Aging Research Centre (ARC) Home PageAging Research Centre   Release 11.7WelcomeWeare dedicated to providing a service that allows researchers in thisfield to find information that is related to the study of the aging process. We also endeavor to introduce this field to laymen who wouldlike to know more about the research that is being conducted in thisfield. ResearchWeare engaged in many areas of research such as systems biology, brainimaging via automated imaging microscopy, the study of neuroendocrinechanges in the hypothalamus, whole body scanning systems, the study ofan entire organism as it ages and the effects of hormonal changes on the aging process PublicationsA computational systems biology approach toneuroendocrine aging: Initial results. Experimental Gerontology, Volume42, Issues 1-2 , January-February 2007, Page 142Novel methods in computer-assisted tissue analysis:Customized regional targeting of both cytoplasmic and nuclear-stainedtissue. Experimental Gerontology, Volume 42, Issues 1-2 ,January-February 2007, Pages 141-142Tracking changes in hypothalamic IGF-1 sensitivity with aging and caloric restriction. Experimental Gerontology, Volume 42,Issues 1-2 , January-February 2007, Pages 11-12.Insulin-like growth factor-1 receptor immunoreactivecells are selectively maintained in the paraventricular hypothalamus ofcalorically restricted mice. Int J Dev Neurosci. 2007 Feb;25(1):23-8Age-dependent loss of insulin-like growth factor-1receptor immunoreactive cells in the supraoptic hypothalamus is reducedin calorically restricted mice. Int J Dev Neurosci. 2006Nov;24(7):431-6.A study of insulin-like growth factor-I receptorimmunoreactivity in the supraoptic nucleus of young and old femaleB6D2F1 mice. FASEB Journal, April 2006, 357.5 Caloric restriction reduces cell loss and maintainsestrogen receptor-alpha immunoreactivity in the pre-optic hypothalamusof female B6D2F1 mice, Neuro Endocrinol Lett. 2005 Jun;26(3):197-203.A survey of estrogen receptor-alpha immunoreactivity inthe hypothalamus of young, old, and old-calorie restricted femaleB6D2F1 mice, Experimental Gerontology, Volume 39, Issues 11-12,November-December 2004, Page 1771Phenomics: a new direction for the study ofneuroendocrine aging. Experimental Gerontology, Volume 38 (2003),Issues 1-2, Page 218A comparison of estrogen receptor-alphaimmunoreactivity in the arcuate hypothalamus of young and middle-agedC57BL6 female mice. Experimental Gerontology, Volume 38 (2003), Issues1-2, Page 220Creating Three-Dimensional Neuronal Maps of the MouseHypothalamus Using an Automated Imaging Microscope System. ExperimentalGerontology, Volume 35 numbers 9-10, December 2000, page 1421Automated Imaging Microscope System, Linux Journal2000, Issue 70, Februrary, Page 32-35 ProjectsAutomated Imaging Microscope System (AIMS)Regional targeting ofcytoplasmic and nuclear-stained tissueOntological bodysystem mapsMapping bodysystems    . - Items of major interest - Meetings 61st Annual Scientific Meeting of the Gerontological Society of America. Date: November21-25, 2008 Location: National Harbor, Maryland http://www.geron.org/ Ninth International Symposium on Neurobiology and Neuroendocrinology of Aging Location: Bregenz Austria Date: TBAJuly 2010 The objective of these Symposia is to bring togetherscientists who havemade recent major advances in the study of aging ranging fromneuroendocrinology, neurobiology, genetics, and molecular mechanisms topractical issues of treatment and care of the elderly and patients withage-related CNS diseases. Our goals are to bring together speakers whonormally would not meet at a meeting devoted to Alzheimer's disease,molecular biology of aging, clinical geriatrics, or other commonlycovered topics. For more information, please write, send a facsimile oremail: Dr. Andrzej Bartke Director of Research, Geriatrics Initiative, Southern Illinois University School of Medicine, P.O. Box 19636 Springfield, IL 62794-9636, USA E-Mail: abartke@siumed.edu or Dr. Richard E Falvo, Department of Cell and Molecular Physiology, Medical Biomolecular Research Building, 103 Mason Farm Road, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7545, USA E-Mail: rfalvo@med.unc.edu WWW Site: http://www.neurobiology-and-neuroendocrinology-of-aging.org/ - Recent Books - Bio Tool Box - Biotech Companies - Journals - Real Audio and other Programs .. Nov 24th, 2006Age-dependent loss of insulin-like growth factor-1 receptor immunoreactive cells in the supraoptic hypothalamus is reduced in calorically restricted mice.Both life-long caloric restriction (CR) and the suppression of insulin-like growth factor-1 (IGF-1) signaling reliably extend the mammalian lifespan. The neuroendocrine system, regulated by the hypothalamus, remains the most convincing site of action for both these modes of life extension. Yet, determining whether CR actions are mediated by the modulation of neuroendocrine IGF-1 signaling remains unclear. Of the hypothalamic nuclei that express the IGF-1 receptor (IGF-1R), the cells of the supraoptic nucleus (SON) display some of the most robust IGF-1R expression. Taking IGF-1R immunoreactivity as an index of sensitivity to IGF-1, we counted IGF-1R immunoreactive and non-immunoreactive cells in the SON of young-ad-libitum fed (young-Al, 6 weeks), old-ad-libitum fed (Old-Al, 22 months), and old-calorie-restricted (Old-CR, 22 months) female B6D2F1 mice. An automated imaging microscopy system (AIMS) was used to generate cell counts for each section of supraoptic hypothalamus. Results show that while the total number of cells in the SON of ad-libitum fed mice does not change significantly with aging, a significant reduction in IGF-1R immunoreactive cells does occur in ad-libitum fed mice with aging. In contrast to this, calorie restricted mice show both a decline in the total number of cells and IGF-1R immunoreactive cells in the SON with