Life Extension Magazine®

Silhouette of people sitting at table for 2016 aging conference

2016 Conferences on Aging

Scientists are not only discovering new ways to slow biological aging, but data revealed at recent conferences has uncovered potential methods to reverse it.

Scientifically reviewed by Dr. Gary Gonzalez, MD, in August 2023. Written by: Ben Best, BS, Pharmacy.

Ben Best
Ben Best

Aging is damage to tissues and organs that accumulates with time.

There is no single cause of aging, because there are many sources of damage and many kinds of damage. There may be, however, ways to address many of these causes with perhaps one or more therapies.1

Inflammatory factors in the bloodstream increase with age. This chronic inflammation is a cause of cancer and damage to organs and tissues. A major source of this inflammation is cells that cease dividing, a condition known as cellular senescence. Senescent cells secrete inflammatory cytokines, cancer-inducing growth factors, and other harmful substances.

Cellular senescence is caused by DNA damage, shortened chromosome ends (telomeres), and other factors. Cellular senescence and inflammation can result in stem cells ceasing to function. Healthy stem cells heal injuries and replace worn-out cells in the intestines, the skin and the blood (including the white blood cells that provide immunity).2

In 2016, I attended several conferences dealing with aging. In contrast to earlier conferences, I was impressed by how much researchers are now not only discovering new causes of aging or means to slow it, but are also finding ways to reverse aging and significantly extend mammalian life spans.

Interventions Testing Program

Randy Strong, PhD
Randy Strong, PhD

Randy Strong, PhD (professor of pharmacology, University of Texas Health Science Center, San Antonio) is one of the Directors of the National Institute on Aging’s Interventions Testing Program (ITP). The ITP tests potential anti-aging substances on mice at three independent laboratories: the University of Texas, the University of Michigan, and the Jackson Laboratory in Maine.3,4

The ITP has been able to report lifespan benefits for a number of substances, but often these were effective only in male mice. Median (but not maximum) lifespan was increased for males by 12% with the antioxidant (nordihydroguaiaretic acid),5 by 8% with aspirin,5 and by 7% using a proprietary blend of milk thistle, bacopa, ashwagandha, green tea, and turmeric extracts.6

Interestingly, an estrogen (17-alpha-estradiol) increased median lifespan by 19% and maximum lifespan by 12% in male mice.6

The antidiabetic drug acarbose increased male mouse median lifespan by 6% and maximum lifespan by 12%, most likely by reducing the amount of glucose absorbed into the bloodstream.6

For female mice, acarbose increased median lifespan by 2% and maximum lifespan by 6%.6

ITP showed rapamycin increased median and maximum lifespan in both male and female mice.7 Insulin resistance and impaired glucose tolerance are associated with poor health and reduced lifespan. Rapamycin has these side effects.8 The combination of metformin and rapamycin increased median lifespan by 23% in both male and female mice.6

Rapamycin as an Anti-Aging Drug

Matt Kaeberlein, PhD
Matt Kaeberlein, PhD

Matt Kaeberlein, PhD (professor of pathology, University of Washington, Seattle) wants to validate rapamycin as an anti-aging drug. In 2009, rapamycin was shown to increase median and maximal lifespan of mice when given at 20 months of age (about equivalent to the age of a 60-year-old human).7 No additional lifespan extension was seen by beginning the rapamycin at 9 months of age, and the earlier (more lengthy) dosing increased the incidence of cataracts and testicular degeneration.9 A three-fold increase in the dose of rapamycin, however, approximately doubled the lifespan extension of 9-month-old mice.10

Rapamycin reduces inflammation, especially in the heart,11,12 and inhibits cells from becoming senescent.13 Rapamycin increases cognitive function in mice.14 A rapamycin-like drug improved the response to influenza vaccination in elderly humans.15

Dr. Kaeberlein’s team showed that a 3-month rapamycin treatment of 20-month-old mice could increase life expectancy by at least 50%.16 Although this experiment indicates that brief exposure (in human time frame) to rapamycin in elderly mice could have substantial long-term benefit, the required dosing period for humans to show a comparable benefit would probably be considerably longer.17

