AGE-MEMORY | Identification of insulin signalling factors that delay age-related memory impairment

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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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

CLOSED

Call topic

MSCA-IF-2015-EF

Update Date

28-04-2024
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Horizon 2020
H2020-EU.1. EXCELLENT SCIENCE
H2020-EU.1.3. EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions (MSCA)
H2020-EU.1.3.2. Nurturing excellence by means of cross-border and cross-sector mobility
H2020-MSCA-IF-2015
MSCA-IF-2015-EF Marie Skłodowska-Curie Individual Fellowships (IF-EF)