A Message From The PROGRAM
Biological Sciences Chair It is intended that the Biological Sciences Program at
The Gerontological Society of America’s 62nd Annual
Scientific Meeting will provide a broad overview of the
GSA’s 62nd Annual
direction of recent research in the biology of aging,
Scientific Meeting is quickly
approaching. I invite you to and provide a guide to how future research will evolve.
join us for what promises to
be an outstanding program Symposia will focus on current areas of rapidly
planned by the Society’s
progressing research into basic biological mechanisms
Biological Sciences Section.
underlying the processes of aging and age-associated
The meeting, taking place
diseases, work that is providing the foundation on
November 18–22 in
Atlanta, GA, has long been one of the premier which to develop strategies for maintaining the
gatherings for biogerontologists. This year’s theme health and vitality of the elderly.
is “Creative Approaches to Healthy Aging.”
We have developed numerous symposia that focus The program will also include several award lectures
on the latest research into the basic biological given by eminent researchers, and paper and poster
mechanisms underlying the processes of aging and
sessions featuring professionals and emerging
age-associated diseases. The work that will be
discussed provides the foundation on which to scholars in the field.
build strategies for maintaining the health and
vitality of people as they age. Below are highlights of the program.
Among the topics to be covered are the pathobiology
of Alzheimer-type dementias; comparative
perspectives on aging and life history evolution; The Pathobiology of Dementias of the
nutrition intervention, aging, and cancer; anti-aging Alzheimer Type: Recent Advances
medicines; evolutionary biogerontology of slow aging
Chair, George Martin, MD, University of Washington, Seattle, WA.
and negligible senescence; genome and epigenome
instability in aging; immune deficiency in aging; “Dementias of the Alzheimer Type” (DAT) is a terminology that
protein alterations in aging and aging disease; and reminds us that “Alzheimer’s disease”, while having certain
contemporary approaches to biogerontology. common histopathological and clinical features, may yet prove to
reflect several pathogenetic subsets. Scot Small and Karen Duff
Additionally, GSA will host a special session have recently suggested a ‘‘dual pathway’’ model of causality,
organized by the Federation of American Societies whereby the neurotoxic A beta peptide and abnormal forms of tau
for Experimental Biology (FASEB) on the subject of can be linked by separate mechanisms driven by a common
science policy. upstream driver (Neuron 60:534, 2008). Todd Golde will then bring
The meeting will also feature the increasingly us up-to-date on the genesis of the family of A beta molecules and
popular Late Breaker Poster session, which allows current views on which species are the toxic moieties. Synapses
for rapid dissemination of the latest research seem to be a major target of such toxicity, but some of us may
findings. These posters reflect abstracts submitted have more to spare than others; John Morris will give us the latest
as recently as one month prior to the conference. evidence of this “synaptic reserve” hypothesis. Frank La Ferla will
Please see the back page for information on how conclude by turning to some good news—the possibility of
you can submit your own abstracts for this session. developing a novel therapy based upon modulations of histone
deacetylase activities. Remarkably, this story finally provides a
We also offer a robust awards program to bridge to current research on the basic biology of aging.
recognize excellence in the field. These marks of
distinction are given to outstanding graduate
students, new investigators, research fellows, The Wilder Side of Aging: Comparative
postdoctoral researchers, and basic and clinical Perspectives on Aging and Life History
researchers. To learn more, please visit
Chair, Donna Holmes, PhD, Washington State University, Pullman, WA.
Biogerontology has benefited historically from a broad,
interdisciplinary perspective. At its best, the biology of aging
Ari Gafni, PhD
integrates state-of-the art approaches to understanding the interplay
Chair, Biological Sciences Section
between the “ultimate” (evolutionary, comparative, and population-
level) and “proximate” (molecular, cellular and physiological)
mechanisms responsible for organismal senescence. This The Search for Anti-Aging Medicines
intellectual integration is critical for assessing the generality and
Chair, Richard Miller, MD, PhD, University of Michigan,
clinical relevance of specific mechanisms—like cellular resistance
Ann Arbor, MI.
