Aging  Research  Centre
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Release 11.7
Welcome
We are dedicated to providing a service that allows researchers in this field to find information that is related to the study of the aging process. We also endeavor to introduce this field to laymen who would like to know more about the research that is being conducted in this field.             
 
Steven A. Garan, Director 		Research
We are engaged in many areas of research such as systems biology, brain imaging via automated imaging microscopy, the study of neuroendocrine changes in the hypothalamus, whole body scanning systems, the study of an entire organism as it ages and the effects of hormonal changes on the aging process
 
 
 


 
Publications
             


 

Projects




Automated Imaging
Microscope System
 (AIMS)
Regional targeting of
cytoplasmic and
nuclear-stained tissue
Ontological body system maps
Mapping body systems
aims
aims






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Nov 24th, 2006

Age-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, 2005

Caloric restriction reduces cell loss and maintains estrogen receptor-alpha immunoreactivity in the pre-optic hypothalamus of female B6D2F1 mice.

Life-long calorie restriction (CR) remains the most robust and reliable means of extending life span in mammals. Among the several theories to explain CR actions, one variant of the neuroendocrine theories of aging postulates that changing hypothalamic sensitivity to endocrine feedback is the clock that times phenotypic change over the life span. If the feedback sensitivity hypothesis is correct, CR animals should display a significantly different pattern of hormone-sensitive cell density and distribution in the hypothalamus. Of the many endocrine signal receptors that may be involved in maintaining hypothalamic feedback sensitivity, our study has selected to begin mapping those for estrogen (E). Altered hypothalamic sensitivity to E is known to schedule reproductive maturation and influence reproductive senescence. Taking estrogen receptor-alpha (ERalpha) immunoreactivity as an index of sensitivity to E, we counted ERalpha immunoreactive and non-immunoreactive cells in the pre-optic hypothalamus of young (6 weeks), ad-libitum (Old-AL) fed old (22 months), and calorie restricted (Old-CR) old (22 months) female B6D2F1 mice. An automated imaging microscopy system (AIMS) was used to generate cell counts for each sampled section of pre-optic hypothalamus. Results show a 38% reduction in ERalpha immunoreactive cells and an 18% reduction in total cell numbers in AL-old mice in comparison to young mice. However, CR mice only show a 19% reduction in ERalpha immunoreactive cells and a 13% reduction in total cell numbers in comparison to young mice. This indicates CR prevents age-related cell loss and maintains estrogen sensitivity in the pre-optic hypothalamus of old female B6D2F1 mice.

REFERENCES:

Neuroendocrinology Letters 2005 Jun;26(3):197-203.

May 27th, 2004

Premature aging in mice expressing defective mitochondrial DNA polymerase

Researchers in Sweden have created homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mitochondrial DNA (mtDNA) polymerase. The mice encountered a threefold to fivefold increase in the levels of point mutations as well as increased amounts of deleted mtDNA. The deterioration in the experimental mice started at 25 weeks young adulthood in normal mice. They prematurely experienced a range of familiar age-related complaints, including baldness, osteoporosis, anemia, curvature of the spine and reduced fertility. The lifespan of the experimental mice was markedly reduced, with the median age of death at 48 weeks. The oldest of the experimental mice died before 61 weeks. Normal mice live approximately 110 weeks.

REFERENCES:

Nature 2004 May 27; 429, 357 - Ageing: Mice and mitochondria

Nature 2004 May 27; 429, 417 - 423 - Premature aging in mice expressing defective mitochondrial DNA polymerase

April 1st, 2004

Scientists release draft of the rat genome

An international research team, supported by the National Institutes of Health (NIH), today announced it has completed a high-quality, draft sequence of the genome of the laboratory rat, and has used that data to explore how the rat's genetic blueprint stacks up against those of mice and humans. In the Nature article, the researchers reported that, at approximately 2.75 billion base pairs, the rat genome is smaller than the human genome, which is 2.9 billion base pairs, and slightly larger than mouse genome, which is 2.6 billion base pairs. Rat genome contains about the same number of genes as the human and mouse genomes. Furthermore, almost all human genes known to be associated with diseases have counterparts in the rat genome and appear highly conserved through mammalian evolution, confirming that the rat is an excellent model for many areas of medical research. The rodent lineage, which gave rise to the rat and mouse, and the primate lineage, which gave rise to humans, diverged about 80 million years ago. Humans have 23 pairs of chromosomes, while rats have 21 and mice have 20.

