Category Archives: Dr. David Sinclair

UNSW’s Labratory for Ageing Research. Left to right, Lindsay Wu, Myung-Jin Kang, Frank Stoddart, David Sinclair, Ashley Wong, Hassina Massudi. Credit: Britta Campion

Fighting the Aging Process at a Cellular Level

Jonathon Fulkerson
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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Article Here via Medical Xpress

It was about 400 BC when Hippocrates astutely observed that gluttony and early death seemed to go hand in hand. Too much food appeared to ‘extinguish’ life in much the same way as putting too much wood on a fire smothers its flames. If obesity led to disease and death, he thought, then perhaps restraint was the secret to a longer life?

It would be a couple of millennia before science confirmed, in 1935, a link between reducing and living longer. This discovery was just the beginning. In the , further advances have led to an extraordinary leap in ; a child born in Australia today can expect to live at least 25 years longer than a child born a century ago. Yet longer life has also unleashed a cocktail of diseases and , attacking us in tandem, to blight our final years.

Scientists are now increasingly focusing on the biology of ageing itself as the key to warding off this multitude of illnesses. “We currently study diseases in isolation, so we look, for example, at , cancer, diabetes, and Alzheimer’s separately,” said Dr Lindsay Wu, organiser of the recent inaugural Australian Biology of Ageing Conference, hosted by UNSW. “But they all have an underlying process of cellular ageing – so if we are able to treat the biological process of ageing, then we can have a huge impact on all sorts of diseases.”

Significant progress is being made on several frontiers. In New York, a human drug study is for the first time targeting ageing rather than a specific disease. US researchers have also recently managed to kill off age-damaged cells in mice to restore vitality, body function and extend life by up to 35%.

And at UNSW’s Laboratory for Ageing Research, and its sister lab at Harvard Medical School, scientists have identified and isolated a compound found in red wine that has prolonged life and improved health in animals as varied as worms, fruit flies and mice. Lead researcher, David Sinclair – who splits his time between his roles as head of the UNSW Lab and as Professor of Genetics at Harvard – has long been taking the compound himself.

Targeting ageing cells

Australian and international researchers are focusing on two key processes. One promising approach is to target naturally occurring ‘senescent’ cells, the label given to any type of cell as it acquires age-related damage or loss of function. Our immune systems should clear out these cells, but as we age this housekeeping function becomes less and less effective. This means senescent cells accumulate rather than divide, and in turn, they secrete inflammatory agents that can damage adjacent cells, causing the kind of chronic inflammation associated with age-related diseases.

Dr Darren Baker, of the US Mayo Clinic, who was in Australia for the Biology of Ageing conference, and colleagues, recently published their breakthrough results in Nature. Their study demonstrated the elimination of senescent cells in mice not only extended their lives but improved their general health, curiosity and energy levels, with no apparent ill effects.

“What we are thinking about is extending healthy life, not just extending life, per se … we don’t want to increase people’s time in care,” says Baker.

His Mayo Clinic group is now trying to develop components or compounds that can selectively kill senescent cells, without relying on the genetic manipulation used in the mouse study. “If you had asked me five years ago, I would have said we are decades away from human interventions, but we are now moving much faster than we anticipated.”

The loosening of DNA

A second prominent research area focuses on the anti-ageing molecules known as sirtuins, particularly the ‘SIRT1’ enzyme. “When we are young, our DNA is very tightly wound and it’s the SIRT1 molecules that keep this structure intact,” says Wu. “As we age, DNA structure naturally loosens and can turn on the wrong genes, causing dysfunction that can lead to diseases like cancer.” Researchers at UNSW are working on ways to energise the enzyme SIRT1, which Sinclair and his team have been working on for close to two decades, so it works more effectively.

“We think the loosening of DNA is driving whole-of-body ageing, so if we can boost the levels of fuel in our SIRT1 molecules to maintain our DNA in a youthful state, we can slow down ageing,” Wu says.