age, but with the decrease in the latter being notably attenuated when compared to the degree of loss seen in ad-libitum fed mice. Thus, while CR induces greater loss in the total number of cells in the SON with age, it reduces the degree of age-dependent loss seen in IGF-1R expressing cells. As a result, when compared to Old-AL mice, the SON of Old-CR mice displays a greater proportion of IGF-1R cells and thus possibly enhanced IGF-1 sensitivity with aging.REFERENCES: International Journal of Developmental Neuroscience 2006 Nov;24(7):431-6.June 26th, 2005Caloric restriction reduces cell loss and maintains estrogenreceptor-alpha immunoreactivity in the pre-optic hypothalamus of femaleB6D2F1 mice.Life-long calorie restriction (CR) remains the most robust andreliable means of extending life span in mammals. Among the severaltheories to explain CR actions, one variant of the neuroendocrinetheories of aging postulates that changing hypothalamic sensitivity toendocrine feedback is the clock that times phenotypic change over thelife span. If the feedback sensitivity hypothesis is correct, CRanimals should display a significantly different pattern ofhormone-sensitive cell density and distribution in the hypothalamus. Ofthe many endocrine signal receptors that may be involved in maintaininghypothalamic feedback sensitivity, our study has selected to beginmapping those for estrogen (E). Altered hypothalamic sensitivity to Eis known to schedule reproductive maturation and influence reproductivesenescence. Taking estrogen receptor-alpha (ERalpha) immunoreactivityas an index of sensitivity to E, we counted ERalpha immunoreactive andnon-immunoreactive cells in the pre-optic hypothalamus of young (6weeks), ad-libitum (Old-AL) fed old (22 months), and calorie restricted(Old-CR) old (22 months) female B6D2F1 mice. An automated imagingmicroscopy system (AIMS) was used to generate cell counts for eachsampled section of pre-optic hypothalamus. Results show a 38% reductionin ERalpha immunoreactive cells and an 18% reduction in total cellnumbers in AL-old mice in comparison to young mice. However, CR miceonly show a 19% reduction in ERalpha immunoreactive cells and a 13%reduction in total cell numbers in comparison to young mice. Thisindicates CR prevents age-related cell loss and maintains estrogensensitivity in the pre-optic hypothalamus of old female B6D2F1 mice.REFERENCES:Neuroendocrinology Letters 2005 Jun;26(3):197-203.May 27th, 2004Premature aging in mice expressing defective mitochondrial DNApolymeraseResearchers in Sweden have created homozygous knock-in mice thatexpress a proof-reading-deficient version of PolgA, the nucleus-encodedcatalytic subunit of mitochondrial DNA (mtDNA) polymerase. The miceencountered a threefold to fivefold increase in the levels of pointmutations as well as increased amounts of deleted mtDNA.The deterioration in the experimental mice started at 25 weeks younghood in normal mice. They prematurely experienced a range offamiliar age-related complaints, including baldness, osteoporosis,anemia, curvature of the spine and reduced fertility. The lifespan oftheexperimental mice was markedly reduced, with the median age of deathat 48 weeks. The oldest of the experimental mice died before 61 weeks.Normal mice live approximately 110 weeks.REFERENCES:Nature2004 May 27; 429, 357 - Ageing: Mice and mitochondriaNature2004 May 27; 429, 417 - 423 - Premature aging in mice expressingdefective mitochondrial DNA polymeraseApril 1st, 2004Scientists release draft of the rat genomeAn international research team, supported by the National InstitutesofHealth(NIH), today announced it has completed a high-quality, draftsequence of the genome of the laboratory rat, and has usedthat data to explore how the rat's genetic blueprint stacks upagainst those of mice and humans.In the Nature article, the researchers reported that, at approximately2.75 billion basepairs, the rat genome is smaller than the human genome, which is 2.9billion base pairs,and slightly larger than mouse genome, which is 2.6 billion base pairs.Rat genomecontains about the same number of genes as the human andmouse genomes. Furthermore, almost all human genes known to beassociated withdiseases have counterparts in the rat genome and appear highlyconserved throughmammalian evolution, confirming that the rat is an excellent model formany areas ofmedical research.The rodent lineage, which gave rise to the rat andmouse, and the primate lineage, which gave rise to humans, divergedabout 80 millionyears ago. Humans have 23 pairs of chromosomes, while rats have 21 andmice have 20.REFERENCES:The Journal Nature- Scientists release draft of the rat genomeNature.2004 Apr 1;428(6982):493-521. - Genome sequence of the BrownNorway rat yields insights into mammalian evolution.October 10, 2003Dr. Andrzej Bartke is awarded $850,000.00 for aging researchfromthe Ellison Medical Foundation (EMF)This award to Dr. Bartke is a four-year national grant for the studyofthe effects of genes and hormones on aging. Total budgetfor the grant is $850,000. The study will look at the growth andthyroid hormones and their roles in regulating glucose metabolism anddetermining therate of aging and length of life in Ames dwarf mice. Dr. Bartke'sresearch is providing new insights into themechanisms that control the aging process.REFERENCES:October10, 2003 - SIU Med School Faculty Member Receives National ResearchAwardSelectedpapersSeptember, 2003Ageing is reversed, and metabolism is reset to young levels inrecovering dauer larvae of C. elegans.Houthoofd K, Braeckman BP, Lenaerts I, Brys K, De Vreese A, VanEygenS, Vanfleteren JR.The nematode Caenorhabditis elegans responds to unfavourableenvironmentalconditions by arresting development and entering diapause as a dauerlarva. Dauers cansurvive several times the normal life span and the duration of thedauer state has noeffect on