REFERENCES:

The Journal Nature - Scientists release draft of the rat genome
Nature. 2004 Apr 1;428(6982):493-521. - Genome sequence of the Brown Norway rat yields insights into mammalian evolution.

October 10, 2003

Dr. Andrzej Bartke is awarded $850,000.00 for aging research from the Ellison Medical Foundation (EMF)

This award to Dr. Bartke is a four-year national grant for the study of the effects of genes and hormones on aging. Total budget for the grant is $850,000. The study will look at the growth and thyroid hormones and their roles in regulating glucose metabolism and determining the rate of aging and length of life in Ames dwarf mice. Dr. Bartke's research is providing new insights into the mechanisms that control the aging process.

REFERENCES:

October 10, 2003 - SIU Med School Faculty Member Receives National Research Award

Selected papers

September, 2003

Ageing is reversed, and metabolism is reset to young levels in recovering dauer larvae of C. elegans.

Houthoofd K, Braeckman BP, Lenaerts I, Brys K, De Vreese A, Van Eygen S, Vanfleteren JR.

The nematode Caenorhabditis elegans responds to unfavourable environmental conditions by arresting development and entering diapause as a dauer larva. Dauers can survive several times the normal life span and the duration of the dauer state has no effect on postdauer life span. This led to the suggestion that dauers are non-ageing, and that dauers eventually perish as the consequence of depletion of stored nutrients. We have investigated physiological changes associated with long-term diapause survival, and found that dauer larvae slowly develop senescence-like symptoms, including decrease of metabolic capacity, aconitase enzyme activity, and ATP stores, and increase of lipofuscin- and oxidised flavin-specific fluorescence. However, these changes are reversed when the dauers recover. Thus senescence can occur before attainment of reproductive maturity, and furthermore, is reversible. Other life processes, including respiration rate and heat output, remain unaltered over four weeks of diapause at 24 degrees C. Possible determinants of the enhanced life maintenance include increased resistance to oxidative stress provided by enhanced superoxide dismutase and catalase activities, and a shift to a highly reducing redox status.

REFERENCES:

Pubmed - Exp Gerontol. 2002 Aug-Sep;37(8-9):1015-21
Exp Gerontol. - Exp Gerontol. 2002 Aug-Sep;37(8-9):1015-21

May 15th, 2003

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Eriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, Scott L, Erdos MR, Robbins CM, Moses TY, Berglund P, Dutra A, Pak E, Durkin S, Csoka AB, Boehnke M, Glover TW, Collins FS

Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by features reminiscent of marked premature ageing. Here, we present evidence of mutations in lamin A (LMNA) as the cause of this disorder. The HGPS gene was initially localized to chromosome 1q by observing two cases of uniparental isodisomy of 1q-the inheritance of both copies of this material from one parent-and one case with a 6-megabase paternal interstitial deletion. Sequencing of LMNA, located in this interval and previously implicated in several other heritable disorders, revealed that 18 out of 20 classical cases of HGPS harboured an identical de novo (that is, newly arisen and not inherited) single-base substitution, G608G(GGC > GGT), within exon 11. One additional case was identified with a different substitution within the same codon. Both of these mutations result in activation of a cryptic splice site within exon 11, resulting in production of a protein product that deletes 50 amino acids near the carboxy terminus. Immunofluorescence of HGPS fibroblasts with antibodies directed against lamin A revealed that many cells show visible abnormalities of the nuclear membrane. The discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing.

REFERENCES:

Nature - 2003 May 15;423(6937):293-8
Pubmed - Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
Arclab - May 11, 2003 to May 17, 2003

May 8th, 2002

Scientists release draft of the mouse genome

US and British Scientists released a draft copy of the mouse genome online for researchers to use freely. The information that is contained in the mouse genome will help researchers who use the rodent for studying a host of human ailments. In 2001 Celera Gennomics developed their own map of the mouse genome, but they change a fee in order to access their information, where as the US and British Scientists released their data for free. The mouse genome consists of approximately 2,700,000,000 base pairs that code for approximately 30,000 genes.