SIRT1 is also the key to Sinclair’s landmark discoveries about resveratrol, a naturally occurring compound found in red wine. In 2003, Sinclair first demonstrated that resveratrol made SIRT1 run faster and could extend the life of single organisms. In 2013, the prestigious Science journal published his work, proving this single anti-ageing enzyme could be effectively targeted, paving the way for the development of a new class of anti-ageing drug that could potentially prevent some 20 diseases ranging from cancer, to type 2 diabetes and Alzheimer’s disease.

The science of diet and exercise

It has also been uncovered that sirtuins (SIRT3 and 4) are behind the link between longevity and dietary restraint that has fascinated so many thinkers since Hippocrates. In the 1500s, the Venetian nobleman, Alvise Cornaro, famously refined Hippocrates’ theory and experimented on himself, limiting his daily intake of food to 12 oz (340 g) and 14 oz (397 g) of wine. He reportedly lived until 100, attributing his health, vigour and contentment to this regime.

Calorie restriction and exercise are now both known to activate sirtuins, explaining in part the protective nature of a good diet and regular physical activity. However, scientists have also greatly refined the link between diet and longevity. Professor David Le Couteur, from the University of Sydney, told the recent conference that a low-protein, high-carbohydrate diet is associated with a , with nutrients ideally balanced in a ratio of about 1:10. This ratio, he said, correlates with the traditional diet of the people of the Japanese island of Okinawa, famous for its high number of centenarians.

Sinclair is confident human life spans of 150 years are likely in the foreseeable future; other researchers suggest 100 will be more commonly attainable. Although Sinclair’s resveratrol is on the market as a supplement, it has not yet been formulated as an anti-ageing drug. However, the first human trials of a potential anti-ageing drug, metformin, are taking place in the US. Metformin is actually a common anti-diabetes drug that has been in use for some 60 years.

Research has consistently shown many diabetics taking metformin live longer than non-diabetics, even if they have additional risk factors, like being overweight. This association is so pronounced metformin is now being tested as an anti-ageing drug.

There are, however, simple steps everyone can take right now if they want to live longer, healthier lives, says Baker. “If you exercise a lot you have fewer senescent cells, and if you have a decent diet you also see fewer of these cells, so just by modifying your behaviour you can influence your rate of accumulation of these kinds of cells.”

“It is always better to look after yourself … than to just wait for an anti-ageing pill.”

Explore further: Anti-ageing drug breakthrough

More information: Darren J. Baker et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan,Nature (2016). DOI: 10.1038/nature16932

 

Personallity Profile – Dr. David Sinclair – Harvard

Jonathon Fulkerson
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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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Been following Dr. David Sinclair’s work for quite sometime, and although I have not mentioned it as much on here thus far. That changes starting now, for his work was just as influential in my dedication to Anti-Aging science as anyone’s. Thank you Dr. Sinclair.

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Via Harvard.edu  David Sinclair, Ph.D.

David Sinclair, Ph.D. is Co-Director of the Paul F. Glenn Center for the Biology of Aging, a Professor of Genetics at Harvard Medical School, Associate Member of the Broad Institute for Systems Biology, and co-founder of Sirtris Pharmaceuticals, Waltham, MA. Dr. Sinclair’s research aims to identify conserved longevity control pathways and devise small molecules that activate them, with a view to preventing and treating diseases caused by aging. His lab was the first to identify small molecules called STACs that can activate the SIRT pathway and extend lifespan of a diverse species. They also discovered key components of the aging regulatory pathway in yeast and is now focused on finding genes and STACs that extend the healthy lifespan of mice.

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Dr. Sinclair obtained a BS with first-class honors at the University of New South Wales, Sydney, and received the Commonwealth Prize for his research. In 1995, he received a Ph.D. in Molecular Genetics and was awarded the Thompson Prize for best thesis work. He worked as a postdoctoral researcher with Dr. Leonard Guarente at M.I.T. being recruited to Harvard Medical School at the age of 29. Dr. Sinclair has received several additional awards including a Helen Hay Whitney Postdoctoral Award, and a Special Fellowship from the Leukemia Society, a Ludwig Scholarship, a Harvard-Armenise Fellowship, an American Association for Aging Research Fellowship, and is currently a New Scholar of the Ellison Medical Foundation. He’s also won the Genzyme Outstanding Achievement in Biomedical Science Award for 2004.