postdauer life span. This led to the suggestion that dauersare non-ageing, andthat dauers eventually perish as the consequence of depletion of storednutrients. Wehave investigated physiological changes associated with long-termdiapause survival,and found that dauer larvae slowly develop senescence-like symptoms,includingdecrease of metabolic capacity, aconitase enzyme activity, and ATPstores, andincrease of lipofuscin- and oxidised flavin-specific fluorescence.However, thesechanges are reversed when the dauers recover. Thus senescence can occurbeforeattainment of reproductive maturity, and furthermore, is reversible.Other life processes,including respiration rate and heat output, remain unaltered over fourweeks of diapauseat 24 degrees C. Possible determinants of the enhanced life maintenanceincludeincreased resistance to oxidative stress provided by enhancedsuperoxide diaseand catalase activities, and a shift to a highly reducing redox status.REFERENCES:Pubmed- Exp Gerontol. 2002 Aug-Sep;37(8-9):1015-21ExpGerontol. - Exp Gerontol. 2002 Aug-Sep;37(8-9):1015-21May 15th, 2003Recurrent de novo point mutations in lamin A causeHutchinson-Gilford progeria syndromeEriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, Scott L, ErdosMR,Robbins CM, Moses TY, Berglund P, Dutra A, Pak E, Durkin S, Csoka AB,Boehnke M, Glover TW, Collins FSHutchinson-Gilford progeria syndrome (HGPS) is a rare geneticdisorder characterized byfeatures reminiscent of marked premature ageing. Here, we presentevidence of mutations inlamin A (LMNA) as the cause of this disorder. The HGPS gene wasinitially localized tochromosome 1q by observing two cases of uniparental isodisomy of 1q-theinheritance of bothcopies of this material from one parent-and one case with a 6-megabasepaternal interstitialdeletion. Sequencing of LMNA, located in this interval and previouslyimplicated in several otherheritable disorders, revealed that 18 out of 20 classical cases of HGPSharboured an identical denovo (that is, newly arisen and not inherited) single-basesubstitution, G608G(GGC > GGT), withinexon 11. One additional case was identified with a differentsubstitution within the same codon.Both of these mutations result in activation of a cryptic splice sitewithin exon 11, resulting inproduction of a protein product that deletes 50 amino acids near thecarboxy terminus.Immunofluorescence of HGPS fibroblasts with antibodies directed againstlamin A revealed thatmany cells show visible abnormalities of the nuclear membrane. Thediscovery of the molecularbasis of this disease may shed light on the general phenomenon of humanageing.REFERENCES:Nature- 2003 May 15;423(6937):293-8Pubmed- Recurrent de novo point mutations in lamin A cause Hutchinson-Gilfordprogeria syndromeArclab- May 11, 2003 to May 17, 2003May 8th, 2002Scientists release draft of the mouse genomeUS and British Scientists released a draft copy of the mouse genomeonlinefor researchers to use freely. The information that is contained in themouse genome will help researchers who use the rodent for studying ahost of humanailments. In 2001 Celera Gennomics developed their own map of the mousegenome, but they change a fee in order to access their information,where asthe US and British Scientists released their data for free.The mouse genome consists of approximately 2,700,000,000 base pairsthat code for approximately 30,000 genes.REFERENCES:MouseGenome Resources - National Institutes of Health (NIH), USAMouse Genome Centre -Medical Research Council, UKFebruary, 2001The effects of aging on gene expression in the hypothalamus andcortex of miceCecilia H. Jiang, Joe Z. Tsien, Peter G. Schultz, and Yinghe HuProc. Natl. Acad. Sci. USA, Vol. 98, Issue 4, 1930-1934A better understanding of the molecular effects of aging in thebrain may help to reveal important aspects oforganismal aging, as well as processes that lead to age-related braindysfunction. In this study, we have examineddifferences in gene expression in the hypothalamus and cortex of youngand aged mice by using high-densityoligonucleotide arrays. A number of key genes involved in neuronalstructure and signaling are differentiallyexpressed in both the aged hypothalamus and cortex, includingsynaptotagmin I, cAMP-dependent protein kinaseC , apolipoprotein E, protein phosphatase 2A, and prostaglandin D.Misregulation of these proteins maycontribute to age-related memory deficits and neurodegenerativediseases. In addition, many proteases that play essential roles inregulatingneuropeptide metabolism, amyloid precursor protein processing, andneuronal apoptosis are up-regulated in the aged brain and likelycontribute significantly to brain aging. Finally, a subset of thesegenes whose expression is affected by aging are oppositely affected byexposure of mice to an enriched environment, suggesting that thesegenes may play important roles in learning and memory.REFERENCES:Theeffects of aging on gene expression in the hypothalamus and cortex ofmice - Proc. Natl. Acad. Sci. USA, Vol. 98, Issue 4, 1930-1934December 15th, 2000Extended Life-Span Conferred by Cotransporter Gene Mutations inDrosophilaBlanka Rogina, Robert A. Reenan, Steven P. Nilsen, Stephen L. HelfandScience 2000 290: 2137-2140Aging is genetically determined and environmentally modulated. Inastudy of longevity in the fruit fly, Drosophila melanogaster, we found that fiveindependent P-element insertionalmutations in a single gene resulted in a near doubling of the average life-span without adecline in fertility or physical activity. Sequence analysis revealedthat the product of this gene,named Indy (for I'm not dead yet), is most closely related to amammalian sodiumdicarboxylate cotransporter--a membrane protein that transports Krebscycle intermediates.Indy was most abundantly expressed in the fat body, midgut, andoenocytes: the principal sitesof intermediary metabolism in the fly. Excision of