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Acknowledgment
Program Updates
Exhibit Information |
 George
M. Martin, MD, University of
Washington, asks
How is the evolutionary biological
theory of aging holding up against
mounting attacks?
 Read additional comments on Dr. Andrzej
Bartke's discussion on
"Why dwarf mice are long-lived and what
does this tell us?"
We invite comments on both topics.
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Welcome to our AGE New Members!
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-
 Update on
AGE: The Journal of the American Aging
Association
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2005 ANNUAL MEETING |
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- EARLY REGISTRATION: Remember that the cutoff date for the
Early Bird registration is April 10!
Click here to register today!
- STUDENT PROGRAM: don't forget
to reserve your seat at the
STUDENT-ONLY Data Blitz and Round Table
- read additional details here.
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book soon!
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grateful for the support of: NIH/NIA,
Ellison Medical Foundation, BioMarker
Pharmaceuticals, Inc., The Wild
Blueberry Association of North America,
GeroNova, Axxora, Linus Pauling Institute, British
Society for Research on Ageing.
Click here to read more about our
supporters.
- PROGRAM UPDATES: Dr. Richard
Miller will speak on
"Size,
Stress, and Aging" during the 8:00 am
session of Sunday, the 5th of June.
Also, please note that the Session
"IGF-1," chaired by Dr. Norm Wolf, is
now scheduled for Monday, the 6th of
June, at 10 am, while the Session
"Genomics and Proteomics, chaired by Dr.
John Holloszy, is now set for Sunday,
the 4th of June, 10:00 am.
- EXHIBIT: Want to exhibit at the meeting?
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Annual Meeting offers great
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registrants. See
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DISCUSSION |
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How
is the evolutionary biological theory of aging
holding up against mounting attacks?
Dr.
George M. Martin, Department of Pathology,
University of Washington
(This
is an invited discussion piece submitted by Dr.
George M. Martin. Responses to and
discussion of this piece are invited from all
readers of this Newsletter for publication in
the next issue. Dr. Martin's replies will
be published in that same issue.)
I cannot imagine any theoretical construct more
central to biogerontology than the evolutionary
biological theory of aging (SN Austad, Why We
Age, Wiley, NY, 1997). The theory applies to
age-structured populations and to ecologies that
dominated the early history of particular animal
species. These early nature-nurture interactions
shaped the genomes so that their life histories
maximized reproductive fitness. In ecologies
with high hazard functions, the more optimal
life history would be one that involved rapid
development, large numbers of progeny beginning
shortly after the attainment of sexual maturity,
and relatively short life spans. For the case of
low hazard environments, a different life
history strategy, one involving slower rates of
development, longer periods of fecundity and
longer life spans, might prove to lead to
greater reproductive fitness. Tom Kirkwood's
formulation invokes trade offs between the need
for energetic resources for reproduction versus
the need for energetic resources to maintain the
soma (Kirkwood and Holliday, Proc R Soc Lond
Biol Sci 205:531, 1979).
For species that evolved in either high or low
hazard environments, all phenotypes that had not
reached some significant level of expression
until the latter part of the life span will have
escaped the force of natural selection. This is
because the bulk of the gene pool passed on to
subsequent generations represent alleles from
the very large group of young, actively
reproducing individuals, not the very small
group of rather rare old survivors. These
alleles that escape the force of natural
selection could be "good" alleles (e.g., those
that code for more robust maintenance of
homeostasis in the face of endogenous and
exogenous injuries) as well as "bad" alleles
(e.g., those that code for relatively
inefficient maintenance of homeostasis).
Surprisingly, there was very little attention
given to evolutionary biology at the many
meetings on the biology of aging I attended
during the 1960's, 1970's and for much of the
1980's, although there were a few of us who were
impressed by the ideas of Peter Medawar. (The
late George Sacher, incidentally, was singularly
unimpressed.) A few of us knew about the
famous 1957 paper by George C. Williams. But it
was Tom Kirkwood and Robin Holliday in the UK
and Michael Rose (UK, Canada and US) who brought
the issues up forcefully in the late 1970's and
1980's. I particularly recall the
participation by Tom Kirkwood and Michael Rose
at a number of meetings on the biology of aging
at about that time, including Tom’s
participation at the Santa Barbara Gordon
Conference I chaired in 1979 (http://sageke.sciencemag.org/cgi/content/full/2002/34/re4/DC4).
Michael's educational fervor prompted him (with
Graves) to publish a paper entitled "What
evolutionary biology can do for gerontology" (J
Gerontol 44:B27, 1989). As Jim Vaupel
pointed out at one of our meetings, however,
when most gerontologists finally understood and
accepted the theory (some forty years after
Medawar), demographers began to question it!
