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Rejuvenation ResearchVol. 16, No. S1 Program and AbstractsStrategies for Engineered Negligible Senescence (SENS): Sixth ConferenceQueens' College, Cambridge, UKSeptember 3–7, 2013Open AccessSponsors of SENS6Published Online:14 Aug 2013https://doi.org/10.1089/rej.2013.16.sens6absAboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail Meeting ProgramTuesday September 3rdSession 1: Calorie restriction in primates16:15Donald IngramPennington Biomedical Research Center, USAMonkeying around with calorie restriction: is a calorie a calorie?16:35Rozalyn AndersonUniversity of Wisconsin, USAImpact of CR on aging in rhesus monkeys – a focus on metabolism16:55Donald Ingram/Rozalyn AndersonPennington Biomedical Research Center, USA/University of Wisconsin, USAOutcomes from parallel CR monkey studies at NIA and UW Madison17:10Donald Ingram/Rozalyn AndersonPennington Biomedical Research Center, USA/University of Wisconsin, USAQ&A Session17:30Luigi FontanaWashington University, USA/Salerno University, ItalyWill calorie restriction work in humans?18:00CoffeeSession 2: Small-molecule interventions effective at late age18:30Dongsheng CaiAlbert Einstein College of Medicine, USAHypothalamic control of aging and longevity19:00Danica ChenUniversity of California at Berkeley, USASirtuin regulation of metabolism and stem cells19:30Frank MadeoUniversity of Graz, AustriaSpermidine induces autophagy in multiple species and mimics calorie restriction20:00Arie BudovskyBen-Gurion University of the Negev, IsraelScreening of medicinal plants in the Judea region (Israel) for geroprotective activities20:15Dinner21:15Poster SessionWednesday September 4thSession 3: Telomeres and cancer08:30Zhenyu JuHangzhou Normal University, ChinaTelomere dysfunction and stem cell aging09:00Haroldo SilvaSENS Research Foundation, USAALTered cancer cells: Uncovering the genetic basis of ALT (Alternative Lengthening of Telomeres)09:30Rigdon LentzGeorgetown University, USAApheresis of TNF and IL-2 disrupts tumour immunoevasion10:00CoffeeSession 4: Combating persistent viruses10:30Charles CaoUniversity of Florida, USANanoparticle-based artificial RNA silencing machinery for antiviral therapy11:00Paul LehnerCambridge University, UKLatency-associated degradation of the MRP1 drug transporter presents a novel therapeutic target for latent human cytomegalovirus infection11:30Todd RiderMassachusetts Institute of Technology, USAPANACEA broad-spectrum antiviral therapeutics12:00LunchSession 5: Short talks, cell senescence and anergy13:15Gregory ChinSENS Research Foundation, USASRF Education: Training Future SENS Researchers13:30Lia GinaldiUniversity of L'Aquila, ItalyEffect of senescence on bone remodelling: the role of inflammageing13:45Alexandra StolzingFraunhofer Institute for Cell Therapy and Immunology, GermanyTransplantation of in vitro derived microglia14:00John SedivyBrown University, USAChromatin and epigenetic dynamics in senescence phenotypes14:30Kevin PerrottBuck Institute for Aging Research, USATargeting the senescence-associated secretory phenotype15:00Janko Nikolich-ZugichUniversity of Arizona, USALife-long persistent viral infection alters the naïve T-cell pool, impairing CD8 T-cell immunity in late life15:30Jan van DeursenMayo Clinic, USAStem and progenitor cell senescence in aging16:00CoffeeSession 6: Disruptive medicine16:30Alan RussellCarnegie Mellon University, USAThe disruptive potential of tissue engineering17:00Richard BarkerCASMI, UKAccelerating translational research processes from bench to clinic17:30Sam ParniaSUNY Stony Brook, USARedefining and reversing death: what has resuscitation science taught us about death and what happens when we die?18:00CoffeeSession 7: Cardiovascular aging18:30Elizabeth CorderMatrix Genomics, Inc., USALow risk for coronary artery disease and findings in the TERC region on 3q2619:00David SpiegelYale University, USAChemical and biological approaches to understanding advanced glycation end-products (AGEs)19:30Brian O'NuallainHarvard University, USAInnate and vaccine-generated antibodies against transthyretin amyloids20:00Dinner21:00Poster sessionThursday September 5thSession 8: Beyond organ transplantation08:30John JacksonWake Forest Institute