REFERENCES:

Mouse Genome Resources - National Institutes of Health (NIH), USA
Mouse Genome Centre - Medical Research Council, UK

February, 2001

The effects of aging on gene expression in the hypothalamus and cortex of mice


Cecilia H. Jiang, Joe Z. Tsien, Peter G. Schultz, and Yinghe Hu
Proc. Natl. Acad. Sci. USA, Vol. 98, Issue 4, 1930-1934

A better understanding of the molecular effects of aging in the brain may help to reveal important aspects of organismal aging, as well as processes that lead to age-related brain dysfunction. In this study, we have examined differences in gene expression in the hypothalamus and cortex of young and aged mice by using high-density oligonucleotide arrays. A number of key genes involved in neuronal structure and signaling are differentially expressed in both the aged hypothalamus and cortex, including synaptotagmin I, cAMP-dependent protein kinase C , apolipoprotein E, protein phosphatase 2A, and prostaglandin D. Misregulation of these proteins may contribute to age-related memory deficits and neurodegenerative diseases. In addition, many proteases that play essential roles in regulating neuropeptide metabolism, amyloid precursor protein processing, and neuronal apoptosis are up-regulated in the aged brain and likely contribute significantly to brain aging. Finally, a subset of these genes whose expression is affected by aging are oppositely affected by exposure of mice to an enriched environment, suggesting that these genes may play important roles in learning and memory.

REFERENCES:

The effects of aging on gene expression in the hypothalamus and cortex of mice - Proc. Natl. Acad. Sci. USA, Vol. 98, Issue 4, 1930-1934

December 15th, 2000

Extended Life-Span Conferred by Cotransporter Gene Mutations in Drosophila


Blanka Rogina, Robert A. Reenan, Steven P. Nilsen, Stephen L. Helfand
Science 2000 290: 2137-2140

Aging is genetically determined and environmentally modulated. In a study of longevity in the adult fruit fly, Drosophila melanogaster, we found that five independent P-element insertional mutations in a single gene resulted in a near doubling of the average adult life-span without a decline in fertility or physical activity. Sequence analysis revealed that the product of this gene, named Indy (for I'm not dead yet), is most closely related to a mammalian sodium dicarboxylate cotransporter--a membrane protein that transports Krebs cycle intermediates. Indy was most abundantly expressed in the fat body, midgut, and oenocytes: the principal sites of intermediary metabolism in the fly. Excision of the P element resulted in a reversion to normal life-span. These mutations may create a metabolic state that mimics caloric restriction, 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 in Drosophila
Arclab - Dec 10, 2000 to Dec 16, 2000

November 8th, 2000

The Center for Research and Education in Aging (CREA) will be officially launched November 8th, 2000

On November 8th, 2000 the Center for Research and Education in Aging, which has a mission of "investigating the basic processes that cause aging, with the goal of improving and extending human health span." will be officially launched.   For more information about this important and groundbreaking organization or to find out how you can help CREA achieve its mission, please visit CREA's website at:

http://crea.berkeley.edu

October 6th, 2000

Regulation of C. elegans life-span by insulinlike signaling in the nervous system


Wolkow CA, Kimura KD, Lee MS, Ruvkun G
Science 2000 Oct 6;290(5489):147-50

An insulinlike signaling pathway controls Caenorhabditis elegans aging, metabolism, and development. Mutations in the daf-2 insulin receptor-like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold. To identify tissues where this pathway regulates aging and metabolism, we restored daf-2 pathway signaling to only neurons, muscle, or intestine. Insulinlike signaling in neurons alone was sufficient to specify wild-type life-span, but muscle or intestinal signaling was not. However, restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism. These findings point to the nervous system as a central regulator of animal longevity.

