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International Journal of Cell Biology
Volume 2012, Article ID 759583, 11 pages
Review Article

Caloric Restriction and the Nutrient-Sensing PGC-1 in Mitochondrial Homeostasis: New Perspectives in Neurodegeneration

1Department of Biology, University of Rome “Tor Vergata”, Via della Ricerca Scientifica 1, 00133 Rome, Italy
2Research Center, IRCCS San Raffaele La Pisana, Via di Val Cannuta 247, 00166 Rome, Italy

Received 7 May 2012; Accepted 8 June 2012

Academic Editor: Giuseppe Filomeni

Copyright © 2012 Daniele Lettieri Barbato et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondrial activity progressively declines during ageing and in many neurodegenerative diseases. Caloric restriction (CR) has been suggested as a dietary intervention that is able to postpone the detrimental aspects of aging as it ameliorates mitochondrial performance. This effect is partially due to increased mitochondrial biogenesis. The nutrient-sensing PGC-1 is a transcriptional coactivator that promotes the expression of mitochondrial genes and is induced by CR. It is believed that many of the mitochondrial and metabolic benefits of CR are due to increased PGC-1 activity. The increase of PGC-1 is also positively linked to neuroprotection and its decrement has been involved in the pathogenesis of many neurodegenerative diseases. This paper aims to summarize the current knowledge about the role of PGC-1 in neuronal homeostasis and the beneficial effects of CR on mitochondrial biogenesis and function. We also discuss how PGC-1 -governed pathways could be used as target for nutritional intervention to prevent neurodegeneration.