the neural circuitry of memory and dementia

Informations projet

MECEDGE

N° de convention de subvention: 796535

DOI

10.3030/796535

Projet clôturé le 21 Novembre 2018

Date de signature de la CE 6 Mars 2018

Date de début 1 Mai 2018

Date de fin 29 Novembre 2020

Financé au titre de

• EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions

Coût total

€ 196 400,40

Contribution de l’UE

€ 196 400,40

Coordonné par

NORGES TEKNISK-NATURVITENSKAPELIGE UNIVERSITET NTNU
Norway

Periodic Reporting for period 1 - MECEDGE (Transgenic dissection of the neural circuitry of memory and dementia)

Période du rapport: 2018-05-01 au 2020-04-30

Résumé du contexte et des objectifs généraux du projet

As the most common form of age-related dementia, Alzheimer's disease (AD) is an enormous and growing problem for an aging society. AD is a neurodegenerative disorder like Parkinson's disease (PD), but the former presents as a cognitive disorder, and the latter as a motor disorder (at least in early stages). The reason for this is not so much what happens (ultimately cell death in both cases), but *where* it happens (respectively, the entorhinal cortex, or EC, or the substantia nigra). This project attempts to explore what is it about the EC that makes it particularly susceptible to the pathological processes underlying AD, with particular emphasis on the role of activity. To do this, we combine transgenic lines we have created which allow us to manipulate the activity of neurons in this region with transgenic models of AD, and record the effects on both activity and AD-like phenotypes.

Travail effectué depuis le début du projet jusqu’à la fin de la période considérée dans le rapport et principaux résultats atteints jusqu’à présent

Unfortunately, after the first four months of the project, the researcher had to return to the United States due to family reasons. Therefore, the project did not get past the initial stage of characterization of the transgenic models.

Progrès au-delà de l’état des connaissances et impact potentiel prévu (y compris l’impact socio-économique et les conséquences sociétales plus larges du projet jusqu’à présent)

While the project unfortunately had to be terminated due to the reason stated above, the success of the initial characterization of the lines will enable others in the lab to continue the research program. This could lead to a greater understanding of the role of activity in the progression of AD, and thereby new potential therapeutic avenues.

Anatomical characterization of EC LIII-specific Transgenic DREADD Expression