REFERENCES:

Regulation of C. elegans life-span by insulinlike signaling in the nervous system - Science 2000 Oct 6;290(5489):147-50

June 26, 2000

International Human Genome Sequencing Consortium Announces "Working Draft" of Human Genome

The Human genome consists approximately 3.12-gigabases that code for 80,000 genes. The work, carried out in 16 centres across the world, means that 85% of the human genome has been accurately deciphered. Further work, still to be finally checked, means in total 97% of the human genome has been read. The existence of this genetic map will lay the foundation for a revolution in medical diagnosis and treatment.

REFERENCES:

March 23rd, 2000

The Drosophila melanogaster genome has been fully sequenced.

REVIEW The 180-megabase genomic sequence of Drosophila melanogaster reveals 13,601 genes. In Drosophila, 60 Mb of the 180-Mb genome consists of centric heterochromatin. The C. elegans was fully sequenced on December 11th, 1998 and it had 97-megabases and 19,000 genes.

REFERENCES:

Dec 1, 1999

First human chromosome is fully sequenced

Scientists with the Human Genome Project have sequenced chromosome 22, the first chromosome to have been fully mapped. The results of this affort are published in the December 2nd issue of the journal Nature. The sequence obtained consists of 12 contiguous segments spanning 33.4 megabases, contains at least 545 genes and 134 pseudogenes, and provides the first view of the complex chromosomal landscapes that will be found in the rest of the genome. More than 30 human disorders are already associated with changes to genes of chromosome 22. These include schizophrenia, disorders of fetal development and the nervous system. The next chromosome to be fully sequenced will most likely be chromosome 7.

NIH Link to Chromosome 22
Human Genome Organisation link to Chromosome 22
The Sanger Centres link to Chromosome 22
The DOE's Joint Genome Institute

Real Audio 80K clip on the sequenceing of chromosome 22

Real Audio 28K clip on the sequenceing of chromosome 22

Nov 18, 1999

Suppression of p66shc protein, extends the life span of mice 30%

The following describes mutant mice that seem to live almost one-third longer than wild-type animals. These mice, which have a single targeted mutation in the gene encoding the p66shc protein, develop and eat normally, and have a normal body weight. But the absence of p66shc confers a heightened cellular resistance to agents that cause oxidative damage. Although the conclusions must be regarded as provisional until larger groups of animals are studied, the results support the proposal2 that oxidative damage is involved in ageing. They also indicate that modification of the response to oxidative damage can have a considerable effect on lifespan, without apparent negative side effects.

NIH OMIM link - SHC TRANSFORMING PROTEIN

NIH LocusLink - SHC TRANSFORMING PROTEIN
Nature 1999 Nov 18;402(6759):309-13 The p66shc adaptor protein controls oxidative stress response and life span in mammals.
ABC News - Scientists Find Gene Switch Makes Mice Live Longer

Oct 4, 1999

Buck Center for Research in Aging celebrates the opening of the Research, Support and Education Building

From September 30th 1999 to October 1st 1999 the Buck Center for Research in Aging in Novato, California, held an inaugural symposiam on aging to celebrate the opening of the center. The Buck Center is located 20 miles north of the Golden Gate Bridge in northern Marin County. The Buck Center receives 5.5 millions annually from the Buck Trust and is governed by its own Board of Directors.

Buck Center for Research in Aging

May 4, 1999

Geron acquires Roslin Bio-Med and forms research collaboration with the Roslin Institute

MENLO PARK, CA and ROSLIN, MIDLOTHIAN, SCOTLAND - May 4, 1999

For more details

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March 26, 1999

Dr. Judith Campisi is awarded $964,000.00 for aging research

Berkeley, CA - March 26, 1999 - The Ellison Medical Foundation has awarded Dr. Judith Campisi $964,000.00 to support her basic investigations into the causes of aging. The Foundation was setup by Larry Ellison, CEO of Oracle, one of the largest database software corporations in the United States. Judith Campisi is a researcher in the Department of Cell and Molecular Biology at the Lawrence Berkeley National Laboratory in Berkeley, California.