the P elementresulted in a reversion tonormal life-span. These mutations may create a metabolic state thatmimics caloricrestriction, which has been shown to extend life-span.REFERENCES:Science- 2000 Dec 15;290(5499):2048.Pubmed- Extended Life-Span Conferred by Cotransporter Gene Mutations inDrosophilaArclab- Dec 10, 2000 to Dec 16, 2000November 8th, 2000The Center for Research and Education in Aging (CREA) will beofficially launched November 8th, 2000On November 8th, 2000 the Center for Research and Education inAging,which has a mission of"investigating the basic processes that cause aging, with the goal ofimproving andextending human health span." will be officially launched. For more information aboutthis important and groundbreaking organization or to find out how youcan help CREA achieveits mission, please visit CREA's website at:http://crea.berkeley.eduOctober 6th, 2000Regulation of C. elegans life-span by insulinlike signaling inthenervous systemWolkow CA, Kimura KD, Lee MS, Ruvkun GScience 2000 Oct 6;290(5489):147-50An insulinlike signaling pathway controls Caenorhabditis elegansaging, metabolism, and development.Mutations in the daf-2 insulin receptor-like gene or the downstreamage-1 phosphoinositide 3-kinasegene extend life-span by two- to threefold. To identify tissueswhere this pathway regulatesaging and metabolism, we restored daf-2 pathway signaling to onlyneurons, muscle, or intestine. Insulinlike signaling inneurons alone was sufficient to specify wild-type life-span, but muscleor intestinal signaling was not.However, restoring daf-2 pathway signaling to muscle rescued metabolicdefects, thus decoupling regulationof life-span and metabolism. These findings point to the nervous systemas a central regulator of animal longevity.REFERENCES:Regulationof C. elegans life-span by insulinlike signaling in the nervous system- Science 2000 Oct 6;290(5489):147-50June 26, 2000International Human Genome Sequencing Consortium Announces"WorkingDraft" of Human Genome The Human genome consists approximately 3.12-gigabases that code for80,000 genes.The work, carried out in 16 centres across the world, means that 85% ofthe human genome has been accurately deciphered. Further work, still tobefinally checked, means in total 97% of the humangenome has been read. The existence of this genetic map will lay thefoundation for a revolution in medical diagnosis and treatment.REFERENCES: Joint Genome Institute TheInsitute for GenomicResearch Universityof Utah: Human Genetics Department Universityof Washington Genome Center National HumanGenome Research Institute (NHGRI) • The Human Genome Project • TheHuman Genome Project: From Maps to Medicine HumanGenome Sequencing The HumanGenome Organisation (HUGO) Genome Sequence Centre(Canada) Sanger Centre (U.K.) CDC - Office ofGenetics Departmentof Energy-Life Sciences Division Celera Genome Research • GenomicsEducation Cooperative HumanLinkage Center WhiteheadInstitute for Biomedical Research, MIT GenethonGenome Research (France) Centre forHuman Genome Research (Denmark) Los Alamos NationalLaboratory: Center for Human Genome Studies Stanford HumanGenome Center Advanced Center forGenome Technology, University of Oklahoma CNN- 26 June 2000 - Genome announcement a milestone, but only a beginning BBC- 26 June 2000 - Scientists crack human code CBC- 26 June 2000 - Mapping the genetic code TIME- JULY 3, 2000 VOL. 156 NO. 1 - MAPPING THE GENOME NOTE: Also refer to the article on sequencing of Drosophilamelanogaster, dated March 23rd, 2000. NOTE: Also refer to the article on sequencing of C. elegans, datedDecember 11th, 1998. March 23rd, 2000The Drosophila melanogaster genome has been fully sequenced.REVIEW The 180-megabase genomic sequence of Drosophila melanogasterreveals 13,601genes. In Drosophila, 60 Mb of the 180-Mb genome consists of centricheterochromatin.The C. elegans was fully sequenced on December 11th, 1998 and it had97-megabases and 19,000 genes.REFERENCES: Science2000 Mar 24;vol 1287, issue 5461. page 2181 TheBerkeley Drosophila GenomeProject (BDGP) TheEuropean Drosophila GenomeProject FlyBase - At HarvardUniversity NOTE: Also refer to the article on C. elegans dated December11th,1998. Dec 1, 1999First human chromosome is fully sequencedScientists with the Human Genome Project have sequencedchromosome 22, the first chromosome to have been fullymapped. The results of this affort are published in the December 2ndissueof the journal Nature.The sequence obtained consists of 12 contiguous segments spanning 33.4megabases,contains at least 545 genes and 134 pseudogenes, and provides the firstview of thecomplex chromosomal landscapes that will be found in the rest of thegenome.More than 30 human disorders are already associated with changes togenes of chromosome 22. These include schizophrenia, disorders offetal development and the nervous system.The next chromosome to be fully sequenced will most likely bechromosome 7.NIHLink to Chromosome 22Human Genome Organisation link to Chromosome 22The Sanger Centres link to Chromosome 22The DOE's Joint Genome Institute Real Audio 80K clip on the sequenceing ofchromosome 22Real Audio 28K clip on the sequenceing ofchromosome 22Nov 18, 1999Suppression of p66shc protein, extends the life span of mice 30%The following describes mutant mice that seem to live almostone-thirdlonger than wild-typeanimals. These mice, which have a single targeted mutation in the geneencoding the p66shcprotein, develop and eat normally, and have a normal body weight. Butthe absence of p66shcconfers a heightened cellular resistance to agents that cause oxidativedamage. Although theconclusions must be regarded as provisional until larger groups ofanimals are studied, the resultssupport the proposal2 that oxidative damage is involved in ageing. Theyalso indicate thatmodification of the response to oxidative damage can have aconsiderable effect on lifespan,without