to oxidative damage—to aging and related disease processes
across a wide taxonomic range of animal species, including A drug that could slow the human aging process to the same
humans. Contributors to this symposium will feature recent work extent that caloric restriction or pituitary dwarfing genes do
illustrating how comparative and evolutionary approaches using for mice would extend healthy lifespan by about 10-fold
“nontraditional” study animals and natural population systems more than a cure for cancer or heart disease. The scientific
can reveal specific physiological correlates of organismal aging search for effective anti-aging medications has to tread the
and life span. Themes include a focus on membrane lipids, narrow path between the hype of hucksters and the hopeless
mitochondrial oxidative metabolism, and resistance to aging- pessimism of most scientists and expert commentators. This
related cellular and molecular damage in animal species ranging session will feature four perspectives on this touchy topic.
from long-lived bird and bats to snakes and field crickets. All Roger McCarter will review the 70 years of literature on
four speakers employ data from outbred, wild animal caloric restriction, to summarize which proposed CR
populations to explore the physiological basis of life span mechanisms have been ruled out, and which are still
variation. Hulbert, Bronikowski and Rossinni have all developed plausible. David Allison will provide a critical discussion of
innovative laboratory approaches for studies of new vertebrate strategies aimed at discovering pharmaceuticals that might
model species or populations that are exceptionally long- or mimic the beneficial effects seen in calorically restricted
short-lived for their body sizes, metabolic rates, or taxonomic rodents. Matt Kaeberlein will discuss sirtuin activators,
groups. Zera and Bronikowski are evolutionary biologists who including resveratrol, balancing reasons for enthusiasm
couch their research in terms of tests of specific predictions of against reasons for caution. Richard Miller will present the
evolutionary life history theory, using naturally occurring most recent findings of the NIA Interventions Testing
variation in wild populations of insects and reptiles, respectively. Program, including data on NDGA, aspirin, and rapamycin as
Carefully directed research comparing basic correlates of aging well as other agents in the ITP screening pipeline.
in long-lived or outbred species to traditional shorter-lived,
inbred model animals has the potential to reveal physiological,
biochemical or genetic variation responsible for innate resistance Evolutionary Bio-Gerontology of Slow
to aging and disease processes. Aging and Negligible Senescence
Chair, Caleb Finch, PhD, University of Southern California,
Los Angeles, CA.
Nutrition Intervention, Aging and Relative to most other mammals, humans have very slow rates
Cancer of aging. This symposium will summarize evidence and theory
Chair, Ahmad Heydari, PhD, Wayne State University, Detroit, MI. for the popular concept of negligible senescence with four
Over 70 years ago, McCay and his colleagues demonstrated speakers. Senescence is only one possible path of life for a
that a reduction in food intake significantly increased both species. It is time to expand the evolutionary theory of ageing
mean and maximum life span of laboratory rodents to embrace age-patterns of mortality, fertility and growth that
demonstrating the impact of food on phenotypes of aging and include not only senescence but also sustenance and
cancer. Recent studies demonstrate that alterations in improvement. While classical theory argues that senescence is
components of food independent from caloric restriction could inevitable because the force of selection declines with age, it
impact ageing and cancer. It has been proposed that can also be argued that a declining force of selection does not
alterations in the balance of stress response genes are the key preclude the evolution of non-senescent life history strategies.
factors in the effectiveness of functional food. For example, Alternatively, adulthood could follow a simple path of
life-long methionine restriction in rodents has been shown to maintenance or even of continued growth and enhancement.
increase life span and inhibit age-related disease processes, Various animal and plant groups in which extremely long-life
while impacting oxidative stress. These findings, while are now well defined by their particular ecological niche and
controversial, have raised great excitement among researchers. anatomical/physiological traits. The principles revealed by this
Currently, “there are great opportunities for the expanded use analysis allow predictions for other species in which negligible
of functional foods to achieve genetic potential and reduce the senescence has not yet been described but should be
risk of disease; the real challenge is to identify the population recognizable with sufficient investigation.
who will benefit the most and identifying those who may be
placed at risk with dietary intervention”. In other words, there
are genetic and environmental differences which precipitate Genome and Epigenome Instability in
into conditions impacting aging and disease. In this session, Dr. Aging
John Richie would discuss the impact of methionine restriction Chair, Jan Vijg, PhD, Albert Einstein College of Medicine,
on aging and cancer; and Drs. Diane Cabelof and Eva Schmelz New York, NY.
would present their findings on impact of folate and
Evidence is now accumulating that erosion of genome and
sphingolipids on aging and cancer. Dr. John Milner would
epigenome informational integrity is a critical factor not only
conclude this session by presenting a seminar discussing
in cancer but also in non-cancer, age-related cell and tissue
challenges with regard to translational approach of the recent
degeneration. Highly conserved pathways have evolved to
discoveries and identifying population in need.
