Scott E. Gordon, Ph.D.
Assistant Professor
Department of Exercise and Sport Science
Human Performance Laboratory
East Carolina University
Targeted Rescue of Protein Translation and Synthesis in Aged Skeletal Muscle
The gradual but significant loss of skeletal muscle mass and strength is a major component of age-related decline in the ability to accomplish basic activities of daily living. The goal of Dr. Gordon's investigation is to determine if blocking AMPK, an enzyme demonstrating elevated activity in aged skeletal muscle, may act as a target for allowing the synthesis of new proteins to prevent muscle wasting in aged rats. Ultimately, his work may result in new therapies for humans that could have advantages over current hormonal replacement therapy.
Click here to read more about Dr. Gordon's work.
James Harper, Ph.D.
Research Investigator
Department of Pathology
University of Michigan Medical School
Modulation of Stress Resistance and Aging in Mice
An enhanced ability to withstand the effects of toxic compounds appears to be an important mediator of life span in a variety of animals, and this increase in stress resistance may be the result of a reduction in the level of specific hormones involved in growth. In Dr. Harper's experiment with mice, he will reduce the level of these hormones using dietary and pharmacological interventions to determine its effects on stress resistance and aging. If Dr. Harper's lab can show that an enhanced ability to resist stress is important for successful aging, then determining which hormones are involved will give us the ability to improve our resistance to stress using specific drugs or dietary intervention in order to keep the elderly population healthier longer.
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Christopher G. Janus, Ph.D.
Assistant Professor
Department of Neuroscience
Mayo Clinic, Jacksonville
Memory Recovery as a Function of Aging and Tau Transgene Suppression
Despite considerable scientific progress, our understanding of the pathogenesis of specific forms of dementia, including Alzheimer's, is still poorly understood, and it is not surprising that current treatments merely focus on the symptoms. The identification of genes associated with neurodegenerative diseases provide an opportunity for creating mouse models designed to replicate the relevant features found in these diseases, including both brain pathology and associated cognitive changes. Dr. Janus' research capitalizes on this novel technology, and using a mouse model attempts to elucidate the causes of cognitive decline. Dr. Janus will investigate the interaction between the effects of aging and the presence of the mutated human tau gene on memory decline. By switching the gene on or off at various ages of the mice life he will attempt to determine how the severity of dementia depends on the age of onset of the disease, which types of memory (simple learning or memory of complex environments) are most affected, and how much memory can be recovered when genes are switched off by the early or late stage of the disease. Such findings may help us test therapeutic approaches to ameliorate dementia caused by neurodegeneration and/or aging.
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Dana Leanne Jones, Ph.D.
Assistant Professor
Department of Biology
Salk Institute for Biological Studies
Identification of Factors Regulating Aging of the Stem Cell Niche
Decreased tissue and organ function is a hallmark of aging, and such changes have been attributed to altered stem cell function. Stem cells are the building blocks during development of organisms and are used for the maintenance and regeneration of tissue throughout an individual's lifetime. Most studies have focused on how stem cells age while Dr. Jones' research seeks to understand how stem cells, the stem cell environment, and the relationship between the two change during aging. Ultimately, her work may facilitate the use of stem cells in tissue replacement therapies, also known as regenerative medicine. (Regenerative medicine can be defined as a group of new techniques that rely on replacing diseased or dysfunctional cells with healthy ones.) In the future, these therapies may be applied to a wide range of human disorders, including many types of cancer, diabetes, muscle degeneration, and neurological diseases such as Parkinson's disease.
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Matt R. Kaeberlein, Ph.D.
Assistant Professor
Department of Pathology
University of Washington
Molecular Genetics of Life Span Extension by Dietary Restriction in C. elegans
Life span extension from dietary restriction has been observed in many different organisms, but the details of this phenomenon remain poorly understood. Dr. Kaeberlein hopes to understand the mechanisms underlying how reduced food consumption slows aging and increases life span in the nematode, C. elegans. The discoveries from his efforts will guide future studies in more complex organisms, including humans, and ultimately help to identify potential targets for therapies that will be beneficial for many different age-associated diseases in humans.