For more details

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March 4, 1999

Mouse model demonstrates role of telomeres and telomerase in aging, cancer and lifespan

Menlo Park, CA - March 4, 1999 - Geron Corporation announced that researchers at the Dana-Farber Cancer Institute of Harvard Medical School and colleagues at Johns Hopkins School of Medicine have published in the March 5 issue of Cell that telomerase-negative mice show telomere loss with age and experience a host of age-related changes. This study expands on a growing body of in vivo proof that age-related telomere erosion contributes to pathology, including cancer. Significant new findings in this work include a causal link between telomere loss and two hallmarks of human aging: an impaired ability to recover from stress and an increased rate of cancer formation. Consistent with other data linking telomerase activity with tumor progression, the authors suggest that telomere loss contributes to cancer formation, but lack of telomerase inhibits long-term tumor growth.

For more details

December 28th, 1998

Geron announces first in Vivo data indicating telomerase expression in normal human cells extends their replicative lifespan without oncogenic transformation.

Geron Corp and the University of Texas Southwestern Medical Center at Dallas announced today the publication of two papers in the Jan 1, 1999, issue of Nature Genetics.

December 17th, 1998

Human cells cloned.

A group at Kyunghee University Hospital in Seoul, South Korea, combined an egg and a cell from a single donor to produce the first stages of a human embryo. The experiment was terminated by the reseachers after a few cell divisions had taken place.

December 11th, 1998

Genome sequence of the nematode C. elegans: A platform for investigating biology the C. elegans sequencing consortium.

REVIEW The 97-megabase genomic sequence of the nematode Caenorhabditis elegans reveals over 19,000 genes. More than 40 percent of the predicted protein products find significant matches in other organisms. There is a variety of repeated sequences, both local and dispersed. The distinctive distribution of some repeats and highly conserved genes provides evidence for a regional organization of the chromosomes

Science 1998 Dec 11;282(5396):2012-8

The genetics of aging as it relates to the C. elegans

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December 9th, 1998

First Cows are Cloned

Eight calves, four of which died during birth, are cloned from a single caw by a team led by Dr. Yukio Tsunoda of Kinki University in Nara, Japan

November 6th, 1998

Embryonic Stem Cell Lines Derived from Human Blastocysts.

Thomson JA, Itskovitz-Eldor J, Shapiro SS, Waknitz MA, Swiergiel JJ, Marshall VS, Jones JM J. A. Thomson, M. A. Waknitz, J. J. Swiergiel, V. S. Marshall

Wisconsin Regional Primate Research Center, University of Wisconsin, Madison, WI 53715, USA. J. Itskovitz-Eldor, Department of Obstetrics and Gynecology, Rambam Medical Center, Faculty of Medi cine, 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):1145-1147

Human blastocyst-derived, pluripotent cell lines are described that have normal karyotypes, express high levels of telomerase activity, and express cell surface markers that characterize primate embryonic stem cells but do not characterize other early lin eages. After undifferentiated proliferation in vitro for 4 to 5 months, these cells still maintained the developmental potential to form trophoblast 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). These cell lines should be useful in human developmental biology, drug discovery, and transplantation medicine.

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Embryonic Stem Cell Lines Derived from Human Blastocysts Science Volume 282, Number 5391 Issue of 6 Nov 1998, pp. 1145 - 1147

New Potential for Human Embryonic Stem Cells Science Volume 282, Number 5391 Issue of 6 Nov 1998, pp. 1061 - 1062

Derivation of pluripotent stem cells from cultured human primordial germ cells

Michael J. Shamblott*, Joyce Axelman*, Shunping Wang*, Elizabeth M. 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 Ho pkins Bayview Hospital, Baltimore, MD 21224