This was the result of the studies of Jim Carey
and colleagues on medflies and subsequent
related studies with other organisms (Vaupel et
al., Science 280:855, 1998). Given extremely
large populations, it became clear that there
were departures from the Gompertz curves. Age
specific mortalities declined in very old
animals, something that had not been predicted
by the evolutionary biological theory of aging.
My simplistic and probably naïve take on this
controversy is that when animals become
extremely aged, they stop moving around or
flying and are therefore less likely to become
injured. The evidence for declines in
age-specific mortality in very old humans is
less striking and could reflect secular trends
in the institution of unusual interventions,
such as central heating and air conditioning and
immunizations against pneumococcus and
influenza. Moreover, extremely aged human
subjects also do not move around much and are
therefore less likely to break their hips and
die in the hospital from some
antibiotic-resistant pneumonitis. I call this my
"cocoon" hypothesis!
There
had been, in fact, much earlier challenges. One
idea had its inspiration in the work of
engineers who had to calculate the times to
failure of components of complex machines such
as airplanes. Some argued that we too are
complicated machines and that inherent
deficiencies in design were sufficient to lead
to aging and failure without the necessity of
invoking evolutionary theories. But one could
argue, as have the Gavrilovs, that such ideas
are indeed compatible with evolutionary theory (Gavrilov
and Gavrilova, J Theoret Biol 213:527, 2001).
The evolutionary theory predicts a polygenic
basis for aging and the likelihood that multiple
mechanisms are involved. Then how, many would
ask, can the theory be reconciled with the
mounting evidence that single gene mutations in
worms, flies and mice can lead to enhanced life
spans? And how to reconcile the fact that a
single environmental intervention - caloric
restriction - can enhance the life spans of so
many species? My answer is that the gene
actions involved in these interventions have
certainly not escaped the force of natural
selection. They evolved as types of
diapauses to permit prolonged survival in times
of environmental stresses that precluded
successful reproduction. Such diapauses
would be eventually trumped by the evolutionary
biological theory of aging.
A growing number of scientists now believe that
the evolutionary biological theory might be
falsified by evidence that there have been
behavioral phenotypes in grandparental
generations that have not escaped the force of
natural selection and that these phenotypes are
seen even today among elders living among
primitive tribes (e.g., Kaplan and Robson, Proc
Natl Acad Sci USA 99:10221, 2002). But we really
do not know how many such elders survived among
our ancestral populations and how effective the
behaviors of those relatively few survivors
might have been in enhancing the reproductive
fitness of their grandchildren. Moreover, in
experimental situations with mammals living in
the wild, support for the "grandmother
hypothesis" was lacking (Parker, Tatar and
Collins, Nature 392:807, 1998).
The most recent challenge has come from a field
biologist, David Reznick. I was delighted
to have heard his presentation at the last
meeting of the American Aging Association in St.
Petersburg, Florida. He presented
surprising data, in his work with different
populations of guppies; the predicted
relationship between environmental hazards and
life span (at least for the case of predation)
was not holding up. (David's paper on the
subject has just appeared) (Reznick et al.,
Nature 431:1095, 2004.) His conclusions are thus
quite different from what emerged from Steve
Austad's classical research on Virginia Opossums
(Austad, J. Zoology (London) 229: 695, 1993).
The
fact that such an icon as the evolutionary
theory of aging is under challenge is a tribute
to the viability of our field. No theory
should ever be immune from new challenges.
I nevertheless continue to embrace the theory as
"the best game in town." Other views would be
most welcome, however!
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SUBMIT A COMMENT ON THIS TOPIC/PAPER AND ENTER TO WIN
A FREE MEETING REGISTRATION AT THE 34TH ANNUAL
MEETING OF THE AMERICAN AGING ASSOCIATION
(hotel and airfare not included).
Winner will be announced in our May edition
of the Newsletter.
Comments will be published in subsequent
editions of the AGE Newsletter.
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To
comment on this paper, please
Email us |
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Comments and Responses on Dr. Andrzej
Bartke's
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"Why dwarf mice are long-lived and what
does this tell us?"
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COMMENT BY Richard Miller, Univ. of Michigan
- I've read Austad's commentary on the
Bartke paper in the American Aging Association
Newsletter, and I wish to take up his challenge
to find a situation in which a dwarfing mutation
has slowed aging without leading to some ill
effects (such as, for example, the tendency of
Snell dwarf mice to be slow, cold, infertile,
and poor fighters, despite their excellent
vision, kidneys, joints, intelligence, oxygen
resistance, and youthful-looking skin and
tendons).
This is, I think, an easy challenge to meet: viz
Chihuahuas, toy poodles, and other miniature
breeds. Not all dwarfing mutations produce
healthy and vigorous sports, but some do, and
dog breeders have kept these for a variety of
purposes, such as sitting on laps, living in
cramped apartments, and darting down rat-holes.