Dr. Kaeberlein believes that substantial benefit without serious side effects can result from large doses of rapamycin given for brief periods.18 He maintains that this prospect is best tested in middle-aged large companion-animal (pet) dogs, because these dogs age about seven times more rapidly than humans.19 He has been actively recruiting owners of pet dogs for participation in this research using the website

Sirtuins and NAD+ for Rejuvenation

David Sinclair, PhD
David Sinclair, PhD

David Sinclair, PhD (professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biological Mechanisms of Aging, Boston, Massachusetts) has been a pioneer in studying the sirtuin anti-aging proteins, as well as substances that activate those proteins (such as resveratrol).20

Sirtuin activators that are hundreds of times more powerful than resveratrol increase insulin sensitivity, and have therefore been proposed as a treatment for type II diabetes.21 Powerful sirtuin-activators have also been shown to improve the general health and lifespan of mice fed a normal diet.22 Sirtuins can rejuvenate cells by stimulating the recycling of damaged cellular components (autophagy).23

Sirtuins require the substance NAD+ to function. Sirtuins are important for DNA repair and for efficient function of the energy-producing cellular organelles, mitochondria.24

NAD+ declines with age because an enzyme in inflammatory cells that destroys NAD+ increases with age.25 Reducing inflammation, inhibiting the inflammatory enzyme, and replacing NAD+ by supplementing with substances (such as nicotinamide riboside) that lead to NAD+ formation, can restore the benefits of sirtuin and NAD+ (improved insulin sensitivity, mitochondrial function, and DNA repair).25 Moreover, NAD+ restoration rejuvenates stem cells, improving the regenerative capacity of organs and tissues.26

Two-Year Study of Calorie Restriction in Normal Humans

Evan Hadley, MD
Evan Hadley, MD

Evan Hadley, MD (Director of the Division of Geriatrics and Clinical Gerontology, National Institute on Aging, Bethesda, Maryland) reported on the two-year clinical trial conducted by the National Institute on Aging to determine the effects of calorie restriction on healthy, non-obese adults between the ages of 21 to 50.

Calorie restriction with adequate nutrition (CR) has been shown to increase health and lifespan in a wide variety of organisms, but the benefits have been difficult to prove for humans.27

Subjects in the clinical trial were volunteers randomized to either eat normally or restrict calories by 25%. Average body mass index (BMI) for the subject was 25.1 (on the border between normal and overweight). 218 volunteers began the study, with 82% of the CR group and 95% of the normally eating group completing the two-year study.28

The CR group was able to reduce calories by 19.5% during the first six months, but only by an average of 9.1% for the following 18 months.28 The CR group showed significant reduction of blood cholesterol, triglycerides, and TNF-alpha (an inflammatory protein).28 The stress hormone cortisol was only elevated for the first year.29 The study showed improved quality of life and no harmful outcomes for those in the CR group.30,31

Elimination of Senescent Cells for Rejuvenation

Norman Sharpless, MD
Norman Sharpless, MD

Norman Sharpless, MD (professor of medicine & genetics, University of North Carolina) is concerned with how senescent cells contribute to aging, and with means to eliminate senescent cells. Senescent cells cease dividing due to various defects, including short telomeres. Senescent cells produce inflammatory factors which can trigger their removal by the immune system.2

With age, the immune system becomes increasingly incapable of removing senescent cells, which become a major source of chronic inflammation.32 Chronic inflammation can lead to cancer.33 Senescent cells impair the function of the tissues and organs in which they occur.34 These cells have been shown to accelerate aging in mice (reducing health and shortening lifespan).35

To eliminate senescent cells requires differentiating them from healthy cells in tissues. Unfortunately, there are no markings that are consistently specific to senescent cells as opposed to healthy ones.36

Dr. Sharpless has focused his attention on a protein called p16, which is often seen on senescent cells. He has found that p16 in human body cells increases tenfold over 60 years of adult aging.37 He has found that increased p16 is seen in many aging-associated diseases, including atherosclerosis, diabetes, neurodegeneration, frailty, cancer, and cataracts,38 and that p16 indicates reduced stem cell function.39

