Basic Biology of Aging Lecture Series 

The Nathan Shock Center of Excellence in the Basic Biology of Aging, and the Genetic Approaches to Aging Training Grant present the Basic Biology of Aging Seminar Lecture Series.

No upcoming seminars are currently posted.

Past Basic Biology of Aging Lecture Series

Aging and mitochondria

Toren Finkel, MD, PhD
National Heart Lung and Blood Institute
National Institue of Health

Thursday, June 11, 2015 - 2:30 PM
Foege, N-130

Hydrogen sulfide metabolism in dietary restriction-mediated longevity and stress resistance

James R. Mitchel, PhD
Harvard School of Public Health

Thursday, June 4, 2015 - 2:30 PM
Foege, N-130

Oxidative stress and the progression of Alzheimer disease: The triangle of death for neurons associated with altered glucose metabolism, mTOR signaling, and protein phosphorylation

Allan Butterfield, PhD
Sanders-Brown Center on Aging
University of Kentucky

Thursday, May 21, 2015 - 2:30 PM
Foege, N-130

Exploring the Roles of the Mitochondrial Sirtuins in Aging and Disease

Bradford W. Gibson, PhD
The Buck Institute for Research on Aging

Thursday, April 30, 2015 - 2:30 PM
Foege, N-130

Role of growth hormone in delayed aging: Impact of dietary intervention and epigenetics

Holly Brown-Borg, PhD
University of North Dakota

Thursday, April 16, 2015 - 2:30 PM
Foege, N-130

Why Attend?
Mice with hereditary dwarfism (Ames dwarf) and growth hormone deficiency exhibit delayed aging, living more than a year longer than normal siblings, differences in antioxidant defense capacity and lower DNA damage. In contrast, mice with high plasma GH concentrations live half as long as normal, wild type siblings and exhibit a depressed antioxidative defense capacity. The overall hypothesis is that the Ames dwarf mouse has a biologic advantage over normal wild type mice with better enzymatic scavenging of toxic metabolic byproducts and less mitochondrial membrane leakage underlying their enhanced longevity. Determining the pathways and mechanisms that GH utilizes may suggest potential therapeutic interventions that could lead to strategies to delay aging, treat aging-related disorders and extend life span in humans.

Adaptive signaling responses to mitochondrial dysfunction: The mitochondrial UPR

Cole Haynes, PhD
Memorial Sloan Kettering Cancer Center

Thursday, May 8, 2014 - 2:30 PM
Foege, N-130

Why Attend?
Mitochondria are required for numerous cellular processes and mitochondrial dysfunction contributes to many diseases, including diseases of aging. The Haynes laboratory studies the molecular pathways that protect mitochondrial function, particularly at the level of protein folding and protein homeostasis. Similar to the endoplasmic reticulum and cytoplasm, mitochondria have a dedicated chaperone and protease network that maintains the organelle's folding capacity, facilitates protein folding and protects against the accumulation of deleterious, aggrega-tion-prone proteins. Dr. Haynes' work has characterized in detail this "mitochondri-al unfolded protein response" and communication network between mitochondria and nucleus that acts to maintain cellular homeostasis in the face of mitochondrial stress.

A metabolomic perspective on aging

Daniel Promislow, D. Phil
Director of the Canine Longevity Consortium
University of Washington

Thursday, April 24, 2014 - 2:30 PM
Foege, N-130

Studies of aging in lab-adapted organisms have identified single genes with major effects on aging. However, in natural populations, including humans, aging is influenced by a large number of loci with relatively small effects, making these genes extremely difficult to identify. To bridge this gap between genotype and phenotype in studies of aging, the Promislow lab has turned to high-resolution metabolomic profiling. Recent work in the lab has found that genotype, age, and the interaction between the two have dramatic effects on metabolome profiles. Moreover, the lab has shown that manipulations that slow aging also alter underlying network structure of the metabolome. This novel approach, easily translated to humans, holds out the promise of identifying previously unrecognized pathways that influence aging in natural populations.