apparent negative side effects.NIHOMIM link - SHC TRANSFORMING PROTEINNIHLocusLink - SHC TRANSFORMING PROTEINNature 1999 Nov 18;402(6759):309-13The p66shc adaptor protein controls oxidative stress response and lifespan in mammals.ABC News - Scientists Find Gene Switch Makes Mice Live Longer Oct 4, 1999Buck Center for Research in Aging celebratesthe opening of the Research, Support and Education BuildingFrom September 30th 1999 to October 1st 1999 the Buck Center forResearch inAging in Novato, California, held an inaugural symposiam on aging tocelebratethe opening of the center. The Buck Center is located 20 milesnorth of the Golden Gate Bridge in northern Marin County.The Buck Center receives 5.5 millions annually from the Buck Trustand is governed by its own Board of Directors.Buck Center for Research inAgingMay 4, 1999Geron acquires Roslin Bio-Med andforms research collaboration with the Roslin InstituteMENLO PARK, CA and ROSLIN, MIDLOTHIAN, SCOTLAND - May 4, 1999 Alliance bringstogether three complementarybreakthrough technologies: human pluripotent stem cells, telomeraseexpression and nuclear transfer. The combinedtechnologies are expected toenhance and accelerate the development of new transplantation therapiesfor numerous degenerative diseases such as diabetes, Parkinson’sdisease, cancer and heart disease. Geron andthe Roslin Institute are pioneers inthese technologies and together are in a strong position to capitalizeon their potential. For more details.March 26, 1999Dr. Judith Campisi is awarded $964,000.00 for aging researchBerkeley, CA - March 26, 1999 - The Ellison Medical Foundation hasawarded Dr. Judith Campisi $964,000.00 to support her basicinvestigations into the causes of aging. The Foundation was setup byLarry Ellison, CEO of Oracle,one of the largest database software corporations in the United States.Judith Campisi is a researcher in theDepartment of Cell and Molecular Biology at the Lawrence BerkeleyNational Laboratory inBerkeley, California.For moredetails.March 4, 1999Mouse model demonstrates role of telomeres and telomerase inaging,cancer and lifespanMenlo Park, CA - March 4, 1999 - Geron Corporation announced thatresearchers at the Dana-FarberCancer Institute of Harvard Medical School and colleagues at JohnsHopkins School of Medicine havepublished in the March 5 issue of Cell that telomerase-negative miceshow telomere loss with age andexperience a host of age-related changes. This study expands on agrowing body of in vivo proof thatage-related telomere erosion contributes to pathology, includingcancer. Significant new findingsin this work include a causal link between telomere loss and twohallmarks of human aging: animpaired ability to recover from stress and an increased rate of cancerformation. Consistentwith other data linking telomerase activity with tumor progression, theauthors suggest thattelomere loss contributes to cancer formation, but lack of telomeraseinhibits long-term tumorgrowth.For moredetailsDecember 28th, 1998Geron announces first in Vivo data indicating telomeraseexpressionin normal human cells extends their replicative lifespan withoutoncogenic transformation.Geron Corp and the University of Texas Southwestern Medical Centerat Dallas announced today the publication of two papers in the Jan 1,1999,issue of Nature Genetics.December 17th, 1998Human cells cloned.A group at Kyunghee University Hospital in Seoul, South Korea,combinedan egg and a cell from a single donor toproduce the first stages of a human embryo. The experimentwas terminated by the reseachers after a few cell divisionshad taken place.December 11th, 1998Genome sequence of the nematode C. elegans: A platform forinvestigatingbiology the C. elegans sequencing consortium.REVIEW The 97-megabase genomic sequence of the nematodeCaenorhabditiselegans reveals over 19,000genes. More than 40 percent of the predicted protein products findsignificant matches in other organisms.There is a variety of repeated sequences, both local and dispersed. Thedistinctive distribution of some repeatsand highly conserved genes provides evidence for a regionalorganization of the chromosomesScience 1998 Dec 11;282(5396):2012-8The genetics of aging as it relates to the C. elegans Lifeextension and stress resistance in Caenorhabditis elegans modulated bythe tkr-1 gene. Moleculargenetics of life span in C. elegans: how much does it teach us? Geneticcontrol of programmed cell death and aging in the nematodeCaenorhabditis elegans. Agenetic pathway conferring life extension and resistance to UV stressin Caenorhabditis elegans. Directisolation of longevity mutants in the nematode Caenorhabditis elegans. Defininggenes that govern longevity in Caenorhabditis elegans. Identificationgenes that are differentially expressed during aging in Caenorhabditiselegans .December 9th, 1998First Cows are ClonedEight calves, four of which died during birth,are cloned from a single caw by a team led by Dr. Yukio Tsunodaof Kinki University in Nara, JapanNovember 6th, 1998Embryonic Stem Cell Lines Derived from Human Blastocysts.Thomson JA, Itskovitz-Eldor J, Shapiro SS, Waknitz MA, Swiergiel JJ,Marshall VS, Jones JMJ. A. Thomson, M. A. Waknitz, J. J. Swiergiel, V. S. MarshallWisconsin Regional Primate Research Center, University ofWisconsin,Madison, WI 53715, USA. J. Itskovitz-Eldor, Department of Obstetricsand Gynecology, Rambam Medical Center, Faculty of Medicine, Technion, Haifa 31096, Israel. S. S. Shapiro and J. M. Jones,Department of Obstetrics and Gynecology, University of Wisconsin,Madison, WI 53715, USA.Science 1998 Nov 6;282(5391):1145-1147Human blastocyst-derived, pluripotent cell lines are describedthat have normal karyotypes, express high levels of telomeraseactivity, and express cell surface markers that characterize primateembryonic stem cells but do not characterize other early lineages. After undifferentiated