PNAS Vol. 95, Issue 23, 13726-13731, November 10, 1998

Human pluripotent stem cells would be invaluable for in vitro studies of aspects of human embryogenesis. With the goal of establishing pluripotent stem cell lines, gonadal ridges and mesenteries containing primordial germ cells (PGCs, 5-9 weeks postfertil ization) were cultured on mouse STO fibroblast feeder layers in the presence of human recombinant leukemia inhibitory factor, human recombinant basic fibroblast growth factor, and forskolin. Initially, single PGCs in culture were visualized by alkaline ph osphatase activity staining. Over a period of 7-21 days, PGCs gave rise to large multicellular colonies resembling those of mouse pluripotent stem cells termed embryonic stem and embryonic germ (EG) cells. Throughout the culture period most cells within t he colonies continued to be alkaline phosphatase-positive and tested positive 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 to characterize embryonic stem and EG cells. The cul tured cells have been continuously passaged and found to be karyotypically normal and stable. Both XX and XY cell cultures have been obtained. Immunohistochemical analysis of embryoid bodies collected from these cultures revealed a wide variety of differe ntiated cell types, including derivatives of all three embryonic germ layers. Based on their origin and demonstrated properties, these human PGC-derived cultures meet the criteria for pluripotent stem cells and most closely resemble EG cells.

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Derivation of pluripotent stem cells from cultured human primordial germ cells Proceedings of the National Academy of Sciences Vol. 95, Issue 23, 13726-13731, November 10, 1998

November 6th, 1998

The 77 year old John Glenn and his shuttle mission.

John Glenn's science experiments that pertain to the study of aging.

July 22nd, 1998

50 mice cloned by researchers at the University of Hawaii

Over 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 of females but is not an egg cell,then they extracted the nucleus and placed it inside a hollowed-out egg cell using a tiny pipette. Then they implanted the egg cell into the uterus of a female animal. Cloning shows that adult cells can be reprogrammed to start over and develop into a whole creature, the question is will the cloned animals age normally or will they age at a faster rate? Details of the experiment were published in the July 22nd, 1998 issue of Nature.

Nature

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Gene found which is linked to Alzheimer's disease

A Gene has been found which is linked to Alzheimer's diseas. The new discovery was reported on the 22 July 1998 at a conference in Amsterdam. Geneticist Rudolph E. Tanzi and his research team at Massachusetts General Hospital in Boston identified a gene called A2M which is responsible for producing a protein which strongly interacts with proteins produced by two of the genes-called LRP and APOE- linked to familial Alzheimer's.The study shows that people with the defective form of the gene are three and one half times more likely to develop late-onset Alzheimer's. The disease is believed to be caused by the accumulation of waxy plaques, composed largely of a protein called beta-amyloid, which kills brain cells. The study will be published in the August 1st, 1998 issue of Nature Genetics.

Nature - Genetics

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Fruit flies bred with copies of the human SOD1 gene live as much as 40 percent longer.

June 2, (1998).

Gabrielle Boulianne, a neurobiologist at the Hospital for Sick Children and a professor of molecular and medical genetics at the University of Toronto reports in an article in the June issue of the journal Nature Genetics that she and her co-workers bred Drosophila melanogaster with copies of the human SOD1 gene and the result was a fly that could live as much as 40 percent longer.

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ABSTRACT:

Extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons

Tony L. Parkes1, Andrew J. Elia2, Dale Dickinson1, Arthur J. Hilliker1, John P. Phillips1 & Gabrielle L. Boulianne2

Reactive oxygen (RO) has been identified as an important effector in ageing and lifespan determination1-3. The specific cell types, however, in which oxidative damage acts to limit lifespan of the whole organism have not been explicitly identified. The association between mutations in the gene encoding the oxygen radical metabolizing enzyme CuZn superoxide dismutase (SOD1) and loss of motorneurons in the brain and spinal cord that occurs in the life-shortening paralytic disease, Familial Amyotrophic Lateral Sclerosis (FALS; ref. 4), suggests that chronic and unrepaired oxidative damage occurring specifically in motor neurons could be a critical causative factor in ageing. To test this hypothesis, we generated transgenic Drosophila which express human SOD1 specifically in adult motorneurons. We show that overexpression of a single gene, SOD1, in a single cell type, the motorneuron, extends normal lifespan by up to 40% and rescues the lifespan of a short-lived Sod null mutant. Elevated resistance to oxidative stress suggests that the lifespan extension observed in these flies is due to enhanced RO metabolism. These results show that SOD activity in motorneurons is an important factor in ageing and lifespan determination in Drosophila.