Astaxanthin, Mother Nature's Most Powerful Antioxidant

Yasuhiro Furuichi, PhD
GeneCare Research Institute in Japan
AstaReal Co., Ltd

Tuesday, April 22, 2014 - 1:30 PM
Health Science Building, K-069

The pigment responsible for the red color of cooked shrimp and some other sea- foods is astaxanthin (Ax), initially produced by the microalgae Haemtococcus pluvialis. The unique molecular structure of Ax makes it hundreds of fold stronger than any other antioxidant molecule, including superior quenching action against singlet oxygen (important in UV-induced photo-aging) and scavenging of peroxyl radicals, hydroxyl radicals, superoxide anion and lipid peroxide. Many lines of bio- chemical and cell biological evidence and several clinical studies have supported roles for Ax in the amelioration of cellular deterioration and senescence and the enhancement of muscle endurance. Dr. Furuichi will discuss these mechanisms of action as well as dosimetry, safety and potential medical applications of Ax. As the discoverer of the 5 capping of mRNA and the author of a soon-to-be-published comprehensive review on its mechanisms, Dr. Furuichi will also be able to answer questions on that subject. Co-Sponsored by the Nathan Shock Center for Excellence in the Basic Biology of Aging and the Genetic Approaches to Aging Training Grant.

Selective Autophagy: Fighting Aging One Protein at a Time

Ana Maria Cuervo, MD, PhD
Co-Director Einstein Institute for Aging Research
Albert Einstein College of Medicine

Thursday, April 10, 2014 - 2:30 PM
Foege Building, Bioengineering Conference Room, Rm. N-130

Faculty Sponsor: Peter Rabinovitch, MD, PhD

Why Attend?
Dr. Cuervo studies the role of protein-degradation in aging and age-related disorders, with emphasis in neurodegeneration. Her group has linked alterations in lysosomal protein degradation (autophagy) with different neurodegenerative diseases including Parkinson's, Alzheimer's and Huntington's disease. They have also proven that restoration of normal lysosomal function prevents accumulation of damaged proteins with age, demonstrating in this way that removal of these toxic products is possible. Dr. Cuervo is a world-leader in the field of protein degradation in relation to biology of aging and is currently co-editor-in-chief of Aging Cell and associate editor of Autophagy.

The Mitochondria in Heart Failure: A Promising Therapeutic Target

Hani N. Sabbah, Ph.D.
Director of Cardiovascular Research Henry Ford Health System, Detroit, MI
Professor of Medicine
Wayne State University

Monday, October 7, 2013 - 2:00 PM
South Lake Union Campus, 850 Republican Street, Brotman Auditorium

Why Attend?
Dr. Sabbah is distinguished for his work to understand the pathophysiology of heart failure and on the development and testing of novel therapeutic modalities for its treatment. This seminar will include recent data examining the role of mitochondria in heart failure and the therapeutic benefit of the mitochondrial targeted drug SS-31/Bendavia.

Caloric Restriction and Aging: Past, Present, and Future

Richard Weindruch, PhD
Department of Medicine
University of Wisconson, Madison

Tuesday, September 24, 2013 - 10:00 AM
Health Sciences Building, K-069

Faculty Sponsor: Matt Kaeberlein and Peter Rabinovitch

Why Attend?
Dr. Weindruch is one of the pioneers of aging research in caloric restriction, and his institute on aging is one of two that have reported data from non-human primates. He has an inside perspective that he will share with us.

Presented by the Nathan Shock Center of Excellence in the Basic Biology of Aging and the Department of Pathology.