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Direct Contact

Harvard Medical School
Department of Genetics
77 Avenue Louis Pasteur
Boston MA 02115 USA
Telephone: (617) 432-3931
Fax: (617) 432-6225
Email:
Lab Website: http://genetics.med.harvard.edu/sinclair/

Selected Publications

Howitz, KT., Bitterman, KJ., Cohen, HY., Lamming, DW., Lavu, S., Wood, JG., Zipkin, RE., Chung P., Kisielewski, A., Zhang, L., Scherer, B., Sinclair DA. (2003) Small molecule sirtuin activators that extend S. cerevisiae lifespan.Nature, 425:191-196 PMID: 12939617

Cohen, HY, Miller, C, Bitterman, KJ, Wall, NR, Hekking, B, Kessler, B, Gorospe, M, de Cabo, R.,Sinclair, DA. (2004) Calorie restriction promotes cell survival by inducing SIRT1. Science, 305:390-2. PMID:15205477

Wood, J, Rogina, B, Lavu, S, Howitz, KT, Helfand, SL, Tatar, M, Sinclair, DA. (2004). Sirtuin activators mimic calorie restriction and delay aging in metazoans. Nature, 430:686-9. PMID:15254550

Lamming, D, Latorre-Esteves, M, Medvedik, O, Wong, S.N., Tsang, F.A, Wang, C, Lin, S-J, Sinclair, DA (2005) HST2mediates SIR2-independent lifespan extension by calorie restriction. Science, 309(5742):1861-4. PMID:16051752

Baur, J, Pearson, K., 25 authors, deCabo, R, Sinclair, DA. (2006) Resveratrol increases health and survival of mice on a high calorie diet. Nature 444(16): 337-342. PMID:17086191

Yang, HY, Baur, J and Sinclair DA. (2007) Design and synthesis of SIRT1 activators that extend yeast lifespan. Aging Cell, 6(1):35-43. PMID:17156081

Milne, J., Sinclair, D., Olefsky, J., Jirousek, M, Westphal, C. (2007) Novel Small Molecule Activators of SIRT1 as Therapeutics for Treatment of Type 2 Diabetes. Nature, 450(7170):712-6. PMCID: PMC2753457

Yang, HY, Yang, T, Baur, JA, Perez, E, Matsui, T, Carmona, JJ, Lamming, DW, Souza-Pinto, NC, Bohr, VA, Rosenzweig, A, de Cabo, R, Sauve, AA, Sinclair, DA. (2007) Nutrient-regulated NAD+ levels in mitochondria dictate cell survival. Cell, 130(6):1095-107. PMC336668

Firestein, RA, Blander, G. and Michan, S., Bhimavarapu, A, Luikenhuis, S., de Cabo, R., Hahn, WC, Guarente, LP, and Sinclair, DA. (2008) SIRT1 is a tumor suppressor in a model of colon cancer. 2008; PLoS One, 3(4):2020

Pearson, K*, Baur, J*, Lewis, KN, Peshkin, L, Price, NL. Navas, P., Ingram, D., Wolf, N., Ungvari, Z, Sinclair, DA*, de Cabo, RA* (2008). Resveratrol delays age-related deterioration and mimics aspects of dietary restriction in mice on a standard diet. CellMetabolism, 8(2):157-68. PMC2538685

Oberdoerffer, P., Michan, S. McVay, M. – 8 authors – Mills, K., Bonni, A., Yankner, B., Scully, R., Prolla, TA., Alt, FW. and David A. Sinclair, D. (2008). DNA damage-induced alterations in chromatin contribute to genomic integrity and age-related changes in gene expression. Cell,135(5):907-18. PMCID: PMC2853975