for Regenerative Medicine, USACharacterization of decellularized thymus scaffolds for use in engineering thymus tissue09:00Eric LagasseMcGowan Institute for Regenerative Medicine, USAEctopic organogenesis in lymph node09:30Steve Van SickleArigos Inc.Improved technology for organ cryopreservation by vitrification10:00CoffeeSession 9: Cellular regeneration10:30Robin FranklinCambridge University, UKMyelin regeneration and ageing11:00Graca Almeida-PoradaWake Forest Institute for Regenerative Medicine, USAEngineering stem cells for liver and gut regeneration11:30Malcolm MadenUniversity of Florida, USARegeneration in the adult organism - a cure for ageing?12:00LunchSession 10: SENS Lecture and short talks13:30George ChurchHarvard University, USASENS Lecture: Technologies for Reading, Writing & Interpreting Omes14:30Justin ReboSENS Research Foundation, USATreating Cytopenia with ESC Derived Blood Cells14:45James LarrickPanorama Research Institute, USASodium-Potassium ATPase modulation for Aging Related Disease15:00João de MagalhãesUniversity of Liverpool, UKSequencing the genome of the longest-lived mammal to identify longevity assurance mechanisms15:15Jean HébertAlbert Einstein College of Medicine, USAWhat good is an old brain in a young body – a strategy for regenerating the neocortex15:30John FurberLegendary Pharmaceuticals, USAInducing exocytosis to remove lipofuscin15:45Axel KowaldUniversity of Newcastle, UKIs transcription the key to the selection advantage of mitochondrial deletion mutants?16:00CoffeeSession 11: Mitochondria16:30Richard YouleNational Institute for Neurological Disorders and Stroke, USAMitochondrial quality control: links to Parkinson's disease and aging models17:00Rafal SmigrodzkiGencia Corporation, USATargeted mitochondrial therapeutics in aging17:30Matthew O'ConnorSENS Research Foundation, USARescue of mtDNA mutations by allotopic expression of engineered mitochondrial genes18:00CoffeeSession 12: Advances in gene delivery18:30Matthew ScholzImmusoft CorporationUtilizing B cells to recreate the biochemical environment of youth19:00Yanru Chen-TsaiStanford University, USAPhage integrase for targeted gene therapy in mouse models19:30Dirk HockemeyerUniversity of California at Berkeley, USAMolecular mechanisms of telomerase regulation in genetically defined human stem cell models20:00Dinner21:00Poster SessionFriday September 6thSession 13: Lysosomes08:30Michael GoligorskyNew York Medical College, USACardiovascular stressors induce lysosomal dysfunction, sirtuin-1 depletion and premature senescence of vascular endothelium09:00Jacques MathieuRice University, USAStrategies for the clearance of age-related lysosomal residuals: 7-ketocholesterol and foam cell formation09:30Ghezal BeliakoffSENS Research Foundation, USATreating age-related macular degeneration through enhanced lysosomal degradation of A2E10:00CoffeeSession 14: “Aging” versus “aging-related disease”10:30James ApplebyGerontological Society of America, USAThe Geroscience Interest Group (GSIG): tracing pathological consequences of fundamental aging processes11:00Mike KopeSENS Research Foundation, USAReimagine Aging11:30Tanja DominkoUniversity of Nova Gorica, SloveniaSlovenia's bid for the world stage in biogerontology12:00LunchSession 15: Short talks13:15Phil MicansInternational Antiaging Systems, USAWhy orthodox medicine must change - the need for preventative/regenerative medicine13:30Karen KurtakGrossman Wellness Institute, USADietary and Nutritional Manipulation of the Nuclear Transcription Factors, PPAR's and SREBP's, as a Tool for Reversing the Primary Diseases of Premature Death and Aging13:45Patricia d'AlessioAISA Therapeutics/University Paris Sud-11, FranceHealthy aging: how stay bonny & transcend inflammation?14:00Calogero CarusoUniversity of Palermo, ItalyKlotho polymorphisms and longevity: a systematic review14:15Giulia AccardiUniversity of Palermo, ItalyInsulin pathway and its correlation with ageing and age-related diseases14:30Anastasia ShindyapinaLomonosov Moscow State University, RussiaBioinformatic analysis of factors involved in age-related mineralization of soft tissues14:45Josh MitteldorfMassachusetts Institute of Technology, USAHow does the body know how old it is?15:00Didier CoeurnelleHeales (Healthy Life Extension Society), BelgiumCollective consequences of a very long life. The right to life extension could / should be considered a human right.15:15Ilia StamblerBar Ilan University, IsraelOn the history of life-extension research: Does the whole have parts?15:30Scott NeedhamLeading Technology Group, AustraliaTowards priorities for aging research15:45Daria KhaltourinaCouncil for Public Health and Demography, RussiaLegal problems of registering substances and therapies to cure aging16:00CoffeeSession 16: Is SENS necessary and sufficient?16:30Silvia GravinaAlbert Einstein College of Medicine, USAAging, single-cell methylomes17:00Robert Shmookler-ReisUniversity of Arkansas, USARange of variation in the duration of C. elegans dauer and post-dauer survival: Food intake of parents and first-stage larvae affects adults recovered after 60 days of developmental arrest17:30CoffeeSession 17: Are we rational about the quest to defeat aging?18:00Alex ZhavoronkovBiogerontology Research Foundation, UKNew economic arguments for accelerating aging research18:30Mair UnderwoodUniversity of Queensland, AustraliaWhat reassurances do the community need regarding life extension? Evidence from studies of community attitudes and an analysis of film portrayals19:00Randall KuhnUniversity of Denver, USAInternational Futures: impact of decelerated or abolished aging on human demographic change19:30Thomas PyszczynskiUniversity of Colorado, USAUnderstanding the paradox of opposition to long-term extension of the human lifespan: fear of death, cultural worldviews, and the illusion of objectivity20:00Gala DinnerSaturday September 7th08:00Breakfast09:30Punting on the River Cam11:30Conference adjournsThank you for your attendance and participation!PostersCeRNA bioinformatic analysis on human telomeraseArancio W, Pizzolanti G, Giordano CVascular ageing: causes, mechanisms, complications and possible therapeutic strategiesBalistreri CR, Candore G, Colonna-Romano G, Forte GI, Benedetto F, Spinelli F, Ruvolo G, Caruso C, Lio DDistinctive profile of pro-inflammatory receptors in naive and memory B cells of young, healthy elderly and Alzheimer Disease patients.Bulati M, Buffa S, Martorana A, Gervasi F, Camarda C, Azzarello DM, Candore G, Lio D, Caruso C, Colonna-Romano GThe Human Memome Project: Text-data analytics to find socio-cultural predictors of longevity utilising the quantified self, crowd sourcing and citizen science communitiesCalimport SRG, Bentley BIdentification of three particular morphological phenotypes in sporadic thoracic aortic aneurysm (S-TAA): phenotype III as S-TAA biomarker in aged individualsBalistreri CR, Pisano C, Di Maggio FM, Scola L, Maresi E, Lio D, Caruso C, Ruvolo G, Candore GEffect of cognitive training on the expression of brain-derived-neurotrophic-factor (BDNF) in lymphocytes of mild cognitive impairment (MCI) patientsCasoli T, Giuli C, Balietti M, Giorgetti B, Solazzi M, Fattoretti PLonger telomeres in mitochondrial lineages doubly-selected for extreme longevity and late female reproductionBerrett MG, Cawthon RM, Kerber RA, O'Brien EThe controversal relationship between immunosenescence and apoptosisCiccarelli F, De Martinis M, Ginaldi LA distinct gene-wide pattern in LRRK2 may identify a third of Parkinson's casesCorder EHThe in vitro senescence phenotype of mesenchymal stromal cells and potential ramifications for innate immune functionCurran S, Campisi JThe Digital Ageing Atlas: Integrating the diversity of age-related changes into a unified resourceCraig T, Smelick C, de Magalhaes JPp53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypesDavalos AR, Kawahara M, Malhotra GK, Schaum N, Huang J, Ved U, Beausejour CM, Coppe JP, Rodier F, Campisi JSystems Biology of Human Aging - Network Model 2013Furber JDAging can be fully reversed with actual knowledgeGarcia Guerrero OUnraveling the Gordian knot of lipofuscinGaspar JPolysaccharides from medicinal herbs as potential therapeutics for ageing and age-related neurodegenerationLi HF, Hu MH, Ma FL, Xiao LY, Zhang J, Xiang YX, Huang ZBProtective effect of a sturgeon egg homogenate marine compound but not of EPA/DHA on arterial ultrastructure in spontaneously hypertensive ratsBertuccelli G, Marotta F, Illuzzi N, Nagpal R, Zerbinati