I defy anyone who has owned a West Highland
White Terrier, like our late lamented "Tiger,"
to call these dogs effete or wimpish. Nature,
apparently, can figure out ways to construct
long-lived dwarfs that are healthy and active at
ages at which their wolfhound and Newfoundland
cohort-mates are long gone to their heavenly
reward, though mouse breeders have not yet
caught on to the secret method. Yet.
COMMENT BY Steven N.
Austad, Univ. of Texas Health Sci. Ctr.
- I believe the challenge is a little more
formidable than suggested. As I recall, I was
commenting on dwarfs due to single gene mutants.
I heartily admit that nature produces fit and
feisty dwarves again and again. However humans
crippling a single gene in an otherwise
well-integrated genome is unlikely to produce
such a fit and feisty critter as a result. In
fact, I know of no such example, although I am
waiting to be proven wrong.
RESPONSE BY: Andrzej Bartke, Southern Illinois
Univ. School of Med.-
With regard to the recent exchange of views
about ill effects of dwarfing mutations, I
would like to say how I view the "relevance" of
these animals to the issue of aging. I would
obviously not argue that Snell dwarf, Ames dwarf
or "Laron dwarf" (GHRKO) mice are fully fit or
likely to be successful in competition with
normal animals under natural conditions. I have
spent many years of my professional life on
analysis of reproductive deficits in these
animals and the underlying hormonal mechanisms.
My own fascination with these mice is related to
the fact that they demonstrate the dramatic
impact of specific endocrine defects on aging
and longevity and thus facilitate identification
of the pathways and the mechanisms involved.
The obvious question is to what extent findings
in these mutant animals may apply to genetically
normal individuals. Providing an answer that
would satisfy everyone is not easy. However,
analysis of the relationships between adult body
size (that can reasonably be assumed to
represent a marker of GH and IGF-1 actions) and
longevity in mice strongly suggests that the
major extension of longevity in animals lacking
GH or its action represents an extreme case of a
physiological relationship that exists in normal
animals. I am referring to numerous studies in
different stocks of normal mice as summarized in
a recent meta-analysis by David Rollo and to
analysis of individual differences in longevity
in a stock of genetically heterogeneous normal
mice by Richard Miller. Studies of the same
signaling pathways in various organisms, the
relationships of body size to longevity in other
species, analysis of polymorphism of human genes
related to IGF-1, and studies of glucose
metabolism in exceptionally long-lived people
provide further (although admittedly indirect)
indications that findings in the various types
of dwarf mice can help us understand normal
biological control of the aging process.
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ANNOUNCEMENTS |
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WELCOME TO OUR NEW AGE MEMBERS:
Robert C. Cockrell, MD -
Laguna Beach
Longevity Inst.
Kimberly Greer, PhD - Texas A&M University
Robert Krikorian, PhD - University
of Cincinnati
Rose Reynolds, PhD - University of
Illinois at Urbana-Champaign
.jpg) Svetlana
V. Ukraintseva, PhD -
Reserch interests include
complex relationships between aging,
health, and longevity, with emphasis on
causes and consequences of increasing
human longevity and risks of chronic
diseases (such as cancer, asthma, and
Alzheimer’s disease) in developed
countries; trade-offs between risks of
common pathologies (e.g., asthma-cancer,
or cancer-heart disease) at old ages;
genetics of aging and cancer;
long-term effects of a drug therapy on
health and survival in the elderly;
candidate anti-aging interventions.
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AGE: The Journal
of the American Aging Association
 The
Journal of the American Aging
Association will not be published for
the year 2004. This decision was
prompted by the transition of the
Journal to a new name and publisher.
The journal will appear in 2005 as
AGE: The Journal of the American
Aging Association
and will be published by Springer. The
Editorial Board has been revised and new
editorial features have been
incorporated to the journal.
AGE is a quarterly, international,
peer-reviewed journal that publishes
articles related to research in the
biology of aging and research on
biomedical applications that impact
aging. The scope of articles to be
considered include evolutionary biology,
biophysics, genetics, genomics,
proteomics, molecular biology, cell
biology, biochemistry, endocrinology,
immunology, physiology, pharmacology,
neuroscience, and psychology.
Articles concerning clinical studies
will also be considered if the results
relate to underlying biological
mechanisms of aging. Such studies should
reflect more than issues related to the
care and treatment of geriatric
patients. Papers concerned with social,
economic, and political issues of aging
will generally not be considered unless
they relate directly to biomedical
gerontology.
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FOR SUBMISSION AND INFORMATION ON THE
-
JOURNAL PUBLICATION,
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PLEASE CONTACT
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In addition to manuscripts emerging from
original research, the journal actively
solicits research reviews of important
topics in biomedical gerontology. Other
types of manuscripts are also
acceptable, such as commentaries,
debates, and meeting reports.