Aging, Adipose Tissue Inflammation, and Cellular Senescence

James Kirkland, MD, PhD
Robert and Arlene Kogod Center on Aging
Mayo Clinic

Friday, April 5, 2013 - 1:30 PM
Bioengineering Building, Foege N-130

Faculty Sponsor: Peter Rabinovitch and Matt Kaeberlein

Why Attend?
This seminar will show how these three topics are closely intertwined. Adipose tissue is often the largest organ in humans and is at the nexus of mechanisms involved in longevity and age-related metabolic dysfunction. Fat cell progenitors, preadipocytes, dysdifferentiate in old age, switching into a pro-inflammatory, tissue-remodeling, senescent-like state. Pro-inflammatory processes may amplify each other and have systemic consequences. Senescent, pro-inflammatory cells in fat could have profound clinical consequences because of the large size of the fat organ and its central metabolic role. Consistent with this, clearance of p16INK4a-positive senescent cells delays ageing-associated disorders.

For further information contact Rachel Wilsey:, 206-897-1759 or Peter Rabinovitch:, 206-685-3761.

Is the Life-extending Action of Cu/ZnSOD Overexpression in Mammals Obesity Dependent?

Yuji Ikeno, MD, PhD
Assistant Professor
Pathology Department & the Barshop Institute
University of Texas Health Science Center at San Antonio, Texas

Tuesday, October 2, 2012 - 9:30 AM
Health Sciences Center, Room K-069

Faculty Sponsor: Matt Kaeberlein and Peter Rabinovitch

Why Attend?
Dr. Ikeno’s lab has recently found that Sprague-Dawley rats overexpressing Cu/ZnSOD (SOD1) in (SD) have a significant increase in lifespan and a reduction in age-related pathologies. In contrast, F344 rats that overexpress SOD1 have little increase in lifespan compared to wild-type rats. Interestingly, Sprague-Dawley, but not F344 rats have an age-related increase in body fat and insulin sensitivity. Dr. Ikeno will discuss the hypothesis that overexpression of Cu/ZnSOD is most protective against oxidative stress and attenuates aging and age-related diseases mainly under obese conditions in mammals.

For more information contact Matt Kaeberlein at 543-4849 or Peter Rabinovitch at 685-3761

A Network Perspective on the Biology of Aging

Daniel Promislow, Ph.D.
Department of Genetics
University of Georgia

Wednesday, July 11, 2012 - 10:30 AM
Health Sciences Center, Rm. K-069

Faculty Sponsor: Matt Kaeberlein, PhD

Why Attend?
Knocking out a single gene can more than double the life expectancy of a small worm. Over the past two decades, scientists have uncovered scores of single mutants that increase lifespan in laboratory organisms. But in the case of aging, the links between genotype and phenotype are extremely complex. On closer inspection, the molecular basis of aging involves a large and complex network of genes, proteins and metabolites. In fact, a comprehensive understanding of the genetics of aging calls for an integrated approach, linking not just genes or proteins in molecular networks, but a suite of molecular, behavioral, physiological and demographic traits, from single cells to large populations. Recognizing this complexity, Dr. Promislow's work on the evolution of aging attempts to answer two key questions. First, why is there variation in rates of aging among individuals, and second, why do different processes fail at different rates within individuals? This seminar will describe how a network approach, applied to inbred, laboratory models as well as to genetically heterogeneous populations, can shed new light on these important questions.

For more information contact Matt Kaeberlein at 543-4849 or George Martin at 543-5088

Xenobiotic Surveillance and Response in the Regulation of C. Elegans Longevity and Satiety

Gary Ruvkun, PhD
Department of Genetics
Havard University

Tuesday, June 5, 2012 - 11:30 AM
Bioengineering Building, Foege N-130

Faculty Sponsor: Matt Kaeberlein, PhD

Tumor Suppressor Mechanisms in Long-lived Rodents

Vera Gorbunova, PhD
Associate Professor
Department of Biology
University of Rochester

Tuesday, May 22, 2012 - 11:30 AM
Bioengineering Building, Foege N-130

Faculty Sponsor: Matt Kaeberlein, PhD

The Role of Transsulfuration in the Health and Aging of Drosophila Melanogaster

Scott Pletcher, PhD
Assistant Professor
Molecular Integrative Physiology
University of Michigan Medical School