detect the presence of genome damage, effectuate its repair protein misfolding in aging and in late life disease, delivered
or signal cellular responses, such as apoptosis and by researchers who have recently made important
senescence. Understanding the cellular pathways involved in contributions to this field, each working on a different
these processes during normal cellular development and system. Together, these presentations will serve to portray an
aging and gaining a clear understanding of their updated picture of research in the area of protein misfolding
consequences in terms of possible DNA sequence errors or diseases and their age related occurrence.
chromatin alterations may eventually lead to novel
interventions to delay cellular degeneration and death. Key
questions that need to be addressed involve the type of Contemporary Approaches to
(epi)genomic changes that occur during aging, their organ Biogerontology: New Insights from
and tissue distribution, their effect on cell and tissue
functioning and their relation to age-related disease. This
symposium will focus on the use of novel, high-throughput Chair, Terrie Vasilopoulos, BS, Pennsylvania State University
approaches for studying changes in the genome and The aim of this symposium is to display the work of young
epigenome and their possible consequences during aging in and emerging researchers in the field of biogerontology.
humans and model organisms. Biogerontology is a multifaceted field and is informed by
many areas of biological research. This symposium will
highlight research from the fields of genetics, physiology,
Immune Deficiency in Aging endocrinology, biostatistics etc. and will discuss how these
Chair: Rita B. Effros, PhD, David Geffen School of Medicine fields contribute to our understanding of the biological
at UCLA, Los Angeles mechanisms of aging. Within these fields, the presenters will
also discuss the use of humans, rodents and other models in
A decline in immune function is one of the hallmarks of studying the biology of aging. This symposium intends to not
aging, leading to reduced ability to control infections and only address how these approaches can be utilized to study
cancer, as well as blunted responses to vaccines. This the biology of aging but will also argue the importance of
symposium will cover several cutting edge areas of research these biological mechanisms in the understanding and
that address some of the major age-related immunological improvement of health-span in our global aging population
changes. Dr. Effros will provide an overview of the
importance of the immune system in a variety of age-related
pathologies. The first speaker, Dr. Gregory Sempowski (Duke
Univ.) will discuss the problem of thymic involution and
approaches his lab has taken to develop novel strategies for George Sacher Student Award
thymic reconstitution to enhance immune control over
cancer. Dr. Janet Lord (Univ. of Birmingham, UK) will review The George Sacher Student Award is given to the best
her research on neutrophil killing and links to emotional student presentation in the Biological Sciences Programby a
stress during aging, emphasizing new findings regarding GSA member at the Society's Annual Scientific Meeting.
bereavement effects. Dr. Prakash Sambhara (CDC) will The annual $500 award is designed to encourage research and
discuss the importance of innate immunity with regard to to foster interest among students in the Biological Sciences
both infection and vaccination in the elderly. Finally, Dr. Jack section to play an active role in the Society's annual meetings.
Gorski (Blood Center of Wisconsin) will introduce some new
molecular techniques used in his research to analyze the For more information on eligibility and application
changes in the memory cytotoxic T cell responses to requirements for each award, please visit
influenza in the elderly www.geron.org/Membership/Awards.
Protein Alterations in Aging and Aging
Disease LATE BREAKER POSTER SESSION
Chair, Ari Gafni, PhD, University of Michigan, Ann Arbor, MI The Late Breaker Poster Session is an opportunity to present
The accumulation of conformationally-altered, dysfunctional, your newest, most pressing, and previously unreported
proteins in tissues of aging organisms has been recognized research results to attendees at The Gerontological Society
for many years. Recent work has revealed that, in addition to of America’s (GSA) 62nd Annual Scientific Meeting. This
a loss of native activity, certain age-altered proteins gain a session helps to broaden and enhance the overage of
toxic activity. This phenomenon is at the origin of a large research areas represented at the meeting, gives immediacy
number of severe human diseases including Type-2 diabetes, to the discussions and introduces new ideas.
Alzheimer’s, Parkinson’s and Huntington’s diseases, to name
a few. Why the proteins involved in late life diseases become For more information, please visit the Annual Meeting
conformationally altered, what is the origin of their acquired section of www.geron.org.
toxicity and what are its underlying mechanisms are all
important, hitherto unanswered, questions. This symposium Late Breaker abstract deadline: September 15, 2009
will feature four presentations addressing the effects of