Summary
Elucidation of the biological mechanisms that govern ageing can facilitate the discovery of evolutionarily conserved factors, which denominate physiological deterioration in humans. Here we will study the effect of insulin/insulin like growth factor signalling (IIS), shown to delay ageing in several organisms, on age-related memory impairment (AMI). We will use both C. elegans and Drosophila as experimental platforms, to test evolutionarily conservation of findings. Longevity combined with memory experiments will be applied in several IIS mutants. We will dissect IIS to find putative mediators of IIS effects on cognitive function. To identify relative mechanisms we will measure activity of known AMI regulators in IIS mutants. Depending on our results, our study will expand on transcription profiling worms and flies IIS mutants of different ages. Neuronal genes differentially affected by IIS will be further studied. We will use novel imaging techniques to characterize morphological changes that occur through ageing in the nervous system. This study is a first step to identify universal mechanisms that underlay cognitive function decline. Pharmacological manipulation of such mechanisms could delay AMI in humans.
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More information & hyperlinks
Web resources: | https://cordis.europa.eu/project/id/709015 |
Start date: | 01-06-2016 |
End date: | 31-05-2018 |
Total budget - Public funding: | 164 653,20 Euro - 164 653,00 Euro |
Cordis data
Original description
Elucidation of the biological mechanisms that govern ageing can facilitate the discovery of evolutionarily conserved factors, which denominate physiological deterioration in humans. Here we will study the effect of insulin/insulin like growth factor signalling (IIS), shown to delay ageing in several organisms, on age-related memory impairment (AMI). We will use both C. elegans and Drosophila as experimental platforms, to test evolutionarily conservation of findings. Longevity combined with memory experiments will be applied in several IIS mutants. We will dissect IIS to find putative mediators of IIS effects on cognitive function. To identify relative mechanisms we will measure activity of known AMI regulators in IIS mutants. Depending on our results, our study will expand on transcription profiling worms and flies IIS mutants of different ages. Neuronal genes differentially affected by IIS will be further studied. We will use novel imaging techniques to characterize morphological changes that occur through ageing in the nervous system. This study is a first step to identify universal mechanisms that underlay cognitive function decline. Pharmacological manipulation of such mechanisms could delay AMI in humans.Status
CLOSEDCall topic
MSCA-IF-2015-EFUpdate Date
28-04-2024
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