Transgenic dissection of the neural circuitry of memory and dementia

Project Information

MECEDGE

Grant agreement ID: 796535

DOI

10.3030/796535

Project terminated on 21 November 2018

EC signature date 6 March 2018

Start date 1 May 2018

End date 29 November 2020

Funded under

• EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions

Total cost

€ 196 400,40

EU contribution

€ 196 400,40

Coordinated by

NORGES TEKNISK-NATURVITENSKAPELIGE UNIVERSITET NTNU
Norway

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

Reporting period: 2018-05-01 to 2020-04-30

Summary of the context and overall objectives of the project

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.

Work performed from the beginning of the project to the end of the period covered by the report and main results achieved so far

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.

Progress beyond the state of the art and expected potential impact (including the socio-economic impact and the wider societal implications of the project so far)

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