Dr. Sharpless has shown increased p16 in smokers40 and patients receiving chemotherapy.41

Injecting mice with a drug that eliminates cells having p16 has been shown to improve function of many organs, including kidney and heart, while increasing lifespan.34 Upregulation of anti-apoptotic proteins is often seen in senescent cells. Targeting cells by inhibiting anti-apoptotic proteins has also been shown to eliminate senescent cells in mice.42

Using the herbal product quercetin and the anticancer drug dasatinib for targeting yet other (non-p16) features of senescent cells has been shown to eliminate senescent cells in mice, improving function in the heart and blood vessels.43

Telomere Lengthening for Rejuvenation

Maria Blasco, PhD
Maria Blasco, PhD

Maria Blasco, PhD (director, Spanish National Centre for Cancer Research, Madrid, Spain) is one of the world’s foremost authorities on the role of telomeres in cancer and aging. Her pro-life extension attitude can be seen in her recent Spanish-language book for laypeople: Dying Young at 140.

Telomeres are repeating DNA sequences that protect the ends of chromosomes the way the caps of shoelaces prevent the laces from fraying. Telomeres shorten each time a cell divides. When telomeres have become too short, the cell usually dies or becomes senescent. Longer telomeres can indicate good health.44

People with short telomeres or high rates of telomere shortening have triple the rate of death from cardiovascular disease.45 People over age 100 with longer telomeres have better cognitive function and fewer age-related diseases.46


Telomeres are lengthened by the enzyme telomerase, which is very active early in fetal development, but absent in most adult cells, the exception being stem cells, where some telomerase is present. But even in stem cells, telomerase activity is inadequate to maintain telomere length.44

Short stem cell telomeres result in insufficient replacement of blood cells,47 brain cells,48 and many other tissues.

Dr. Blasco believes that telomere shortening is a major cause of aging,49 because of loss of stem cell function, loss of cells, increased numbers of senescent cells, and the inflammation produced by senescent cells.50 But she also believes that aging due to telomere loss is reversible.51

Most cancer cells become immortal (prevent themselves from aging) by activating telomerase, and the severity of the cancer often corresponds to the amount of telomerase activity.52

Dr. Blasco’s research team achieved a 24% increase in the lifespan of one-year-old mice by delivering a telomerase gene using a virus that does not incorporate the gene into chromosomes.53 There was no increase in cancer.53 Her team has also used the virus to deliver telomerase genes to increase survival of mice suffering from aplastic anemia,54 and of mice who have suffered a myocardial infarction (heart attack).55

Factors from Young Blood to Rejuvenate the Elderly

Thomas Rando, MD, PhD
Thomas Rando, MD, PhD

Thomas Rando, MD, PhD (professor of neurology, Stanford University Medical Center, Stanford, California) supervised a landmark 2005 study which joined the circulatory system of young and old mice (parabiosis).56

The parabiosis experiment showed that the blood of young mice rejuvenated muscle stem cells in old mice, enhancing muscle regeneration after injury.56 But in the young mice, the stem cells lost some of their regenerative potential from exposure to “old” circulating blood.57

One of the students at the time conducting that experiment (Irina Conboy) later showed that the social bonding hormone oxytocin declines with age and contributes to muscle stem cell rejuvenation in old mice.58 She also showed that the growth factor TGF-beta produced by old muscle cells inhibits muscle stem cell function.59

Another student at the time who had participated in the breakthrough 2005 parabiosis study (Amy Wagers) later showed that the growth factors GDF11 and GDF8 (myostatin) decline with age and rejuvenate old mice when administered to them.60

Dr. Rando himself went on to show that repeated injections of young blood plasma improve cognitive function in old mice.61 He also showed that inflammatory factors in the blood that increase with age, such as CCL11 caused reduction in stem cell activity.62

Proposed Clinical Trial with Young Blood Factors

Dipnarine Maharaj, MD
Dipnarine Maharaj, MD

Dipnarine Maharaj, MD (medical director, South Florida Bone Marrow/Stem Cell Transplant Institute, Boynton Beach, Florida) believes that increasing chronic inflammation as a consequence of aging causes decreasing function of stem cells, thereby impairing the function of bodily organs and tissues.