N, Naito Y, Mohania D, Milazzo M, Sapienza C, Italia A, Tomella C, Catanzaro RIs there any beneficial effect of S. boulardi lysates on NK cell activity in otherwise healthy but immunocompromised elderly subjects?Kantah MK, Takadanohara H, Marotta F, Illuzzi N, Naito Y, Celep G, Milazzo M, Sapienza C, Tomella C, Kobayashi R, Catanzaro RNon-senescence seems feasible. But are we ready now for such possibility?Khalyavkin AVWhether is phenoptosis an inevitable programmed aging or it can be avoided?Khalyavkin AVAging and external signalingKhalyavkin AV, Krutko VNAge-associated changes in walking parameters of Japanese adult womenKikkawa K, Okada H, Oishi REfficiency of cellular division when creating small pockets of electric current along the walls of cellsKletetschka G, Zila V, Klimova LEstetrol, molecular chaperones and the epigenetics of longevity and cancer resistanceKrxøll JThree-pathway model of mammalian longevityLehmann G, Muradian KhK, Fraifeld VEOverview of beverages with anti-aging functions in Chinese marketYang F, Song J, Liang M, Ma FL, Mao XL, Li HF, Huang ZBThe hidden phenomenon of oxidative stress in the treatment of subclinical hypothyroidism: a protective nutraceutical interventionTomella C, Catanzaro R, Illuzzi N, Cabeca A, Lorenzetti, A Celep G, Milazzo M, Sapienza C, Zerbinati N, Italia A, Bertuccelli G, Marotta FAnti-inflammatory and anti-mutagenic effect of YHK phytocompound in hepatocytes: in view of an age-management liver protecting approachCatanzaro R, Celep G, Illuzzi N, Milazzo M, Rastmanesh R, Yaduvanshi SK, He F, Solimene U, Sapienza C, Srivastava N, Marotta FThe gene expression patterns of ‘normal’ aging show a high similarity with age-related pathologiesMazuz K, Budovsky A, Fraifeld VEAge dynamics of transcriptomes of long-lived Drosophila strains with GADD45 overexpression in nervous systemMoskalev AA, Plyusnina EN, Kudryavtseva AVSoluble Tumor Necrosis Factors (sTNFR1 and sTNFR2) are increased in an age-dependent manner and in multiple organ malignancies.Obrenovich ME, Emancipator SN, Frackelton JP, Lonsdale DA new telomere/stem cell theory of agingPark ERegeneration of neonatal lymphoid organs in the old organismPishel IMIntermittent hypoxia, oxidative stress and inflammation: The long and stressful road to cardiovascular diseaseShannack MAged mice repeatedly injected with plasma from young mice: a survival studyShytikov DW, Balva OV, Pishel IM, Debonneuil ENicolai Sietnicki - a Nicolai Fedorov follower as transhumanist precursor of a dogmatic philosophy of the extension of life conceptSitnicki ISystem modeling of genetic factors that induce pluripotencySukhera UA, Nawaz MSPrediction of new lifespan regulators in C. elegansTacutu R, Budovsky A, de Magalhães JP, Fraifeld VEThe links between polar mRNA transport and lifespan in budding yeast Saccharomyces cerevisiaeTaranukha D, Budovsky A, Gobshtis N, Braiman A, Porat Z, Aronov S, Fraifeld VENutraceutical properties of extravirgin olive oil: a natural remedy for age-related disease?Virruso C, Accardi G, Colonna-Romano G, Candore G, Vasto S, Caruso CDiabetes type 2 and cancer: an integrative approach to prevention, treatment and rehabilitation.Voronina T, Grechko NWeb intelligence to solve agingWuttke D, Kulaga ASenescent cells—bad neighbors for cancer cells?Yanai H, Tacutu R, Budovsky A, Caliò A, Chilosi M, Fraifeld VEAbstractsAbstracts of invited, oral and poster presentations are printed here as a single list, in alphabetical order of presenting author.Accardi G, Verga S, Emanuele F, Caruso C, Virruso C, Vasto S, Licastro F, Candore GLaboratory of Immunopathology, Department of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo1 INSULIN PATHWAY AND ITS CORRELATION WITH AGEING AND AGE-RELATED DISEASESRecent findings suggest a strong correlation between Type 2 diabetes (T2D) and Alzheimer's disease (AD). It is well known that an impairment of insulin signaling pathway can lead to insulin resistance and T2D, raising blood glucose levels. However, insulin and insulin growth factor-1 (IGF-1) contribute to neuronal survival, cognitive function and learning and memory processes as well. Indeed, many studies demonstrate that hyperinsulinemia, a pre-insulin resistance condition, is linked to higher risk of