Minor, R., Baur, J, Gomes, A., Price, N., Hubbard, B., Westphal, C., Ellis, J., Vlasuk, G., Sinclair, D.A. deCabo, R. (2011) SRT1720 improves survival and healthspan of obese mice. Nature Reports 1, 70. PMC3216557

Ramadori, G., Fujikawa, T., Anderson, J., Berglund, E.J., Frazao, R., Michan, S., Vianna, C., Sinclair,D.A., Elias, C. and Coppari. R. (2011) SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance. Cell Metabolism, 14(3):301-12 PMC3172583

Price, N.L., Gomes, A.P., Ling, A.J., Martin-Montalvo, A, North, B.J., Hubbard, B.P., Agarwal,B. Davis,J., Varamini, B. Hafner, A., Rolo,A., Palmeira,C.M., de Cabo,R., Baur,J., and Sinclair, D.A. (2012) SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. Cell Metabolism, 15(5): 675-0 PMC2538685

Escande, C., Nin, V., Price, N., Capellini, V., Gomes, A., Barbosa, M.T., O’Neil, L., White, T.A, Sinclair, D.A., Chini, E.N. (2012) The flavonoid apigenin is an inhibitor of the NAD+ase CD38. Diabetes, 62(4):1084-93. PMID: 23172919

Han, J., Hubbard, BP., Lee, J., Montagna, C., Lee, HW., Sinclair, DA., and Suh, Y. (2013) Analysis of 41 cancer cell lines reveals excessive allelic loss and novel mutations in the SIRT1 gene. Cell Cycle, epub. Jan 15. PMID: 23255128

Armour, SM., Bennett, EJ., Braun, CR., Zhang, XY., McMahon, SB., Gygi, SP., Harper, JW., and Sinclair, DA. (2013). A high-confidence interaction map identifies SIRT1 as a mediator of acetylation of USP22 and the SAGA coactivator complex. Molecular Cell Biology, 33(8):1487-502. PMID: 23382074.

Hubbard, BP., Gomes, AP., Dai, H., Li, J., Case, AW., Considine, T., Riera, TV., Lee, JE. E, Sy., Lamming, DW., Pentelute, BL., Schuman, ER., Stevens, LA., Ling, AJ., Armour, SM., Michan, S., Zhao, H., et al., Hamuro, Y., Moss, J., Perni, RB., Ellis, JL., Vlasuk, GP., and Sinclair, DA. (2013). Evidence for a common mechanism of SIRT1 regulation by allosteric activators. Science, Vol. 339: 1216-1219. PMID: 23471411

Biason-Lauber, A., Boni-Schnetzler, M., Hubbard, BP., Bouzakri, K., Brunner, A., Cavelti-Weder, C., Keller, C., Meyer-Boni, M., Meier, DT., Brorsson, C., et al., Sinclair, DA., and Donath, MY. (2013) Identification of a SIRT1 mutation in a family with type 1 diabetes. Cell Metabolism, PMID: 23473037

Lai, L., Yan, L., Gao, S., Hu, CL., Ge, H., Davidow, A., Park, M., Bravo, C., Iwatsubo, K., Ishikawa, Y., Auwerx, J., Sinclair, DA, Vatner, SF., and Vatner, DE. (2013) Type 5 adenylyl cyclase increases oxidative stress by transcriptional regulation of manganese superoxide dismutase via the SIRT1/FoxO3a pathway. Circulation, PMID: 23526361

Sinclair, DA. (2013) Studying the Replicative Life Span of Yeast Cells in Biological Aging. Ed. Trygve Tollesbol. Springer, NY, USA.Hubbard BP, Loh C, Gomes AP, Li J, Lu Q, Doyle TL, Disch JS, Armour SM, Ellis JL, Vlasuk GP, Sinclair DA. (2013) Carboxamide SIRT1 inhibitors block DBC1 binding via an acetylation-independent mechanism.Cell Cycle. 20;12(14). PMID: 23797592