A study of elderly adults showed that high levels of chronic inflammation were highly predictive of low cognition, low bodily function, and a higher likelihood of impending death.63 Most of the aging-related diseases (cancer, heart disease, stroke, Alzheimer’s disease, arthritis, diabetes, etc.) are associated with chronic inflammation.64

Impairment of stem cell function reduces the ability of body tissues and organs to heal wounds and prevent impaired function due to cell depletion.65 Elderly people become frail not only with respect to weak muscles and bones, but because of a frail brain, frail hormonal system, and frail immune system.66

Adjoining the circulatory system of young mice to old mice (parabiosis) has shown rejuvenation of the old mice due to blood components of the young mice restoring stem cell function in the old mice.67

Dr. Maharaj wants to conduct clinical trials that demonstrate rejuvenation of elderly humans by infusion of stem cell-mobilized plasma from young, healthy humans. He has patented the procedure he would use in these clinical trials (patent 2014/0336443).

His procedure involves stimulating bone growth with oscillating magnetic fields, mobilizing stem cells from young donors by administering G-CSF (granulocyte-colony stimulating factor),68 infusing plasma (not blood cells) containing growth factors mobilized by the G-CSF from the young donors into elderly subjects, and then assessing the youthfulness of the elderly subjects using eight biomarkers. The biomarkers include measures of inflammation, insulin sensitivity, telomere length, etc.

A Method to Evaluate Rejuvenation Therapies

Steve Horvath, PhD, ScD
Steve Horvath, PhD, ScD

Steve Horvath, PhD, ScD (professor, Human Genetics and Biostatistics, University of California, Los Angeles) has noticed that the addition of methyl groups to DNA increases with age (a process known as epigenetic change). Analyzing 7,844 samples of healthy human tissues, he developed a method of estimating chronological age that is 96% correct.69 Dr. Horvath believes that his method could be useful in evaluating rejuvenation therapies.69

His method demonstrates accelerated aging in HIV infection,70 Parkinson’s disease,71 Down’s syndrome,72 and obesity.73 His method also predicts impending death from any cause.74

Applying his method to the offspring of persons close to 105 years of age, he found the offspring to have an “epigenetic age” about five years younger than age-matched controls.75-77

Age Reversal Funding Options

1) To invest in the fund dedicated to rapidly developing age-reversal therapies, log onto: or call 1-866-554-7108 (24 hours) or email our Chief Operating Officer at:

2) To make a tax deductible donation to exclusively support human age-reversal research, send a check to:

Life Extension Society 3600 West Commercial Blvd. Ft. Lauderdale, FL 33309 Or call 1-866-554-7108

3) To indicate your interest in investing after we become a public company (around May 15, 2017), please log on to:

Concluding Remarks


Based on these findings, we appear to be on the verge of breakthrough methods of rejuvenating human beings.

Sadly, vastly more money is spent on various forms of entertainment than on research to develop these methods.

There are currently initiatives to raise money for this research by the SENS Foundation, Age Reversal Therapeutics, Inc., and other organizations.

Life Extension supporters are encouraged to donate or invest in these organizations for the sake of their health, their longevity, and their survival, and the health, longevity, and survival of their loved-ones.


