Potential Therapeutic Targets for Neurodegenerative Diseases: Lessons Learned from Calorie Restriction
Wenzhen Duan and Christopher A. Ross
Affiliation: Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine. CMSC 8-121, 600 N. Wolfe Street, Baltimore, MD 21287, USA.
Keywords: Calorie restriction, neurodegeneration, sirtuins, neurotrophin, PPAR, chaperone proteins, autophagy, Yeast, Non-human primates, Signaling pathways, Neuroprotection, Calorie restruction, PPARs, Biomarkers, Meal frequency, Glucose tolerance, Triiodothyronine, Alzheimer's disease, Parkinson's disease, Stroke, Substantia nigra, Cerebral occlusion, Huntington's disease, Amyotrophic lateral sclerosis, Calorie intake, Aging, C. elegans, Drosophila, Wallerian degeneration, p53, FOXO, PGC-1α, HSF1, Ku70, Calorie mimetics, NGF, BDNF, GDNF, Mitochondria, Antioxidant, Reservatrol, Multiple sclerosis, Rapamycin, CR mimetics
It is well known that calorie restriction (CR) can retard the aging process in organisms ranging from yeast to non-human primates, and delay the onset of numerous age-related diseases including neurodegenerative disorders. Translation of the knowledge gained from CR research in animal models to disease prevention strategies in humans should provide therapeutic approaches for these diseases. Signaling pathways induced by CR are therefore potentially new therapeutic targets for neurodegenerative diseases. This review summarizes the evidence on key biological mechanisms underlying the beneficial effects of CR based on our current understanding, with particular emphasis on the recent impact of CR on neuroprotection, and on the emerging development of pharmacological agents that target signaling pathways induced by CR. We focus in particular on recent findings on sirtuins for prevention of neurodegenerative diseases.
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