Dr. Tchkonia is an Assistant Professor and Associated Consultant at the department of Physiology and Biomedical Engendering, at Mayo Clinic. Her research interests involve discovery science, translational research, and clinical applications in the field of cellular senescence, and aging- and senescence-associated chronic diseases. With collaborators, she discovered the first senolytic drugs that effectively eliminate senescent cells both in vitro and in vivo and demonstrated that pharmacological targeting of these cells can alleviate age-related frailty and symptoms of multiple diseases. Some of these drugs have already been tested in clinical trials for various indications at different centers in the US and worldwide. Dr. Tchkonia is one of the four co-inventors of a mouse model where senescent cells can be removed selectively and a named inventor on multiple patent applications related to therapeutic approaches for targeting senescent cells in aging and disease.

Dr. Tamar Tchkonia received her Master's degree from Tbilisi State University and her Ph.D. degree in molecular biology from the Institute of Molecular Biology, Moscow Russia. She was a Docent at Tbilisi State University and an invited lecturer at Tbilisi State Medical University. After two years of postdoctoral training at the Boston University Medical Center, Dr. Tchkonia joined the faculty at the Evans Biomedical Research Center at Boston University. Since 2007 Tamar has been an active member of the Robert and Arlene Kogod Center on Aging at Mayo Clinic and a steering committee member of the annual meeting series organized by the Alliance for Healthy Aging.

Administrator
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Dr. Robbins is a Professor of Biochemistry, Molecular Biology and Biophysics and Associate Director of the Institute on the Biology of Aging and Metabolism (iBAM) and the Medical Discovery Team on the Biology of Aging at the University of Minnesota.

Dr. Robbins received his B.A. from Haverford College, his Ph.D. from the University of California at Berkeley and then worked as a post-doctoral fellow in the laboratory of Dr. Richard Mulligan at the Whitehead Institute at MIT. He was a Professor of Microbiology and Molecular Genetics, Director of Basic Research for the Molecular Medicine Institute and Co-Director of the Paul Wellstone Cooperative Muscular Research Center at the University of Pittsburgh School of Medicine. He then was a Professor of Molecular Medicine at Scripps Research in Jupiter, Florida and Director of the Center on Aging prior to moving to the University of Minnesota.

He was one of the first to identify enhancer elements that regulate transcription at a distance, the first to show that the retinoblastoma tumor suppressor regulates transcription and the first to develop gene therapies for autoimmune disease including an ongoing clinical trial for osteoarthritis. More recently, he was part of a collaborative team that was the first to identify senotherapeutic compounds, able to reduce the senescent cell burden and extend healthspan and lifespan in mouse models, that are in more than 15 clinical trials for age related diseases and conditions.

Laura Niedernhofer joined the University of Minnesota in July 2018 to direct the new Institute on the Biology of Aging & Metabolism and Medical Discovery Team on the Biology of Aging. She is also a Professor in the Department of Biochemistry, Molecular Biology and Biophysics at UMN. Dr. Niedernhofer's expertise is in DNA damage and repair, genome instability disorders, cellular senescence and aging. Her research program is centered on studying fundamental mechanisms of aging and developing therapeutics to target them. She contributed to the discovery of a new class of drugs called senolytics. Laura has served on study section for NCI, NIEHS and NIA. She has been awarded for research in aging, cancer and environmental health science and was the 2018 recipient of the Vincent Cristafolo Rising Star in Aging Research awarded by the American Federation for Aging Research (AFAR). She is currently serving on the Advisory Council to the Division of Aging Biology, NIA and on the Board of Directors for American Federation of Aging Research. Laura was recently nominated to The Academy for Health and Lifespan Research.

Director, Institute of the Biology of Aging and Metabolism https://med.umn.edu/aging
Medical Discovery Team Biology of Aging https://med.umn.edu/research/medical-discovery-teams
Professor Biochemistry, Molecular Biology & Biophysics https://cbs.umn.edu/academics/departments/bmbb
University of Minnesota, School of Medicine https://med.umn.edu/

Academic Officer
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Academic Officer
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Simon Bekker-Jensen has a PhD in Cancer Biology from the Technical University of Denmark and the Danish Cancer Research Centre. Prior to establishing his independent group within cellular stress signaling in 2016, he has 10 years of experience in research within the DNA damage response. Amongst others, he holds a Consolidator Grant from The European Research Council and is an EMBO Young Investigator.