  1. Life Extension Foundation. Research Update. March 2017.
  2. Campisi J, d’Adda di Fagagna F. Cellular senescence: when bad things happen to good cells. Nat Rev Mol Cell Biol. 2007;8(9):729-40.
  3. Miller RA, Harrison DE, Astle CM, et al. An Aging Interventions Testing Program: study design and interim report. Aging Cell. 2007;6(4):565-75.
  4. Nadon NL, Strong R, Miller RA, et al. Design of aging intervention studies: the NIA interventions testing program. Age (Dordr). 2008;30(4):187-99.
  5. Strong R, Miller RA, Astle CM, et al. Nordihydroguaiaretic acid and aspirin increase lifespan of genetically heterogeneous male mice. Aging Cell. 2008;7(5):641-50.
  6. Strong R, Miller RA, Antebi A, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an alpha-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016;15(5):872-84.
  7. Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. 2009;460(7253):392-5.
  8. Lamming DW, Ye L, Katajisto P, et al. Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity. Science. 2012;335(6076):1638-43.
  9. Wilkinson JE, Burmeister L, Brooks SV, et al. Rapamycin slows aging in mice. Aging Cell. 2012;11(4):675-82.
  10. Miller RA, Harrison DE, Astle CM, et al. Rapamycin-mediated lifespan increase in mice is dose and sex dependent and metabolically distinct from dietary restriction. Aging Cell. 2014;13(3):468-77.
  11. Dai DF, Karunadharma PP, Chiao YA, et al. Altered proteome turnover and remodeling by short-term caloric restriction or rapamycin rejuvenate the aging heart. Aging Cell. 2014;13(3):529-39.
  12. Flynn JM, O’Leary MN, Zambataro CA, et al. Late-life rapamycin treatment reverses age-related heart dysfunction. Aging Cell. 2013;12(5):851-62.
  13. Sousa-Victor P, Garcia-Prat L, Munoz-Canoves P. Dual mTORC1/C2 inhibitors: gerosuppressors with potential anti-aging effect. Oncotarget. 2015;6(27):23052-4.
  14. Halloran J, Hussong SA, Burbank R, et al. Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice. Neuroscience. 2012;223:102-13.
  15. Mannick JB, Del Giudice G, Lattanzi M, et al. mTOR inhibition improves immune function in the elderly. Sci Transl Med. 2014;6(268):268ra179.
  16. Bitto A, Ito TK, Pineda VV, et al. Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice. Elife. 2016;5.
  17. Dutta S, Sengupta P. Men and mice: Relating their ages. Life Sci. 2016;152:244-8.
  18. Johnson SC, Yanos ME, Bitto A, et al. Dose-dependent effects of mTOR inhibition on weight and mitochondrial disease in mice. Front Genet. 2015;6:247.
  19. Kaeberlein M, Creevy KE, Promislow DE. The dog aging project: translational geroscience in companion animals. Mamm Genome. 2016;27(7-8):279-88.
  20. Haigis MC, Sinclair DA. Mammalian sirtuins: biological insights and disease relevance. Annu Rev Pathol. 2010;5:253-95.
  21. Milne JC, Lambert PD, Schenk S, et al. Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes. Nature. 2007;450(7170):712-6.
  22. Mitchell SJ, Martin-Montalvo A, Mercken EM, et al. The SIRT1 activator SRT1720 extends lifespan and improves health of mice fed a standard diet. Cell Rep. 2014;6(5):836-43.
  23. Kroemer G, Marino G, Levine B. Autophagy and the integrated stress response. Mol Cell. 2010;40(2):280-93.
  24. Gomes AP, Price NL, Ling AJ, et al. Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell. 2013;155(7):1624-38.
  25. Camacho-Pereira J, Tarrago MG, Chini CC, et al. CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab. 2016;23(6):1127-39.
  26. Wu LE, Sinclair DA. Restoring stem cells - all you need is NAD(.). Cell Res. 2016;26(9):971-2.
  27. Cava E, Fontana L. Will calorie restriction work in humans? Aging (Albany NY). 2013;5(7):507-14.