Tuesday, May 15, 2012 - 11:30 AM
Foege Builiding, Bioengineering Conference Room, N-130

Faculty Sponsor: Matt Kaeberlein, PhD

The Brain and Fat: Dissecting Systemic Control of Metabolism and Aging in the NAD World

Shin-ichiro Imai, MD, PhD
Associate Professor
Department of Developmental Biology & Medicine
Washington University School of Medicine

Tuesday, March 20, 2012 - 3:30 PM
Health Sciences Center, Room K-069

Faculty Sponsor: Peter Rabinovitch, MD, PhD

Why Attend
Sirtuins have become established as important factors modulating aging-related disease in mammals. The Imai laboratory studies the role of SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) for the regulation of metabolism and aging. Dr. Imai has proposed a comprehensive concept of a novel systemic regulatory network, named NAD World, for the intricate connection between metabolism and aging. This new concept of the NAD World may provide important insights into the systemic regulation of mammalian aging and longevity and also convey ideas of functional hierarchy and frailty for the induction of aging. By understanding the system dynamics of the NAD World, Dr. Imai's goal is to develop therapeutic and preventive interventions for age-associated diseases, such as type 2 diabetes and Alzheimer's disease. Here are three burning questions that the Imai lab is trying to answer: 1) Which organs/tissues play a major role in the regulation of aging and longevity in mammals? Is there any control center of aging? 2) What hormones/factors mediate the communication between the control center of aging and other modulatory organs/tissues? 3) What molecules/signaling pathways coordinate the regulation of mammalian aging at a systemic level?

Extending Lifespan by promoting proliferative homeostasis in Drosophila

Heinrich Jasper, Ph.D.
Assistant Professor
University of Rochester, New York

Tuesday, June 22, 2010 - 12:30 PM
HSB, K-069

Faculty Sponsor: Peter Rabinovitch
Seminar is now RE-SCHEDULED

Mitochondrial signaling in Disease and Aging

Gerald Shadel, Ph.D.
Medicine and Molecular Genetics
Yale School of Medicine

Tuesday, June 15, 2010 - 12:30 PM
HSB, K-069

Faculty Sponsor: Peter Rabinovitch

Adenylyl cyclase type 5 (AC5), cardiac stress and longevity

Stephen Vatner, M.D.
Dept. of Cell Biology & Molecular Medicine
UMDNJ, New Jersey Medical School

Tuesday, June 8, 2010 - 12:30 PM
HSB, K-069

Faculty Sponsor: Peter Rabinovitch

Genetic Variation in Aging and Longevity

Yousin Suh, Ph.D.
Associate Professor
Medicine and Molecular Genetics
Albert Einstein College of Medicine, New York

Tuesday, May 4, 2010 - 12:30 PM
HSB, K-069

Faculty Sponsor: Peter Rabinovitch

Chemical Modifications of Proteins during Aging

John Baynes, Ph.D.
Carolina Distinguished Professor Emeritus
Dept. of Chemistry & Biochemistry
University of South Carolina

Tuesday, April 20, 2010 - 12:30 PM
HSB, K-069

Faculty Sponsor: Peter Rabinovitch

Diet, Death and Demography

Linda Partridge, Ph.D.
Director, The Institute of Healthy Ageing University College, London
Group Leader, Max Planck Institute for Biology of Ageing, Cologne, Germany

Monday, November 9, 2009 - 11:00 AM
Health Sciences Center, Room K-069

Faculty Sponsor: Peter Rabinovitch

Mitochondria, Age and the Heart

Charles L. Hoppel, M.D.
Departments of Pharmacology and Medicine
Case Western Reserve University

Tuesday, July 28, 2009 - 4:00 PM
Health Sciences Center, K-069

Faculty Sponsor: Peter Rabinovitch, M.D., Ph.D