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Elizabeth A. Kensinger, Ph.D.
Assistant Professor
Department of Psychology
Boston College
How Aging Affects Memory for Emotional Events: Behavioral and Neuroimaging Investigations
The vast majority of research that has focused on understanding age-related changes in memory has examined memory for information that contains no personal significance or emotional importance. Dr. Kensinger will investigate the cognitive (thought-level) and neural (brain-level) processes that young and older adults use to help them remember information that has emotional significance to them (for example, information that is perceived as being pleasant or unpleasant). Dr. Kensinger will examine the extent to which the characteristics of the to-be-remembered information and the memory demands required by the task influence whether older adults show memory enhancement for emotional information. Through the use of functional neuroimaging (fMRI), Dr. Kensinger will also examine the neural processes that young and older adults use to successfully learn and retrieve emotional information, and to investigate whether the processes that are recruited by older adults are the same as, or distinct from, those processes engaged by young adults. Her work may ultimately provide ways to distinguish healthy from pathological aging at a relatively early stage.
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Genevieve Neal-Perry, M.D., Ph.D.
Assistant Professor
Department of Obstetrics & Gynecology
Department of Women's Health
Albert Einstein College of Medicine
Hypothalamic Dysfunction: A Neuroendocrine Basis for Reproductive Aging
Reproductive aging is a complex process that not only affects fertility, but also increases the risk for health-related problems such as osteoporosis, heart disease, diabetes mellitus and cognitive dysfunction. While it is certain that ovarian failure ultimately defines the onset of menopause, the role of the brain in reproductive aging, specifically the hypothalamus (a region of the brain critically involved in reproduction), is less clear. The goal of Dr. Neal-Perry's project is to define the role of the hypothalamus in age-related reproductive failure. Understanding how the brain participates in the onset of age-related reproductive failure may provide a platform for the development of new and non-hormonal treatments that delay the onset of menopause and menopause-related illnesses, thereby improving the overall quality of life of women as they age.
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Paul Schmidt, Ph.D.
Assistant Professor
Department of Biology
University of Pennsylvania
Couch Potato Aging in Drosophila
Reproductive diapause is a form of quiescence, similar to hibernation. Insects use cues such as temperature and light to recognize upcoming periods of stress such as winter. When diapause is expressed, individuals become very stress resistant and long lived.
In the model organism Drosophila melanogaster, some individuals (genotypes) are diapause-capable whereas others are diapause-incapable. Dr. Schmidt's lab has previously shown that these diapause-capable flies age at a slower rate than their diapause-incapable counterparts. Furthermore, genetic analysis has shown that the ability to express diapause is caused by a reduction in the activity of one gene: couch potato (cpo). Because the expression of diapause itself and the ability to express diapause are associated with delayed senescence, the identified gene for diapause represents a new candidate gene (and potentially a novel pathway) involved in the genetic determination of aging. Dr. Schmidt's research is an investigation of the role of this newly identified gene in the aging process. His work may ultimately explain why some individuals have a tendency to live longer and senesce more slowly than others.
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Tao Wei, M.D., Ph.D.
Assistant Professor of Microbiology & Molecular Biology
Department of Biology
University of Texas at San Antonio
Caloric Restriction Represses DNA Damage to Replication Forks and Chromosomal Rearrangements
Aging is multifactorial; numerous theories exist to explain the process. In the area of evolutionary genetics, the antagonistic pleiotropy theory postulates that there are special types of pleiotrope genes that have opposite effects of fitness at different ages, being advantageous in early life, but are harmful at later ages. However, evidence for existence of such genes is lacking, which is what Dr. Wei's work aims to find. His research, which is centered on metabolism and genome stability, will help to shed light on the molecular pathology of cancer-susceptibility pre-mature aging diseases, such as Werner and Bloom syndromes. Ultimately, the results could provide insights into metabolic interventions such as low calorie diet as a means to maintain good health and form molecular bases for development of anti-aging therapies for age-related diseases, and in a broader sense, to enhance longevity and quality of life for the elderly.