  28. Ravussin E, Redman LM, Rochon J, et al. A 2-Year Randomized Controlled Trial of Human Caloric Restriction: Feasibility and Effects on Predictors of Health Span and Longevity. J Gerontol A Biol Sci Med Sci. 2015;70(9):1097-104.
  29. Fontana L, Villareal DT, Das SK, et al. Effects of 2-year calorie restriction on circulating levels of IGF-1, IGF-binding proteins and cortisol in nonobese men and women: a randomized clinical trial. Aging Cell. 2016;15(1):22-7.
  30. Martin CK, Bhapkar M, Pittas AG, et al. Effect of Calorie Restriction on Mood, Quality of Life, Sleep, and Sexual Function in Healthy Nonobese Adults: The CALERIE 2 Randomized Clinical Trial. JAMA Intern Med. 2016;176(6):743-52.
  31. Richardson A, Austad SN, Ikeno Y, et al. Significant life extension by ten percent dietary restriction. Ann N Y Acad Sci. 2016;1363:11-7.
  32. Ovadya Y, Krizhanovsky V. Senescent cell death brings hopes to life. Cell Cycle. 2016:1-2.
  33. Campisi J. Aging, cellular senescence, and cancer. Annu Rev Physiol. 2013;75:685-705.
  34. Baker DJ, Childs BG, Durik M, et al. Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan. Nature. 2016;530(7589):184-9.
  35. Jurk D, Wilson C, Passos JF, et al. Chronic inflammation induces telomere dysfunction and accelerates ageing in mice. Nat Commun. 2014;2:4172.
  36. Hall BM, Balan V, Gleiberman AS, et al. Aging of mice is associated with p16(Ink4a)- and beta-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells. Aging (Albany NY). 2016;8(7):1294-315.
  37. Liu Y, Sanoff HK, Cho H, et al. Expression of p16(INK4a) in peripheral blood T-cells is a biomarker of human aging. Aging Cell. 2009;8(4):439-48.
  38. Jeck WR, Siebold AP, Sharpless NE. Review: a meta-analysis of GWAS and age-associated diseases. Aging Cell. 2012;11(5):727-31.
  39. Sharpless NE, DePinho RA. How stem cells age and why this makes us grow old. Nat Rev Mol Cell Biol. 2007;8(9):703-13.
  40. Sorrentino JA, Sanoff HK, Sharpless NE. Defining the toxicology of aging. Trends Mol Med. 2014;20(7):375-84.
  41. Wood WA, Krishnamurthy J, Mitin N, et al. Chemotherapy and Stem Cell Transplantation Increase p16INK4a Expression, a Biomarker of T-cell Aging. EBioMedicine. 2016;11:227-38.
  42. Yosef R, Pilpel N, Tokarsky-Amiel R, et al. Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL. Nat Commun. 2016;7:11190.
  43. Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell. 2015;14(4):644-58.
  44. Blackburn EH, Epel ES, Lin J. Human telomere biology: A contributory and interactive factor in aging, disease risks, and protection. Science. 2015;350(6265):1193-8.
  45. Epel ES, Merkin SS, Cawthon R, et al. The rate of leukocyte telomere shortening predicts mortality from cardiovascular disease in elderly men. Aging (Albany NY). 2008;1(1):81-8.
  46. Atzmon G, Cho M, Cawthon RM, et al. Evolution in health and medicine Sackler colloquium: Genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians. Proc Natl Acad Sci U S A. 2010;107 Suppl 1:1710-7.
  47. Rossi DJ, Bryder D, Seita J, et al. Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age. Nature. 2007;447(7145):725-9.
  48. Ferron SR, Marques-Torrejon MA, Mira H, et al. Telomere shortening in neural stem cells disrupts neuronal differentiation and neuritogenesis. J Neurosci. 2009;29(46):14394-407.
  49. Flores I, Canela A, Vera E, et al. The longest telomeres: a general signature of adult stem cell compartments. Genes Dev. 2008;22(5):654-67.
  50. Collado M, Blasco MA, Serrano M. Cellular senescence in cancer and aging. Cell. 2007;130(2):223-33.
  51. Bernardes de Jesus B, Blasco MA. Aging by telomere loss can be reversed. Cell Stem Cell. 2011;8(1):3-4.
  52. Xu Y, Goldkorn A. Telomere and Telomerase Therapeutics in Cancer. Genes (Basel). 2016;7(6).