Tilly, JL. and Sinclair, DA. (2013) Germline energetics, aging, and female fertility. Cell Metabolism, 17(6):838-50. NIHMS 482422

Martin-Montalvo, A., 23 authors, Sinclair, D.A., Wolf, N.A., Spindler, S., Bernier, M. and de Cabo, R. (2013) Metformin improves healthspan and lifespan in mice. Nature Communications, in press

Chen, J., Michan, S., Juan, A., Hurst, CG, Hatton CJ, Pei, DT, Joyal, J, Evans, LP, Cui, Z, Stahl, A., Sapieha, P, Sinclair, DA, Smith, LEH. (2013) Neuronal sirtuin1 mediates retinal vascular regeneration in oxygen-induced ischemic retinopathy. Angiogenesis, in press.

Hua, J., Guerin, K., Chen J., Michan, S., Stahl, A., Krah, N., Seaward, M., Dennison, R., Juan, A., Hatton, C., Sapieha, P., Sinclair, D.A., Smith, L. (2013) Resveratrol inhibits pathological retinal neovascularization in vldlr-/-mice. Angiogenesis, in press.

Schmeisser, K., Mansfeld, J., Kuhlow, D., Weimert, S., Zarse, K., Prieve, S., Heiland, I. Birringer, M., Groth, M., Segref, A., Werner, C., Schmeisser, S., Schuster, S., Pfeiffer, A., Guthke, R., Platzer, M., Hoppe, T., Cohen, C., Sinclair, D.A., Ristow, M. (2013) Theniacin metabolite 1-mthylnicotinamide extends lifespan in a PARP/sirtuin-dependent manner by including a transient redox signal. Nature Chemical Biolog in press.

Santos Franco S, De Falco L, Ghaffari S, Brugnara C, Sinclair DA, Mattè A, Iolascon A, Mohandas N, Bertoldi M, An X, Siciliano A, Rimmelé P, Cappellini MD, Michan S, Zoratti E, Janin A, De Franceschi L. Resveratrol accelerates erythroid maturation by activation of FOXO3 and ameliorates anemia in beta-thalassemic mice. 2013.Haematologica. Aug 23

Hubbard BP and Sinclair DA. Measurement of sirtuin enzyme activity using a substrate-agnostic fluorometric nicotinamide assay. Methods Mol Biol. 2013;1077:167-77

Sinclair DA. Studying the replicative life span of yeast cells. Methods Mol Biol. 2013;1048:49-63.

Chen J, Michan S, Juan AM, Hurst CG, Hatton CJ, Pei DT, Joyal JS, Evans LP, Cui Z, Stahl A, Sapieha P, Sinclair DA, Smith LE. Neuronal sirtuin1 mediates retinal vascular regeneration in oxygen-induced ischemic retinopathy.Angiogenesis. 2013;16(4):985-92

Sinclair D.A. and Guarente, L. Small molecule activators of sirtuins for the treatment of age-related diseases. Annual Revews Phramacol. Sci. 2013. 54:363-80.

Hubbard and Sinclair, D.A. Small molecule sirtuin activators. J. Experimental Medicine (2013) In press.

Hubbard BP, Sinclair DA. Measurement of sirtuin enzyme activity using a substrate-agnostic fluorometric nicotinamide assay. Methods Mol Biol. 2013, 1077:167-77.

Sinclair D.A. and Guarente, L. Small molecule activators of sirtuins for the treatment of age-related diseases.Annual Revews Pharmacol. Sci. (2013) 54:363-80.

Hubbard and Sinclair, D.A. Small molecule modulators of sirtuins. Trends in Pharmacol Sci (2014), in press.

Michan, S., Juan, A.M., Hurst, C.G., Cui, Z., Evans, L.P., Hatton, C.J., Pei, D.T., Ju, M., Sinclair, D.A., Smith, L.E.H., Chen, J. Sirtuin1 over-expression does not impact retinal vascular and neuronal degeneration in a mouse model of oxygen-induced retinopathy. PLoS One 2013, 9(1):e85031.