Morten Scheibye-Knudsen did his medical training at the University of Copenhagen including a short scholarship investigating mitochondrial physiology. During medical school he founded his first company, Forsoegsperson.dk, which has grown to be the largest provider of volunteers for clinical trials in Denmark. After medical school he worked as a medical doctor in Denmark and Greenland before moving to basic science as a post doctoral fellow at the National Institute on Aging, NIH, in Baltimore. Here, he utilized computational and wet lab science to investigate how DNA damage contributes to the complex phenotypes seen in premature and normal aging. In 2016 he returned to Copenhagen as an assistant professor to start his own research program focusing on aging. In 2018, he received tenure and was promoted to associate professor. His team (~20 people) utilizes computational science, animal models, gene editing, and high-throughput approaches such as high-content microscopy and omics investigations to understand the molecular basis of aging and age-associated phenotypes. Lab generated data is routinely analyzed through AI-assisted pipelines such as novel cellular senescence classifiers and fully automated animal tracking (www.tracked.bio). He has published his work in some of the best journals in the world including Cell, Cell Metabolism, Nature Aging, New England Journal of Medicine and many others. In addition to his core research, he has been lecturing at Johns Hopkins School of Public Health for 8 years; He is a chief editor at Frontiers in Aging running the Aging Interventions section; He organizes the largest annual conference on Aging Research and Drug discovery (www.agingpharma.org); He is an advisor to Deep Longevity, the Longevity Vision Fund and Ars Salus; He has given invited presentations at top institutions (NIH, MIT, Harvard, NUS, Karolinska and others); and received several awards for his research.

Ageing and major chronic diseases are associated with an accumulation of damage to our DNA. Accordingly, hereditary diseases displaying premature/accelerated aging are most often caused by defects in various DNA repair processes. In this lecture, I will elucidate our work utilising computational approaches, wet lab analysis, animal models and clinical trials to understanding how DNA damage leads to diseases and what we can do to attenuate the consequence of damage to our genome allowing everyone longer and healthier lives.

Lene Juel Rasmussen is Professor at the University of Copenhagen and Executive Director of the interdisciplinary aging center, Center for Healthy Aging, residing within the Faculty of Health and Medical Sciences. Her research aims to unravel the complex molecular basics of aging and the development of aging associated diseases. Within this context, her research group focuses on the molecular understanding of mitochondrial dysfunction and how cells achieve to preserve mitochondrial and nuclear DNA integrity as well as DNA repair.

The hallmarks of aging, includes genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A significant amount of scientific evidence has been generated on the role of individual hallmarks on aging, and how they are involved in loss of function and the etiology of age-related diseases. My research addresses whether a specific hallmark by itself could be the primary driver of all aging phenotypes or if different combinations of interactions produce different aging phenotypes. Taken together, emerging evidence points to complex interactions as being the likely driver of aging. I am specifically investigating the interaction between mitochondrial dysfunction and genomic instability.

I am a lecturer in Translational Biology of Ageing at Newcastle University. I was originally an exercise scientist and became interested in energy metabolism and mitochondria. I took my Ph.D. on mitochondrial function and reactive oxygen species generation in ageing at Cambridge University, and since then this field has become my expertise. Since I came to Newcastle University, I have made critical contributions to the research on the roles of mitochondrial function and their changes in cellular senescence and in organismal ageing, which has been the major strengths in Newcastle.

Through my expertise on mitochondrial and cellular metabolism I also have extensive research collaboration across different biomedical fields since my early career, and have established and led a university core facility for Metabolic analyses using Seahorse Analyzer technology. My work as scientific officer, from conception of ideas, experimental supervision to writing up, has played a key role for over a dozen of high impact publications.

I am a committee member for the Faculty of Medical Sciences Ageing and Geroscience theme and leads a workstream 'Restoring health' for Centre for Healthier Lives.

My current research includes mechanisms of mitochondrial dysfunction during cell senescence, and developments of the therapies against age related conditions and diseases using senescence and mitochondrial targeted approaches. I am also interested in technological and methodological developments and their applications to research, and have a number of local and international industry connections.