  53. Bernardes de Jesus B, Vera E, Schneeberger K, et al. Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Mol Med. 2012;4(8):691-704.
  54. Bar C, Povedano JM, Serrano R, et al. Telomerase gene therapy rescues telomere length, bone marrow aplasia, and survival in mice with aplastic anemia. Blood. 2016;127(14):1770-9.
  55. Bar C, Bernardes de Jesus B, Serrano R, et al. Telomerase expression confers cardioprotection in the adult mouse heart after acute myocardial infarction. Nat Commun. 2014;5:5863.
  56. Conboy IM, Conboy MJ, Wagers AJ, et al. Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature. 2005;433(7027):760-4.
  57. Conboy MJ, Conboy IM, Rando TA. Heterochronic parabiosis: historical perspective and methodological considerations for studies of aging and longevity. Aging Cell. 2013;12(3):525-30.
  58. Elabd C, Cousin W, Upadhyayula P, et al. Oxytocin is an age-specific circulating hormone that is necessary for muscle maintenance and regeneration. Nat Commun. 2014;5:4082.
  59. Carlson ME, Hsu M, Conboy IM. Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells. Nature. 2008;454(7203):528-32.
  60. Poggioli T, Vujic A, Yang P, et al. Circulating growth differentiation factor 11/8 levels decline with age. Circ Res. 2016;118(1):29-37.
  61. Villeda SA, Plambeck KE, Middeldorp J, et al. Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice. Nat Med. 2014;20(6):659-63.
  62. Goodell MA, Rando TA. Stem cells and healthy aging. Science. 2015;350(6265):1199-204.
  63. Arai Y, Martin-Ruiz CM, Takayama M, et al. Inflammation, But Not Telomere Length, Predicts Successful Ageing at Extreme Old Age: A Longitudinal Study of Semi-supercentenarians. EBioMedicine. 2015;2(10):1549-58.
  64. Prasad S, Sung B, Aggarwal BB. Age-associated chronic diseases require age-old medicine: role of chronic inflammation. Prev Med. 2012;54 Suppl:S29-37.
  65. Behrens A, van Deursen JM, Rudolph KL, et al. Impact of genomic damage and ageing on stem cell function. Nat Cell Biol. 2014;16(3):201-7.
  66. Clegg A, Young J, Iliffe S, et al. Frailty in elderly people. Lancet. 2013;381(9868):752-62.
  67. Scudellari M. Ageing research: Blood to blood. Nature. 2015;517(7535):426-9.
  68. Maharaj D. G-csf for use in treating or preventing a disease associated with aging in a patient, for administration with a stem-cell containing composition and/or an electromagnetic signal. Google Patents; 2015.
  69. Horvath S. DNA methylation age of human tissues and cell types. Genome Biol. 2013;14(10):R115.
  70. Horvath S, Levine AJ. HIV-1 Infection Accelerates Age According to the Epigenetic Clock. J Infect Dis. 2015;212(10):1563-73.
  71. Horvath S, Ritz BR. Increased epigenetic age and granulocyte counts in the blood of Parkinson’s disease patients. Aging (Albany NY). 2015;7(12):1130-42.
  72. Horvath S, Garagnani P, Bacalini MG, et al. Accelerated epigenetic aging in Down syndrome. Aging Cell. 2015;14(3):491-5.
  73. Horvath S, Erhart W, Brosch M, et al. Obesity accelerates epigenetic aging of human liver. Proc Natl Acad Sci U S A. 2014;111(43):15538-43.
  74. Marioni RE, Shah S, McRae AF, et al. DNA methylation age of blood predicts all-cause mortality in later life. Genome Biol. 2015;16:25.
  75. Horvath S, Pirazzini C, Bacalini MG, et al. Decreased epigenetic age of PBMCs from Italian semi-supercentenarians and their offspring. Aging (Albany NY). 2015;7(12):1159-70.
  76. Christiansen L, Lenart A, Tan Q, et al. DNA methylation age is associated with mortality in a longitudinal Danish twin study. Aging Cell. 2016;15(1):149-54.
  77. Marioni RE, Shah S, McRae AF, et al. The epigenetic clock is correlated with physical and cognitive fitness in the Lothian Birth Cohort 1936. Int J Epidemiol. 2015;44(4):1388-96.