Identifying neuronal or muscle cell-specific suppressors that rescue motility defects in the ALS model of the nematode worm Caenorhabditis elegans

Project Information

RescueMoDe

Grant agreement ID: 895529

DOI

10.3030/895529

Project closed

EC signature date 23 April 2020

Start date 2 August 2021

End date 27 November 2023

Funded under

• EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions

Total cost

€ 175 572,48

EU contribution

€ 175 572,48

Coordinated by

ACADEMISCH ZIEKENHUIS GRONINGEN
Netherlands

Periodic Reporting for period 1 - RescueMoDe (Identifying neuronal or muscle cell-specific suppressors that rescue motility defects in the ALS model of the nematode worm Caenorhabditis elegans)

Reporting period: 2021-08-02 to 2023-08-01

Summary of the context and overall objectives of the project

I pursued a project to understand the mechanism behind a modifier of proteotoxicity using the nematode worm Caenorhabditis elegans. This modifier induces a protective effect in several worm models of ageing and neurodegeneration by extending lifespan and health span, indicating that it has a broadly neuroprotective effect. Understanding how it protects neurons can potentially lead to the development of new therapeutic strategies against ageing and neurodegenerative diseases.

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

Using novel genetic tools, I identified that this modifier of proteotoxicity improved the health of some types of neurons during ageing, while other types of neurons are less affected. I also optimised a genetic tool that enables rapid depletion of a protein of interest in C. elegans worms. Therefore we are now able to deplete this modifier in any tissue of interest and at any timepoint. Using this optimised tool, we plan to investigate the mechanism of this modifier of toxicity further in several C. elegans models of neurodegeneration.

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)

My data implicates that this modifier of neurodegeneration is working on specific neuronal tissues. Further research is required to understand the exact neuroprotective effect of mechanism, but understanding the tissue localisation of these mechanisms in the future will help researchers develop targeted therapeutic strategies for ageing and neurodegenerative diseases.

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