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REFER TO:

Nature - Genetics

Role of oxidative stress in Drosophila aging.- Mutat Res 1992 Sep;275(3-6):267-279

Expression of bovine superoxide dismutase in Drosophila melanogaster augments resistance of oxidative stress.- Mol Cell Biol 1991 Feb;11(2):632-640

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January 16th, 1998

Extension of Life-Span by Introduction of Telomerase into Normal Human Cells

Science, 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

February 27, 1997

Letter to Nature -- Viable offspring derived from fetal and adult mammalian cells

February 24, 1997

Scientists clone first adult mammal

The Telomerase Picture Fills In

Positional Cloning of the Werners syndrome Gene - Abstract, Summary

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THE NEW SCIENCE OF AGING


A TV series that was shown on PBS Wednesday, June 2, 1999, 8:00 p.m. ET

For information about the videocassettes from PBS

For more details about this documentary

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If you do not have the Real Audio program that you need to listen to the programs below, please click on this message and you may then download the program on to your system.

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Sep 16, 2003 - KQED Forum

Aging Research

Guests:
Cynthia Kenyon
Herbert Boyer Professor of Biochemistry and Biophysics
Director, Hillblom Center for the Biology of Aging
University of California San Francisco
San Francisco, California


Dale Bredesen,
founding president and CEO,
Buck Institute for Age Research

David Sinclair,
Professor of pathology,
Harvard Medical School

Philip Cohen,
San Francisco bureau chief for New Scientist magazine


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May 9, 2003 - NPR Talk of the Nation

Genetics of Aging

Guests:
Ted Gavin
Member, Board of Directors
SpamCon Foundation
San Francisco, California

Phil Goldman
Chief Executive Officer
MailBlocks
Los Altos, California

David Sinclair
Assistant Professor of Pathology
Harvard Medical School
Boston, Massachusetts

Cynthia Kenyon
Herbert Boyer Professor of Biochemistry and Biophysics
Director, Hillblom Center for the Biology of Aging
University of California San Francisco
San Francisco, California

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August 31, 2001 - NPR Talk of the Nation: Science Friday

Longevity and Aging

Guests:
Michael Fossel
Author, "Reversing Human Aging"
Clinical Professor of Medicine
Michigan State University
East Lansing, MI

Steven Austad
Author, "Why We Age: What Science Is Discovering About the Body's Journey Through Life" (Wiley)
Associate Professor, Zoology
Gerontologist
University of Idaho
Moscow, Idaho

Thomas Perls
Author, "Living to 100: Lessons in Living to Your Maximum Potential at Any Age" (Basic Books)
Geriatrician, Gerontology Division and Biometrics Center
Beth Israel Deaconess Medical Center
Associate Professor, Division on Aging
Harvard Medical School
Boston, Massachusetts

Michael McKubre
Director, Energy Research Center
SRI Incorporated
Menlo Park, California

June 26, 2000 - NPR Talk of the Nation

The Human Genome

The ten year race to complete a map of the human genetic code has ended in a tie. The publicly funded Human Genome Project and the private corporation Celera Genomics are announcing today that their work on a rough draft of a map of the human genome is complete. The map won't lead to medical miracles overnight, but once the information has been studied it could lead to the development of new drugs and therapies to treat diseases. Join Juan Williams and guests to discuss what a complete map of the human genome will mean for the future of medicine and humanity.

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June 9, 2000 - NPR Talk of the Nation

The Human Genome and a genetics update 

The public-private race to get the first complete map of the human
genome is nearing the finish line, with both groups expected to
announce a working draft sometime this month. Then the real work
begins: finding the genes along those long stretches of DNA and
determining their function. This hour, we'll get an update on the latest
genetics news.