AD. Moreover, in vivo studies show an increased risk for cognitive decline in diabetic mice. The molecular explanation of this correlation is unclear but insulin resistance and impairment of insulin pathway seem to have a key role. In the brain, altered metabolism makes neurons more sensible to oxidation causing mitochondrial damages. Moreover, AD brains have a lower insulin utilization, a reduced expression of its receptors and of IGF-1, all necessary for neuronal survival and learning and memory processes. The attenuation of AKT, a kinase involved in downstream insulin cascade, causes the augmented activity of GSK-3 beta that, in mice and maybe in human, increases neuronal apoptosis and in human causes hyperphosphorilation of tau protein.SHIP2, a 5-phosphatase, is an antagonist of PI3K and its expression, in brain of diabetic mice is increased. Moreover, its over-expression causes impairment of insulin/IGF-1 signaling, hence the decline of all related functions. This is linked to the reduction of PI(3,4,5)P3 level, also in the central nervous system. Since some single nucleotide polymorphisms (SNPs) of the INPPL1, gene encoding SHIP2, in particular rs2276047, rs9886 and rs144989913, are significantly associated with T2D in European and Japanese people, we performed a case-control study with type 2 diabetic and AD Italian people. Moreover we compared these populations with younger one.Preliminary results suggest a putative correlation between this rs144989913 and ageing rather than age-related diseases. Since this SNP is an insertion/deletion of 28 base pairs, it may cause an alteration in SHIP2 expression, confirming the evidence previous shown in old mice in which SHIP2 levels were raised.Keywords: Alzheimer's disease, Type 2 Diabetes, Ageing, Insulin pathway, SHIP2Almeida-Porada G, Soland M, Boura J, Mokhtari S, Porada CWake Forest Institute for Regenerative Medicine2 ENGINEERING STEM CELLS FOR LIVER AND GUT REGENERATIONMarrow stromal cells (MSC) have several unique properties, which make them well suited both for regenerative medicine and gene delivery. These include the ease of isolation and the ability to be considerably expanded in culture without losing engraftment capacity. Furthermore, MSC have been reported to reduce local inflammation, blunt immune response, and counteract the chemotactic signals released to recruit immune cells to the site of injury/inflammation.Nevertheless, controversy still remains whether these cells, upon transplantation, would be able to be recognized in an allogeneic setting, lessening their therapeutic potential when compared with their autologous counterpart. Since MSC express negligible amounts of HLA-II, but display variable levels of HLA-I on their surface, and harbor several ligands to activating NK cell receptors, it is likely that MSC can become a target of NK and CTL. We genetically engineered MSC to express the HCMV proteins US2, US3, US6, and US11, since they were shown to reduce HLA-I surface levels on somatic cells. Moreover, this reduction in HLA-I levels prevented CTL recognition thereby preventing activation and killing of infected cells during a normal HCMV infection. We demonstrated that US6 and US11 were the most efficient in downregulating expression of HLA-I and therefore reducing MSC immunogenicity, as demonstrated by the correlation between HLA-I expression and the decrease in human PBMNC proliferation using MLR assays. We also investigated the role of the HCMV US proteins US 2, 3, 6 and 11 in protecting MSC from complement lysis, since the complement system, plays an essential role in the inflammatory process, and serves as a critical bridge between the innate and adaptive arms of the immune response. MSC express soluble factor H, the complement regulatory proteins CD46, CD55, and CD59, that enable MSC inhibit activation of the complement system to a certain extent. Still, in the presence of inflammation and complement system activation, these innate mechanisms of protection are insufficient to prevent cellular damage and death. Expression of US2 HCMV protein on MSC had the ability to increase expression of CD46, CD55, and CD59 surface molecules, and functional assays demonstrated a significant reduction in complement lysis