proliferation in vitro for 4 to 5 months,these cells still maintained the developmental potential to formtrophoblast and derivatives of all three embryonic germ layers,including gut epithelium (endoderm); cartilage, bone,smooth muscle, and striated muscle (mesoderm); and neural epithelium,embryonic ganglia, and stratified squamous epithelium (ectoderm). Thesecell lines should be useful in human developmental biology, drugdiscovery, and transplantation medicine..EmbryonicStem Cell Lines Derived from Human BlastocystsScience Volume 282, Number 5391 Issue of 6 Nov 1998, pp. 1145 - 1147NewPotential for Human Embryonic Stem CellsScience Volume 282, Number 5391 Issue of 6 Nov 1998, pp. 1061 - 1062Derivation of pluripotent stem cells from cultured humanprimordialgerm cells Michael J. Shamblott*, Joyce Axelman*, Shunping Wang*, ElizabethM.Bugg*, John W. Littlefield, Peter J. Donovan, Paul D. Blumenthal,George R. Huggins, and John D. Gearhart,Departments of Gynecology and Obstetrics and Physiology,Johns Hopkins University School of Medicine, Baltimore, MD 21287; Kimmel Cancer Institute, Jefferson Medical College, Philadelphia,PA 19107; and Department of Gynecology and Obstetrics, Johns Hopkins Bayview Hospital, Baltimore, MD 21224PNAS Vol. 95, Issue 23, 13726-13731, November 10, 1998Human pluripotent stem cells would be invaluable for in vitrostudies of aspects of human embryogenesis. With the goal ofestablishing pluripotent stem cell lines, gonadal ridges andmesenteries containing primordial germ cells (PGCs, 5-9 weekspostfertilization) were cultured on mouse STO fibroblast feeder layers in thepresence of human recombinant leukemia inhibitory factor, humanrecombinant basic fibroblast growth factor, and forskolin. Initially,single PGCs in culture were visualized by alkaline phosphatase activity staining. Over a period of 7-21 days, PGCs gave riseto large multicellular colonies resembling those of mouse pluripotentstem cells termed embryonic stem and embryonic germ (EG) cells.Throughout the culture period most cells within the colonies continued to be alkaline phosphatase-positive and testedpositive against a panel of five immunological markers (SSEA-1, SSEA-3,SSEA-4, TRA-1-60, and TRA-1-81) that have been used routinely tocharacterize embryonic stem and EG cells. The cultured cells have been continuously passaged and found to bekaryotypically normal and stable. Both XX and XY cell cultures havebeen obtained. Immunohistochemical analysis of embryoid bodiescollected from these cultures revealed a wide variety of differentiated cell types, including derivatives of all three embryonic germlayers. Based on their origin and demonstrated properties, these humanPGC-derived cultures meet the criteria for pluripotent stem cells andmost closely resemble EG cells..Derivationof pluripotent stem cells from cultured human primordial germ cellsProceedings of the National Academy of Sciences Vol. 95, Issue 23,13726-13731, November 10, 1998November 6th, 1998The 77year old John Glenn and his shuttle mission.JohnGlenn's science experiments that pertain to the study of aging.July 22nd, 199850 mice cloned by researchers at the University of HawaiiOver 50 female mice were cloned by a team led by Ryuzo Yanagimachi,a University of Hawaii scientist.They used a cumulous cell,a type of cell that comes from the ovaries offemalesbut is not an egg cell,then they extracted the nucleus and placed itinsidea hollowed-out egg cell using a tiny pipette. Then they implanted theegg cellinto the uterus of a female animal.Cloning shows that cells can be reprogrammed to start over anddevelop into a whole creature, the question is will thecloned animals age normally or will they age at a faster rate? Detailsofthe experiment were published in the July 22nd, 1998 issue of Nature.Nature..Gene found which is linked to Alzheimer's disease A Gene has been found which is linked to Alzheimer's diseas. Thenew discovery was reportedon the 22 July 1998 at a conference in Amsterdam.Geneticist Rudolph E. Tanzi and his research team at MassachusettsGeneralHospital in Boston identified a gene called A2M which is responsibleforproducing a protein which strongly interacts with proteins produced bytwo ofthe genes-called LRP and APOE- linked to familial Alzheimer's.The studyshows that people with thedefective form of the gene are three and one half times more likely todevelop late-onset Alzheimer's. The disease is believed to be caused bytheaccumulation of waxy plaques, composed largely of a protein calledbeta-amyloid, which kills brain cells.The study will be published in the August 1st, 1998 issue of NatureGenetics.Nature - Genetics..Fruit flies bred with copies of thehumanSOD1 gene live as much as 40 percent longer.June 2, (1998).Gabrielle Boulianne, a neurobiologist at the Hospital for SickChildren anda professor of molecular and medical genetics at the University ofTorontoreports in an article in the June issue of the journal Nature Geneticsthatshe and her co-workers bred Drosophila melanogaster with copies of thehumanSOD1 gene and the result was a fly that could live as much as 40percent longer..ABSTRACT:Extension of Drosophila lifespan by overexpression of human SOD1inmotorneuronsTony L. Parkes1, Andrew J. Elia2, Dale Dickinson1, Arthur J.Hilliker1, John P. Phillips1 & Gabrielle L. Boulianne2Reactive oxygen (RO) has been identified as an important effectorinageingand lifespan determination1-3. The specific cell types, however, inwhichoxidative damage acts to limit lifespan of the whole organism have notbeenexplicitly identified. The association between mutations in the geneencodingthe oxygen radical metabolizing enzyme CuZn superoxide diase (SOD1)andloss of motorneurons in the brain and spinal cord that occurs in thelife-shorteningparalytic disease, Familial Amyotrophic Lateral Sclerosis (FALS; ref.4), suggeststhat chronic and unrepaired oxidative damage occurring specifically inmotorneurons could be a critical causative factor in ageing. To test thishypothesis,we generated transgenic Drosophila which express human SOD1specifically in motorneurons. We show that overexpression of a single gene, SOD1, in asingle celltype, the motorneuron, extends normal lifespan by up to 40% and rescuesthe lifespanof a short-lived Sod null mutant. Elevated resistance to oxidativestress suggeststhat the lifespan extension observed in these flies is due to enhancedRO metabolism.These results show that SOD activity in motorneurons is an importantfactor in ageingand lifespan determination in Drosophila..REFER TO:Nature - GeneticsRoleof oxidative stress in Drosophila aging.