The journal will publish 4 issues per
year and will be available online to
current AGE scientific members. Lay
members and student members can purchase
online subscriptions for $30 per year.
The printed version of the journal is
available to all members for an
additional $50 per year. Review
complete membership benefits
here.
For more information on AGE, please
review the information at the
publisher's site:
http://www.springeronline.com/sgw/cda/frontpage/0,11855,5-40109-70-36731207-0,00.html
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GRANT DEADLINES:
- 1
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Short-term Fellowships
Sponsor: HUMAN FRONTIER
SCIENCE PROGRAM
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Deadline(s): 03/21/05 (password) and
03/30/05 (application)
http://www.hfsp.org/home.php
2.
Research Grants
Sponsor:
United Parkinson Foundation
Deadline(s): 04/01/05
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http://www.pdf.org/Research/internationalresearch.cfm
3.
Glenn/AFAR Breakthroughs in Gerontology
Awards
Sponsor:
American Federation for Aging Research
Deadline(s): none -
http://www.afar.org
4.
FASEB Summer Research Conference Travel
Award
Sponsor: Federation of American
Societies of Experimental Biology
Deadline(s): N/A
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https://career.faseb.org/marc/travel2.html
5.
JSPS Long-Term Fellowships in Japan
Sponsor: NATIONAL INSTITUTES
OF HEALTH/NIH- FOGARTY INTERNATIONAL CENTER
Deadline(s): check website for
criteria:
http://www.fic.nih.gov/programs/jspsinvite.html
6.
Biomedical Pilot Initiative
Sponsor:
ROCKEFELLER BROTHERS FUND
Website:
http://www.rbf.org
7.
Clinical Scholars
Sponsor:
ROCKEFELLER BROTHERS FUND
Website:
http://www.rockefeller.edu/pdfellows.php
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MEETING ANNOUNCEMENTS:
Email
us your meeting announcement
April 2005
01 -
Celebrating Our Cultural Heritage as We Age, 5th
Interdisciplinary Gerontology Conference
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Boca
Raton, Florida, USA
07
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Alzheimer Society of Canada 27th National
Conference
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Regina, Canada
12
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CESAGen International Conference
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London, United Kingdom
12
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Altenpflege+HealthCare
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Nuernberg, Germany
May
2005
06
- Second Congress of the International Academy
of Nutrition and Aging
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St
Louis, USA
12
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Pastoral Care Issues to the Elderly
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Windsor, Canada
19
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Alzheimer's Disease: Update on Research,
Treatment, and Care
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San Diego California
19
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Ethics and Aging in Long-Term Care
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Westchester/Mamaroneck New York, USA
23
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5th International Conference of the
International Society for Gerontechnology
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Nagoya, Japan
June 2005
07
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Improving Care for Older People 2005
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London, United Kingdom
18
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Alzheimer's Association International Conference
on Prevention of Dementia
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Washington, DC, USA
20
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Australian Society for Geriatric Medicine 2005
Annual Scientific Meeting
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Brisbane, Australia
26
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XVIII World Congress of Gerontology: Active
Aging in the XXIst Century -- Participation,
Health and Security
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Rio de
Janeiro, Brazil
July 2005
01
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CFP - International Journal of Medical Sciences
14
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British Society of Gerontology 34th Annual
Scientific Meeting 2005
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Keele,
Stoke-on-Trent, Staffordshire, England, United
Kingdom
20
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Australian Society for Geriatric Medicine Annual
Scientific Meeting
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Brisbane, Australia
26
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13th Annual Alzheimer's Association Dementia
Care Conference
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Chicago,
Illinois, USA
August 2005
16
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HEALTHCOM 2005 International Conference on
Health Communication
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Kuala
Lumpur, Malaysia
22
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Florida Conference on Aging
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Orlando, Florida, USA
September 2005
29
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World Ageing & Generations Congress 2005
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St
Gallen, Switzerland
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NIH ANNOUNCEMENTS:
March
21, 2005 - The Director of the National
Institutes of Health (NIH), Elias A. Zerhouni,
M.D., named a new Director for the NIH Center
for Scientific Review: Dr. Antonio Scarpa,
M.D., Ph.D., who is currently the David and Inez
Myers professor and chair of the Department of
Physiology and Biophysics at Case Western
Reserve University in Cleveland, Ohio.
The
press release and an interview with Dr. Scarpa
are available on CSR's Web site:
http://www.csr.nih.gov;
His CV
is available at
http://pout.cwru.edu/faculty/staff_membrane/scarpa_cv.html
A
high-resolution photo of Dr. Scarpa is available
at
http://www.csr.nih.gov/extrafotos/ExPhotos.htm.
For
additional information, please contact CSR's
Communications Director, Don Luckett, via
e-mail: luckettd@nih.gov.
Email
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