in MSC expressing US2 protein, when compared to the control.In conclusion, we are able to genetically engineer MSC to have an enhanced survival advantage in the presence of an exacerbated inflammatory microenvironment and/or in an allogeneic transplantation setting, as a result of decreased rejection by the immune system. This should extend their survival time and thereby enhance their therapeutic potential.Anderson RM.Department of Medicine, SMPH, UW Madison, and GRECC VA Hospital, Madison, WI3 IMPACT OF CR ON AGING IN RHESUS MONKEYS – A FOCUS ON METABOLISMCaloric restriction (CR) without malnutrition delays aging and extends lifespan in diverse species; however, mechanisms have remained elusive. Furthermore, the translatability of CR to primate species, and thus the applicability of insights from CR to human health, remains an open question. Here I will discuss the longitudinal adult-onset CR study in rhesus monkeys initiated at UW Madison in the late 1980s. In this population of rhesus macaques moderate CR lowered the incidence of aging-related deaths. In addition, CR delayed the onset of age-associated pathologies. Analysis of metabolic rate and energy expenditure indicate that the CR animals differ from controls in metabolic rate and in efficiency of metabolic output. These findings are supported by serum metabonomic data that show the CR animals to be metabolically distinct from their control-fed counterparts. Subsequent studies in skeletal muscle have revealed a metabolic component to the aging process, where a shift in metabolism anticipates the onset of sarcopenia - the age related loss of muscle mass. In CR animals the onset and progression of sarcopenia is delayed and multiple indicators of cellular metabolism suggest a “younger” profile than would be expected based on chronological age. The findings from the UW-Madison study suggest that CR does slow aging in rhesus monkeys and that changes in energy metabolism are central to its mechanisms of action.Keywords: aging, caloric restriction, rhesus monkeys, metabolismIngram DK, Anderson RM.Pennington Biomedical Research Center, LSU, Baton Rouge, LA, USA / Department of Medicine, SMPH, UW-Madison, and GRECC VA Hospital, Madison, WI, USA4 OUTCOMES FROM PARALLEL CR MONKEY STUDIES AT NIA AND UW MADISONCaloric restriction without malnutrition extends lifespan and delays the onset of age-associated disorders in diverse species, from unicellular organisms to laboratory mice and rats. Until recently, evidence of the translatability of CR's effects to human health has been a critical gap in CR research. In the late 1980s two parallel rhesus monkey caloric restriction (CR) studies were initiated to determine the effect of CR on resistance to illness and mortality in nonhuman primates. With more than 20 years of longitudinal data accrued, both studies have demonstrated improvements in health in CR animals compared to controls, significant in the University of Wisconsin (UW) study, and approaching significance in the National Institute on Aging (NIA) study. The impact of CR on survival in nonhuman primates; however, is a point of departure in the two studies. In 2009 the UW-Madison-based research team reported improved survival for animals on CR. In contrast, the NIA-based research team reported in 2012 that there was no difference in survival between CR and Control monkeys. Here we present a comparison of key differences in study design that could explain differences in survival outcome, including the genetic origin of the study cohort, age of onset for the dietary intervention, dietary composition, feeding regimens, and protocols for animal husbandry. The relative contributions of these differences to study outcomes will be discussed, and NIA and UW perspectives on the impact of these findings on CR research and its potential to reveal insights into human health will be presented.Keywords: calorie restriction, primate, survival, study design, geneticAppleby J.Gerontological Society of America5 THE GEROSCIENCE INTEREST GROUP (GSIG): TRACING PATHOLOGICAL CONSEQUENCES OF FUNDAMENTAL AGING PROCESSESThis presentation will focus on the emerging field of geroscience, an interdisciplinary field that aims to understand the relationship between