- Mutat Res 1992Sep;275(3-6):267-279Expressionof bovine superoxide diase in Drosophila melanogaster augmentsresistance ofoxidative stress.- Mol Cell Biol 1991 Feb;11(2):632-640.January 16th, 1998Extension of Life-Span by IntroductionofTelomeraseinto Normal Human CellsScience, Jan 16, (1998). Andrea G. Bodnar, Michel Ouellette, Maria Frolkis Shawn E. Holt,Choy-Pik Chiu,Gregg B. Morin, Calvin B. Harley, Jerry W. Shay, Serge Lichtsteiner,Woodring E.Wright Rel 2.9 - 98/01/29 February 27, 1997Letterto Nature -- Viable offspring derived from fetal and mammaliancells Nature, Volume 385, 810 - 813, February 27, 1997 SeeNature Web Special: Cloned Sheep February 24, 1997Scientistsclone first mammal "They found a way of stopping the clock and programming the genes so they go back to the beginning," James told Reuters in a telephone interview. CNN, February 24, 1997 The Telomerase Picture Fills In SCIENCE - 25 April 1997 - Volume 276 - Number 5312 PositionalCloning of the Wernerssyndrome Gene - Abstract,Summary SCIENCE - 12 Apr 1996; 272 (5259):258-262 ... .THE NEW SCIENCE OFAGINGA TV series that was shown on PBS Wednesday, June 2, 1999, 8:00 p.m. ET For information about the videocassettesfrom PBS For more details about this documentary . If you do not have the Real Audio program that you need to listen tothe programs below,please click on this message and you may then download the program onto your system..Sep 16, 2003 - KQED ForumAging ResearchGuests:Cynthia KenyonHerbert Boyer Professor of Biochemistry and BiophysicsDirector, Hillblom Center for the Biology of AgingUniversity of California San FranciscoSan Francisco, CaliforniaDale Bredesen,founding president and CEO,Buck Institute for Age ResearchDavid Sinclair,Professor of pathology,Harvard Medical SchoolPhilip Cohen,San Francisco bureau chief for New Scientist magazine.May 9, 2003 - NPR Talk of the NationGenetics of AgingGuests:Ted GavinMember, Board of DirectorsSpamCon FoundationSan Francisco, CaliforniaPhil GoldmanChief Executive OfficerMailBlocksLos Altos, CaliforniaDavid SinclairAssistant Professor of PathologyHarvard Medical SchoolBoston, MassachusettsCynthia KenyonHerbert Boyer Professor of Biochemistry and BiophysicsDirector, Hillblom Center for the Biology of AgingUniversity of California San FranciscoSan Francisco, California.August 31, 2001 - NPR Talk of the Nation: Science Friday Longevity and Aging Guests: Michael FosselAuthor, "ReversingHuman Aging"Clinical Professor of MedicineMichigan State UniversityEast Lansing, MI Steven AustadAuthor,"Why We Age: What Science Is Discovering About the Body's JourneyThrough Life" (Wiley)Associate Professor, ZoologyGerontologistUniversity of IdahoMoscow, Idaho Thomas Perls Author,"Living to 100: Lessons in Living to Your Maximum Potential at Any Age"(Basic Books)Geriatrician, Gerontology Division and Biometrics CenterBeth Israel Deaconess MedicalCenterAssociate Professor, Division on AgingHarvard Medical SchoolBoston, Massachusetts Michael McKubre Director, Energy Research Center SRI Incorporated Menlo Park, California June 26, 2000 - NPR Talk of the NationThe Human Genome The ten year race to complete a map of the human genetic code hasended in a tie. The publicly funded Human Genome Project and theprivate corporation Celera Genomics are announcing today that theirwork on a rough draft of a map of the human genome is complete. Themap won't lead to medical miracles overnight, but once theinformation has been studied it could lead to the development of newdrugs and therapies to treat diseases.Join Juan Williams and guests to discuss what a complete map of thehuman genome will mean for the future of medicine and humanity..June 9, 2000 - NPR Talk of the NationThe Human Genome and a genetics update The public-private race to get the first complete map of the humangenome is nearing the finish line, with both groups expected toannounce a working draft sometime this month. Then the real workbegins: finding the genes along those long stretches of DNA anddetermining their function. This hour, we'll get an update on the latestgenetics news.Guests:Bruce RoeGeorge Lynn Cross Research Professor of Chemistry and BiologyDirector, Advanced Center for Genome TechnologyUniversity of OklahomaNorman, OklahomaFred CohenMember, Board of DirectorsDoubleTwistProfessor, Medicine and PharmacologyUniversity of CaliforniaSan Francisco, CaliforniaMaja BucanAssociate Professor, GeneticsCenter for Neurobiology and BehaviorUniversity of Pennsylvania Medical CenterPhiladelphia, Pennsylvania.May 14, 1999 - NPR Talk of the Nation: Science Friday AGING RESEARCH UPDATE Researchers from Columbia University announced that they haveidentified an enzyme crucial to extending the lifespan of roundworms.Articles Discussed: "A cytosolic catalase is needed to extend lifespan in C. elegansdaf-C and clk-1 mutants, "by James Taub, Joe F. Lau, Charles Ma, Jang Hee Hahn, Rafaz Hoque,Jonathan Rothblatt and Martin Chalfie.Nature, May 13, 1999.Guests:Martin ChalfieProfessor, Biological ScienceColumbia UniversityNew York, New YorkSteven AustadAuthor, Why We Age: What Science is Discovering About the Body'sJourney Through Life (John Wiley & Sons)Associate