Strong R, Miller RA, Astle CM, Baur JA, de Cabo R, Fernandez E, Guo W, Javors M, Kirkland JL, Nelson JF, Sinclair DA, Teter B, Williams D, Zaveri N, Nadon NL, Harrison DE. Evaluation of resveratrol, green tea extract, curcumin, oxaloacetic acid, and medium-chain triglyceride oil on life span of genetically heterogeneous mice. Gerontol A Biol Sci Med Sci. 2013 68(1):6-16. PMID: 22451473

Gomes, A.P., Price N.L., Lin A.Y, Moslehi, J., Montgomery, M., Rajman, L., White, J.P., Teodoro, J.S., Wran, C.D., Hubbard, B.P., Mercken, E.M., Palmeira, C., de Cabo, R., Rolo, A.P., Turner, N., Bell, E. and Sinclair, D.A. Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell 2013 155(7):1624-38.

Wu, E.W., Gomes, A.P. and Sinclair, D.A. Geroncogenesis: Metabolic changes during aging as a driver of tumorigenesis. 2014. Cancer Cell, 25:12-19

Yoon, C., Ling, A.Y., Isik, M., Lee, D.D., Steinbaugh, M.J., Sack, L., Boduch. A.N., Blackwell, T.B., Sinclair, D.A*, Elledge, S.J.* GLTSCR2/PICT1 links mitochondrial stress and Myc signaling. Proc. Natl. Acad. Sci., 2014, 111(10):3781-6.

The Sirt1 activator SRT3025 provides atheroprotection in Apoe-/- mice by reducing hepatic Pcsk9 secretion and enhancing Ldlr expression. Miranda MX, van Tits LJ, Lohmann C, Arsiwala T, Winnik S, Tailleux A, Stein S, Gomes AP, Suri V, Ellis JL, Lutz TA, Hottiger MO, Sinclair DA, Auwerx J, Schoonjans K, Staels B, Lüscher TF, Matter CM.Eur Heart J. 2015 Jan 1;36(1):51-9.

Mitchell SJ, Martin-Montalvo A, Mercken EM, Palacios HH2, Ward TM2, Abulwerdi G2, Minor RK, Vlasuk GP, Ellis JL, Sinclair DA, Dawson J, Allison DB, Zhang Y, Becker KG Bernier M, de Cabo R. The SIRT1 Activator SRT1720 Extends Lifespan and Improves Health of Mice Fed a Standard Diet. Cell Rep. 2014 Feb 25.

Mercken, EM*, Mitchell, SJ*, Martin-Montalvo, A,1 Minor, RK, Almeida, M., Gomes, A., Scheibye-Knudsen, M., Palacios, H., Licata, JJ, Zhang, Y, Becker, K.G. Khraiwesh, H., Gonzalez-Reyes, J., Villalba, JM, Baur, JA, Vlasuk, G, Ellis, JL, Sinclair, DA, Bernier, M, and de Cabo, R. SRT2104 extends survival of male mice on a standard diet and preserves bone and muscle mass. Aging Cell 2014, in press

Solon-Biet SM, McMahon AC, Ballard JW, Ruohonen K, Wu LE, Cogger VC, Warren A, Huang X, Pichaud N, Melvin RG, Gokarn R, Khalil M, Turner N, Cooney GJ, Sinclair DA, Raubenheimer D, Le Couteur DG, Simpson SJ. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice.Cell Metab. 2014 Mar 4;19(3):418-30.

North BJ, Rosenberg MA, Jeganathan KB, Hafner AV, Michan S, Dai J, Baker DJ, Cen Y, Wu LE, Sauve AA, van Deursen JM, Rosenzweig A, Sinclair DA. SIRT2 induces the checkpoint kinase BubR1 to increase lifespan. EMBO J.2014 May 12.

Rimmelé P, Bigarella CL, Liang R, Izac B, Dieguez-Gonzalez R, Barbet G, Donovan M, Brugnara C, Blander JM, Sinclair DA, Ghaffari S. Aging-like phenotype and defective lineage specification in SIRT1-deleted hematopoietic stem and progenitor cells.