the basic biology of aging and age-related diseases. Geroscience is “coming of age.” Originally coined by Gordon Lithgow, “geroscience” was just entered into Wikipedia in June of 2013. A central concept of geroscience is that multiple human diseases arise from a common cause, aging itself. Thus, slowing down the process of aging (as it has been done in animal models) represents a potentially fruitful approach to concurrently address and combat the many chronic conditions affecting the elderly.Over the past few decades, researchers studying the biological underpinnings of the aging process have made impressive progress in understanding the genetics, biology and physiology of aging. As a result, basic research in animal models has demonstrated the plasticity of lifespan, with several genetic, behavioral and pharmacological means of extending lifespan in rodents and other model organisms. Most importantly, with some notable exceptions, extension of lifespan is accompanied by a significant delay in the appearance and progression of multiple morbidities, as well as a slowing in age-related functional decline. That is, slowing the aging processes leads to an increase in healthspan, the portion of life spent in good health.This presentation will describe the development of the Geroscience Interest Group (GSIG), a collaborative effort across several NIH Institutes to support the development of new tools, models and paradigms that address the basic biological underpinnings of these multiple diseases. Originally conceived by Felipe Sierra, this NIH Interest Group has quickly become one of the largest such trans-NIH groups. By pooling resources and expertise, the GSIG identifies major cross-cutting areas of research and proposes coordinated approaches to identify hurdles and envision solutions to the health problems of our burgeoning elderly population. While most of the effort of the GSIG focuses on increasing awareness within and across the NIH, some activities are also open to the scientific community at large, and these will be discussed.Keywords: geroscience, GSIG, NIH, healthspanArancio W, Pizzolanti G, Giordano C.University of Palermo6 CERNA BIOINFORMATIC ANALYSIS ON HUMAN TELOMERASEMessenger RNA (mRNA) translation efficiency is regulated by microRNAs. Each microRNA is able to regulate the translation of multiple mRNAs and each mRNA is regulated by multiple microRNAs. Thus, cellular mRNAs pool competes for microRNAs pool and viceversa. The regulatory network between mRNAs and microRNAs can be studied in the perspective of Competing Endogenous RNAs, or ceRNAs.Here it is presented a bioinformatic study on ceRNAs for human telomerase (hTERT). Several genes potentially involved in the regulatory network of hTERT have been harvested by this study.hTERT is essential for telomeres integrity. Telomere dysfunctions have been widely reported to be involved in Ageing, Cancer and Cellular Senescence.Amongst the gene collected, the oncosupressor PTEN and the dynein heavy chain coding gene DNHD1 are top level interactors.Interestingly, many genes of unknown functions result as predicted interactors, suggesting that hTERT may be involved in unexplored networks and scenarios.Keywords: hTERT, telomerase, PTEN, dynein, CeRNABalistreri CR, Candore G, Colonna-Romano G, Forte GI, Benedetto F, Spinelli F, Ruvolo G, Caruso C, Lio D.Immunosenescence Group, Department of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Palermo, Italy7 VASCULAR AGEING: CAUSES, MECHANISMS, COMPLICATIONS AND POSSIBLE THERAPEUTIC STRATEGIESAgeing is increasingly considered as an independent factor for the development of cardiovascular diseases (CDs). During ageing, there are structural and functional changes in the vasculature, including dilated lumen, altered intimal-medial thickness, vascular stiffness, endothelial dysfunction, increased endothelial apoptosis, matrix metalloproteinase dysregulation, increased expression of inflammatory molecules, aggravated oxidative stress and shortened telomere length. These changes leave the body and the arteries more susceptible to hypertension, atherosclerosis, medial degeneration and the onset of a different array of artery complications (i.e. myocardial infarction, stroke, aneurysms). Meta