Coordinatore | MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | Germany [DE] |
Totale costo | 2˙489˙200 € |
EC contributo | 2˙489˙200 € |
Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | ERC-2010-AdG_20100317 |
Funding Scheme | ERC-AG |
Anno di inizio | 2011 |
Periodo (anno-mese-giorno) | 2011-06-01 - 2016-05-31 |
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1 |
MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Organization address
address: Hofgartenstrasse 8 contact info |
DE (MUENCHEN) | hostInstitution | 2˙489˙200.00 |
2 |
MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Organization address
address: Hofgartenstrasse 8 contact info |
DE (MUENCHEN) | hostInstitution | 2˙489˙200.00 |
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'The diseases of older age are a major challenge to human societies. Despite the complexity of ageing, both reduced food intake (dietary restriction) and simple genetic alterations can greatly increase lifespan and provide broad-spectrum protection against diseases of ageing in laboratory animals. Furthermore, there is strong evolutionary conservation of mechanisms. For instance the nutrient-sensing insulin/IGF and TOR signalling network modulates lifespan in yeast, invertebrates and rodents. There is thus a major scientific opportunity to use model organisms to discover how to ameliorate ageing and hence to protect against ageing-related disease in humans. Our recent findings on dietary amino acid balance in the fruit fly Drosophila imply that consumption of nutrients irrelevant to metabolism is life-shortening. Using a novel genomic approach, we shall determine if the same is true in mice and measure the role of dietary imbalance in extension of lifespan by dietary restriction. Late life dietary restriction in invertebrates can increase future survival as much as permanent restriction, implying that chemical mimetics administered late in life could also be fully effective. We shall determine if dietary restriction in mice has similarly acute effects, and use dietary switches to identify candidate mechanisms of increased health and lifespan. Recent evidence has pointed to particular components of nutrient-sensing pathways as promising drug targets for prevention of age-related disease, and we shall investigate two candidates. The work will break new ground in understanding how ageing is modulated by diet and signaling pathways and point to interventions that could protect against the effects of ageing to reduce the burden of ageing-related disease in humans.'