Gomes AP, Sinclair DA. Measuring PGC-1α and its acetylation status in mouse primary myotubes. Methods Mol Biol.2015;1241:49-57.

Moroz N, Carmona JJ, Anderson E, Hart AC, Sinclair, DA, Blackwell TK. Dietary restriction involves NAD⁺-dependent mechanisms and a shift toward oxidative metabolism. Aging Cell. 2014 Dec;13(6):1075-85.

RB2015 Rejuvenation Biotechnology Conference Aug 19-21

Jonathon Fulkerson
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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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RB2015

WHO ATTENDS

  • Academic Researchers
  • Pharmaceutical and Biotech Industry
  • Undergrad, Graduate and Post Doctorial Students
  • Nonprofits
  • Regulatory
  • Investors
  • The General Public

WHY ATTEND

  • Focused tracks covering three key elements of successful drug development: clinical review, therapeutic approaches, industry and policy
  • In depth examination of advances in tissue engineering and gene therapy
  • More interactivity – 6 hours of interactive discussion sessions and 17 hours of networking
  • Jobs Board – review and share the expertise needs of the industry’s leading research and development organizers
  • Understand and shape the scientific and investment opportunities of the new Rejuvenation Biotechnology Industry
  • Extended poster sessions
  • Back by popular demand – our opening evening’s entertainment will be Hal Sparks – Comedian, Actor and Musician.

Early Results of Human Trials For Anti-Aging Drug Are Promising

Jonathon Fulkerson
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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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From http://www.iflscience.com/health-and-medicine/preliminary-results-early-human-trials-anti-aging-formulas-reveal-no-adverseanti aging (1)

David Sinclair of Harvard University has been working toward a molecular fountain of youth. Finding previous success in mice, early human trials have begun in small studies around the globe. Preliminary results of these studies indicate that the treatments are safe and do not induce major adverse side effects, but it is still far too early to tell if the treatments will actually be effective at reversing aging in humans.

A normal part of human aging involves senescence, which is a general wearing out of the body over time. Muscles begin to lose tone and become inflamed over time, and they also can develop insulin resistance. Without being able to use insulin, the cells aren’t able to uptake the glucose needed for activity. These problems contribute to why many elderly people have trouble getting around and athletes aren’t able to sustain certain levels of activity as they age.

Last December, Sinclair’s group published a paper in Cell revealing that they had been able to drastically reduce the functional “age” of muscle tissue. Treating the mice with the metabolic co-enzyme NAD+ effectively reversed the aging process within the skeletal muscle by increasing muscle tone and producing effects similar to eating a healthy diet and exercising.

Over time, NAD+ levels decrease, which limits the cells’ ability to produce ATP in the mitochondria for energy. As the mice grew older and less active, their levels of NAD+ had basically been cut in half. By replenishing this critical compound in the mice, their muscles had been rejuvenated. The natural process that deteriorates skeletal muscle is the same one that affects the heart.

If the relative effects that were seen in the mice could be replicated in humans, it would result in a 60-year-old with the physique of a 20-year-old. The human studies that began this year following a period of financial uncertainty are initially only auditing the treatment’s safety, by taking stock of all side effects that could occur and identify negative interactions with other medications. The first studies have been fairly small, but will continue to grow.

Results from human studies that explore the treatment’s efficacy will not appear for a few more years, though Sinclair is optimistic. He told ABC that this treatment has the potential to allow individuals to lead long, healthy lives. He described the potential of his anti-aging therapy to one day be regarded similarly and ubiquitously as antibiotics.

“Some people say it’s like playing God, but if you ask somebody 100 years ago, what about antibiotics? They probably would have said the same thing,” he told ABC’s Sue Lannin. “Some people worry about big advances in technology and medicine, but once it’s adapted and it’s natural for people to live until they’re 90 in a healthy way … we’ll look back at today like we do at the times before antibiotics when people died from an infected splinter.”