Guests:

Bruce Roe
George Lynn Cross Research Professor of Chemistry and Biology
Director, Advanced Center for Genome Technology
University of Oklahoma
Norman, Oklahoma

Fred Cohen
Member, Board of Directors
DoubleTwist
Professor, Medicine and Pharmacology
University of California
San Francisco, California

Maja Bucan
Associate Professor, Genetics
Center for Neurobiology and Behavior
University of Pennsylvania Medical Center
Philadelphia, Pennsylvania





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May 14, 1999 - NPR Talk of the Nation: Science Friday

AGING RESEARCH UPDATE

Researchers from Columbia University announced that they have identified an enzyme crucial to extending the lifespan of roundworms. Articles Discussed:  "A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-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 Chalfie
Professor, Biological Science
Columbia University
New York, New York
Steven Austad
Author, Why We Age: What Science is Discovering About the Body's Journey Through Life (John Wiley & Sons)
Associate Professor, Zoology
Gerontologist
University of Idaho
Moscow, Idaho

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January 29, 1999 - NPR Talk of the Nation: Science Friday

STEM CELL UPDATE

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Brief Text Description:

Human embryonic stem cell research, which holds the promise of curing many diseases, has been hampered by a lack of funds. But last week, the federal government ruled that much of this work is eligible to receive federal funds, a decision that the National Bioethics Advisory Commission is slated to debate.

John Gearhart
Professor of Gynecology and Obstetrics
Johns Hopkins University School of Medicine
Baltimore, Maryland

Eric Meslin
Executive Director
National Bioethics Advisory Commission
Rockville, Maryland

Bruce Torbett
Researcher
Scripps Research Institute
La Jolla, California

Kent Smith
Research Associate
Scripps Research Institute
La Jolla, California


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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 cells in the lab to live much longer than normal, perhaps paving the way for new treatments for age-related diseases and cancer. In this hour, we'll get an update on the latest aging research. Plus, a new way of thinking about how the brain stores memories.


Guests:

Calvin Harley
Chief Scientific Officer
Geron Corporation
Menlo Park, California

Michael Fossel
Author, Reversing Human Aging, (William Morrow)
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


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September 5, 1997 - NPR Talk of the Nation: Science Friday

GENETICS OF AGING

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Brief Text Description:

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Guests:

Gary Ruvkun
Faculty Member, Department of Genetics,
Harvard Medical School
Boston, Massachusetts

Michael Fossel
Author, Reversing Human Aging, William Morrow and Company
Clinical Professor of Medicine
Michigan State University
East Lansing, Michigan

Mike West
Founder and Vice President,
Geron Corporation,
Menlo Park,
California

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April 12, 1996 - NPR Talk of the Nation: Science Friday

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Brief Text Description:

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THE SCIENCE OF AGING

Guests:
Gerard Schellenberg
Associate Director of Research
Geriatric Research, Education, and Clinical Center
Veterans Affairs Puget Sound Health Care System
Seattle, WA

Stanley Rapoport
Chief of Laboratory of Neuroscience
National Institute on Aging
Bethesda, MD

Michael Fossel
Professor of Clinical Medicine
Michigan State University
East Lansing, MI
Author
Reversing Human Aging

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September 29, 1995 - NPR Talk of the Nation: Science Friday

BIOLOGY OF AGING



Brief Text Description:


Guests:

Dr. Leonard Hayflick
School of Medicine
University of California, San Francisco
San Francisco,CA

Jerry Shay
Professor of Cell Biology and Neuroscience
University of Texas Southwestern Medical Center
Dallas, TX

Dr. Michael Fossel,
Author of forthcoming book, "Reversing Human Aging"
Professor of Medicine
Michigan State University
East Lansing, MI



May 24, 1996 - NPR Talk of the Nation: Science Friday

GENE THERAPY


Brief Text Description:


Guests:

Ronald Crystal
Professor of Medicine and Chief of the Division of Pulmonary
and Critical Care Medicine
The New York Hospital-Cornell Medical Center
New York, N.Y.

Jeffrey Leiden
Professor of Medicine, Professor of Pathology, and Chief of
the Section of Cardiology
The University of Chicago
Chicago, Ill.



Theories of Aging

Papers on different Theories of Aging

Theories of Aging

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Upcoming Meetings and Conferences

Events without dates should be considered as tentative.

Calender of Upcoming Meetings/Conferences

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Journals


Articles pertaining to the aging process can be found in the journals listed below.

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Recent Books

Papers

Bio Tool Box

Scientists Involved in Aging Research

Laboratories Involved in Aging Research

Biotech Companies

Companies Involved in Aging Research

Bill Board - Research Opportunities, Calls For Research and News

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