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Scientists' Open Letter on Aging Research

To whom it may concern,

Aging has been slowed and healthy lifespan prolonged in many disparate animal models (C. elegans, Drosophila, Ames dwarf mice, etc.). Thus, assuming there are common fundamental mechanisms, it should also be possible to slow aging in humans.

Greater knowledge about aging should bring better management of the debilitating pathologies associated with aging, such as cancer, cardiovascular disease, type II diabetes, and Alzheimer's. Therapies targeted at the fundamental mechanisms of aging will be instrumental in counteracting these age-related pathologies.

Therefore, this letter is a call to action for greater funding and research into both the underlying mechanisms of aging and methods for its postponement. Such research may yield dividends far greater than equal efforts to combat the age-related diseases themselves. As the mechanisms of aging are increasingly understood, increasingly effective interventions can be developed that will help prolong the healthy and productive lifespans of a great many people.

Sincerely (56 Signatories),


Signatures From Leading Aging Researchers

Signatures From Additional Leading Scientists

Publications on the Plasticity of Aging

  • 2005 Advances in understanding aging processes and their consequences are leading to the development of therapies to slow or reverse adverse changes formerly considered to be "normal" aging and processes that underlie multiple age-related conditions. Estimating the effectiveness of candidate aging therapies, whose effects on human aging may require many years to determine, is a particular challenge. Evan C. Hadley, Edward G. Lakatta, Marcelle Morrison-Bogorad, Huber R. Warner, and Richard J. Hodes; Cell, Vol 120, 557-567, 25 February 2005.

  • 2005 Mutations in genes affecting endocrine signaling, stress responses, metabolism, and telomeres can all increase the life spans of model organisms. The Plasticity of Aging: Insights from Long-Lived Mutants. Cynthia Kenyon. Cell, Vol 120, 449-460, 25 February 2005.
  • 2004 Ames dwarf mice (Prop1df/df) and Little mice (Ghrhrlit/lit) are used as models of delayed aging and show significant increases in lifespan (50% and 25%, respectively) when compared with their wild-type siblings. Amador-Noguez D, Yagi K, Venable S, Darlington G. Aging Cell. 2004 Dec;3(6):423-41.
  • 2004 In humans, long-term calorie restriction is highly effective in reducing the risk for atherosclerosis. Fontana L, Meyer TE, Klein S, Holloszy JO. Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6659-63.
  • 2003 In RNAi-treated C. elegans, when the reproductive systems is removed, they lived six times as long as normal. Whereas the mean life-span of wild type was 20 days, these animals had mean life-spans of 124 days. Healthy animals with extreme longevity. Arantes-Oliveira N, Berman JR, Kenyon C. Science. 2003 Oct 24;302(5645):611.
  • 2003 In yeast (S. cerevisiae), overexpression of PNC1 extends the replicative life span by 70% in a Sir2-dependent manner. Kevin J. Bitterman, Oliver Medvedik, and David A. Sinclair; Microbiol Mol Biol Rev. 2003 September; 67(3): 376-399.
  • 2003 In humans, Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by features reminiscent of marked premature ageing. The discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing. Eriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, Scott L, Erdos MR, Robbins CM, Moses TY, Berglund P, Dutra A, Pak E, Durkin S, Csoka AB, Boehnke M, Glover TW, Collins FS. Nature. 2003 May 15;423(6937):293-8.

  • 2002 Indefinite postponement of aging - which we term "engineered negligible senescence" - may be within sight. Given the major demographic consequences if it came about, this possibility merits urgent debate. Time to Talk SENS: Critiquing the Immutability of Human Aging; Aubrey D. N. J. de Grey, Bruce N. Ames, Julie K. Andersen, Andrzej Bartke, Judith Campisi, Christopher B. Heward, Roger J. M. McCarter and Gregory Stock; Annals of the New York Academy of Sciences 959:452-462 (2002)
  • 2001 Mutant mice with a combined deficiency of growth hormone (GH), prolactin, and thyrotropin, and knockout mice with GH resistance, live longer than their normal siblings. The extension of life span in these animals is very large (up to 65%), reproducible, and not limited to any particular genetic background or husbandry conditions. Bartke A, Coschigano K, Kopchick J, Chandrashekar V, Mattison J, Kinney B, Hauck S. J Gerontol A Biol Sci Med Sci. 2001 Aug;56(8):B340-9.
  • 2001 Mice homozygous for loss-of-function mutations at the Pit1 (Snell dwarf) locus show a >40% increase in mean and maximal longevity on the relatively long-lived (C3H/HeJ x DW/J)F(1) background. Findings demonstrate that a single gene can control maximum lifespan and the timing of both cellular and extracellular senescence in a mammal. Flurkey K, Papaconstantinou J, Miller RA, Harrison DE. Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6736-41.
  • 2000 In Drosophila, five independent P-element insertional mutations in a single gene resulted in a near doubling of the average adult life-span without a decline in fertility or physical activity. Rogina B, Reenan RA, Nilsen SP, Helfand SL.; Science. 2000 Dec 15;290(5499):2137-40.
  • 1999 In mice, suppression of p66shc protein extends the life span by 30%. Migliaccio E, Giorgio M, Mele S, Pelicci G, Reboldi P, Pandolfi PP, Lanfrancone L, Pelicci PG.; Nature. 1999 Nov 18;402(6759):309-13.
  • 1998 Low caloric intake (caloric restriction) can lengthen the life span of a wide range of animals and possibly even of humans. Specific mutations significantly lengthen life span by up to 50%. Lakowski B, Hekimi S.; Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13091-6.
  • 1998 In Drosophila, overexpression of a single gene, SOD1, in a single cell type, the motorneuron, extends normal lifespan by up to 40% and rescues the lifespan of a short-lived Sod null mutant. Parkes TL, Elia AJ, Dickinson D, Hilliker AJ, Phillips JP, Boulianne GL.; Nat Genet. 1998 Jun;19(2):171-4.
  • 1993 Mutations in the gene daf-2 can cause C. elegans to live more than twice as long as wild type. Kenyon, C.J., Chang, Gensch, E., J. Rudner, A. and Tabtiang, R.; Nature. 1993 Dec 2;366(6454):461-4.

CureAging.org: Independent Open Letter in Support of Aging Research

Email support@cureaging.org for information on adding signatures, etc.

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  Дата публикации: 25.02.2006  
 

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