Professor, ZoologyGerontologistUniversity of IdahoMoscow, Idaho.January 29, 1999 - NPR Talk of the Nation: Science Friday STEM CELL UPDATE .Brief Text Description:Human embryonic stem cell research, which holdsthe promise of curing many diseases, has been hampered by a lack offunds.But last week, the federal government ruled that much of this work iseligibleto receive federal funds, a decision that the National BioethicsAdvisoryCommission is slated to debate.John GearhartProfessor of Gynecology and ObstetricsJohns Hopkins University School of MedicineBaltimore, MarylandEric MeslinExecutive DirectorNational Bioethics Advisory CommissionRockville, MarylandBruce TorbettResearcherScripps Research InstituteLa Jolla, CaliforniaKent SmithResearch AssociateScripps Research InstituteLa Jolla, California.January 16, 1998 - NPR Talk of the Nation: Science Friday AGING UPDATE Brief Text Description: For the first time, scientists have been able to get human cellsinthe lab to live much longer than normal, perhaps paving the way for newtreatments for age-related diseases and cancer. In this hour, we'll getan update on the latest aging research. Plus, a new way of thinkingabout how the brain stores memories.Guests: Calvin Harley Chief Scientific Officer Geron Corporation Menlo Park, California Michael Fossel Author, Reversing Human Aging, (WilliamMorrow) Clinical Professor of Medicine Michigan State University East Lansing, Michigan Kelsey Martin Post-doctoral Fellow Howard Hughes Medical Institute Center for Neurobiology and Behavior Columbia University, New York, New York Dusan Bartsch Post-doctoral Fellow Howard Hughes Medical Institute Center for Neurobiology and Behavior Columbia University, New York, New York.September 5, 1997 - NPR Talk of the Nation: Science Friday GENETICS OF AGING .Brief Text Description:.Guests:Gary RuvkunFaculty Member, Department of Genetics,Harvard Medical SchoolBoston, MassachusettsMichael FosselAuthor, Reversing Human Aging, William Morrow and CompanyClinical Professor of MedicineMichigan State UniversityEast Lansing, MichiganMike WestFounder and Vice President,Geron Corporation,Menlo Park,California.April 12, 1996 - NPR Talk of the Nation: Science Friday.Brief Text Description:.THE SCIENCE OF AGINGGuests: Gerard SchellenbergAssociate Director of ResearchGeriatric Research, Education, and Clinical CenterVeterans Affairs Puget Sound Health Care SystemSeattle, WAStanley RapoportChief of Laboratory of NeuroscienceNational Institute on AgingBethesda, MDMichael FosselProfessor of Clinical MedicineMichigan State UniversityEast Lansing, MIAuthorReversing Human Aging.September 29, 1995 - NPR Talk of the Nation: Science Friday BIOLOGY OF AGING BriefText Description:Guests:Dr. Leonard HayflickSchool of MedicineUniversity of California, San FranciscoSan Francisco,CAJerry Shay Professor of Cell Biology and NeuroscienceUniversity of Texas Southwestern Medical CenterDallas, TXDr. Michael Fossel, Author of forthcoming book, "Reversing Human Aging"Professor of MedicineMichigan State UniversityEast Lansing, MIMay 24, 1996 - NPR Talk of the Nation: Science Friday GENE THERAPY Brief Text Description:Guests:Ronald CrystalProfessor of Medicine and Chief of the Division of Pulmonaryand Critical Care MedicineThe New York Hospital-Cornell Medical CenterNew York, N.Y.Jeffrey LeidenProfessor of Medicine, Professor of Pathology, and Chief ofthe Section of CardiologyThe University of ChicagoChicago, Ill.Theories of AgingPapers on different Theories of AgingTheories of Aging...Upcoming Meetings and Conferences  Events without dates should be considered as tentative.Calender ofUpcomingMeetings/Conferences......JournalsArticles pertaining to the aging process can be found in thejournals listed below. AgingCell AGINGClinical and Experimental Research AgeingResearch Reviews AmericanJournal of RespiratoryCell and Molecular Biology AmericanSociety of Human Genetics Apoptosis Biochemistry andMolecular Biology International Biogerontology Biologyof the Cell Blood- American Society ofHematology CancerCell Cell Celland tissue research CellBiochemistry and Function Cell BiologyInternational CellDeath and Differentiation Cellularand MolecularNeurobiology Cellularimmunology Cellularsignalling CurrentAdvances in Cell & Developmental Biology Cytogenetics and CellGenetics Development Developmentgenes and evolution Development,growth & differentiation DevelopmentalBiology DevelopmentalBrain Research Developmental cell Developmentalgenetics DevelopmentalReview EMBO -European Molecular BiologyOrganization Endocrinereviews Endocrinology Experimental CellResearch ExperimentalGerontology FASEB -Federation of AmericanSocieties for Experimental Biology Free RadicalBiology and Medicine Gene GeneStructure and Expression Genes& Development Genes tocells Genomics Gerontology Glia GrowthHormone & IGF Research HumanMolecular Genetics InternationalJournal of Biochemistry and Cell Biology InternationalJournal of Biological Macromolecules InternationalJournal of Developmental Neuroscience Journalof Anti-AgingMedicine Journal ofCell Biology Journalof Cell Science Journalof Cellular Biochemistry Journal ofEndocrinology Journalof Experimental Biology Journal ofMolecular Biology Journalof Neuroscience Mechanismsof Ageing and Development Mechanismsof Development Molecularand Cellular Biology Molecular and CellularEndocrinology MolecularBiology of the Cell MolecularBrain Research Molecular Immunology MutationResearch MutationResearch-DNA Repair Nature Nature- Genetics Nature- Biotechnology Nature- Neuroscience Neurobiologyof Aging Neuroendocrinology NewScientist Nucleic Acids Research Proceedingsof the National Academyof Sciences Science Seminars in Cell andDevelopmental Biology Trends inBiochemical Sciences Trends inBiotechnology Trends inCell Biology Trends inEndocrinology and Metabolism ... 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