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Raghunatha Yammani, Ph.D.
Instructor
Department of Internal Medicine
Wake Forest University School of Medicine
Aging and S100A4 in Cartilage
Although many factors can lead to the development of osteoarthritis, the primary risk factor is aging. Dr. Yammani's preliminary studies have established that S100A4 (a calcium-binding protein that belongs to a family of S100 proteins that play an important role in a variety of cellular activities in various cell and tissue types) binds to Receptor for Advance Glycation End produces (RAGE) and activate an array of signaling molecules. His current AFAR-sponsored project is to define the role of S100A4 and RAGE-mediated cell signaling pathways in cartilage with age, thus providing basic cellular and molecular mechanisms that link aging to the development of osteoarthritis. This knowledge may ultimately lead to better therapies for those suffering from the disease.
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SOUTHEAST AFFILIATE
Kreton Mavromatis, M.D.
Assistant Professor
Departments of Medicine and Cardiology
Emory University
Effects of Age on Endothelial Progenitor Cell Mobilization in Humans
Coronary atherosclerosis is a leading cause of aging-related death in the world. Naturally occurring stem cells circulating in the bloodstream can regenerate and rejuvenate the injured artery, preventing inflammation and arterial obstruction. Circulating stem cell activity, however, diminishes with age. Dr. Mavromatis will examine circulating stem cells in young and older patients after arterial injury caused by a common procedure, coronary balloon angioplasty. He hopes it will shed light on why a diminishing circulating stem cell response to angioplasty is seen with aging. More specifically, Dr. Mavromatis hopes to understand whether reduced circulating stem cell activity is due to reduced numbers of cells released from the bone marrow, or whether it is due to a decreased ability of individual cells to grow and function; and, what chemical factors signal the cells that arterial injury has taken place. Such a discovery could hold promise for stem cell therapy.
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Zhi Qiang Qu, M.D., Ph.D.
Assistant Professor
Department of Cell Biology
Emory University School of Medicine
A Study on the Mechanisms of the Best Vitelliform Macular Dystrophy
Age-related macular degeneration (AMD) is a common disease among the aged population and is a leading cause of blindness in industrialized countries. The cause of AMD remains unknown and there are currently no effective ways of prevention and treatment of the disease. To reveal the mechanism of AMD, Dr. Qu will study Best vitelliform macular dystrophy (VMD2) as a model for AMD because there are many similarities between the two diseases. He hypothesizes that there probably are common processes in pathological mechanisms for both AMD and VMD2 and that VMD2 can be used as a model for AMD study. Dr. Qu's work will provide important insights into the understanding of AMD and will make the prevention and treatment of AMD possible.
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OHIO AFFILIATE
Jonathan Godbout, Ph.D.
Assistant Professor, Dept. of MVIMG
Associate Faculty Member, IBMR
The Ohio State University
Aging, Cytokines and Depressive Behavior
It is known that the elderly have a higher incidence of depressive disorders concomittant with illness and infection; however, the mechanisms involved are not well understood. One explanation is that there are age-related impairments in the communication between the brain and the immune sytem. A potential consequence of this impairement is a prolonged inflammatory response within the brain when the immune sytem is activated. This is significant because prolonged brain inflammation can be detrimental to mental health and can increase depressive symptoms. The goal of Dr. Godbout's project is to attain a better understanding of the relationship between immune activation, brain inflammation, and depression in the aged. Specifically, the aim of his AFAR project is to understand the biochemistry that underlies why the neuroinflammatory response to immune activation leads to prolonged depressive behavior in aged mice. Dr. Godbout's research will also seek to identify potential targets to prevent neurobehavioral deficits in a susceptible elderly population.
Click here to read more about Dr. Godbout's work.