Administrative Site Contact: [email protected]

Dr. Gavin Richardson, PhD is a Senior Lecturer and acting lead of the Vascular Medicine and Biology Theme at the Biosciences Institute, Newcastle University. Dr. Richardson is the lead of the heart platform for the Quality in Organ Donation (QUOD) biobank and BHF National Centre for Regenerative Medicine collaborator with imperial college London. He obtained his PhD in prostate cancer stem cell biology in Newcastle in 2004 and worked as a postdoctoral researcher at Durham University studying skin dermal stem cells and skin aging. In 2010 Dr. Richardson re-joined Newcastle University on an independent fellowship to apply his expertise in regeneration and aging to study age-related cardiovascular disease. During his career, Dr. Richardson has worked in institutions including Columbia and Harvard Universities as a visiting Fellow. His research aims to understand how senescence contributes to the pathophysiology of cardiovascular disease focusing on senescence-associated inflammation and maladaptive myocardial remodeling. Dr. Richardson’s current work aims to characterize the cardiac senescence signature to identify novel biomarkers of cardiovascular disease and develop new therapies, targeting senescence, to attenuate their detrimental impact on myocardial function.

Professor of Cell Gerontology, Newcastle University

Dr. von Zglinicki is a founding member of the basic biology branch of the Newcastle Ageing Institute and was its scientific director from 2014 to 2019. His principal research interest is in understanding the cellular and molecular signaling pathways connecting DNA damage responses (specifically emanating from dysfunctional telomeres) with mitochondrial function and metabolism, thus causing and maintaining cell senescence, and how these contribute to mammalian aging. He was the first to discover oxidative stress and resulting DNA damage as a major cause of telomere shortening and to propose telomere length as a biomarker of aging in humans. He found that senescent cells induce senescence in bystander cells, which might explain the long-term physiological and pathological consequences of short-term senescence-inducing treatments. He aims to prolong a healthy lifespan in mammals and ultimately humans by interventions that selectively ablate senescent cells and/or suppress bystander signaling. In 2017 he received the Lord Cohen of Birkenhead Medal for Services to Gerontology. He published about 300 papers on cell and molecular biology of aging, resulting in an h-index of 89 (Google Scholar June 2022).

Staff Advisor
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Mark S. Hipp studied Biochemistry at the Eberhard-Karls-University Tübingen, and received his PhD at the University of Konstanz (2005). As a graduate student he worked on the effects of the ubiquitin-like modifier FAT10 on protein degradation in the Department of Biology, with Prof. Marcus Groettrup.

While working as a postdoctoral fellow in the laboratory of Prof. Ron Kopito at Stanford University he discovered that the inhibition of the proteasome observed in Huntington's disease is not direct, but can only be explained by a network-wide effect of the aggregates. He further expanded this hypothesis during his time as a group leader at the Max Planck Institute of Biochemistry in the Department of Prof. F. Ulrich Hartl, where his group characterized the interactions of multiple different disease associated proteins with the cellular quality control machinery.

In 2019 Mark Hipp accepted a position at the University Medical Center Groningen, where he is continuing his investigation of the toxic effects of protein aggregates. Since 2020 he is also affiliated with the Carl von Ossietzky Universität Oldenburg.

Marco Demaria is currently an Associate Professor in Cellular Ageing at the Medical Faculty of the University of Groningen and the Group Leader of the laboratory of Cellular Senescence and Age-related Pathologies of the European Research Institute for the Biology of ageing (ERIBA). He obtained his PhD at the University of Torino, Italy, under the supervision of prof. Valeria Poli. In 2010, he joined the laboratory of prof. Judith Campisi as a postdoctoral fellow at the Buck Institute for Research on Aging in Novato, USA. In 2015, Dr. Demaria returned to Europe and joined the University of Groningen and the European Research Institute for the Biology of Ageing (ERIBA) with a tenure-track position. His work is supported by several agencies and companies. Dr. Demaria serves as Editor in Chief for npj Aging, and as reviewer for several journals and funding agencies. In 2018 he co-founded a start-up company, Cleara Biotech. Since 2022 he is the President of the International Cell Senescence Association (ICSA).

Dr. Demaria is focused towards understanding the molecular basis of aging and age-related disorders, and identifying new molecular and cellular targets to improve health and longevity. At the core of his research is cellular senescence, a potent tumor suppressive mechanism characterized by a strong secretory and pro-inflammatory phenotype. During his postdoctoral studies, he has characterized a new transgenic mouse model for the study of senescence in vivo, and demonstrated that senescent cells accumulate and persist during aging and under genotoxic stress, where they contribute to disease. However, he has also demonstrated that sub-populations of senescent cells cover positive roles during tissue repair. Now, the goal of the Demaria laboratory is to define the conditions and phenotypes that determine whether a senescent cell covers beneficial or detrimental functions. The laboratory is developing the following projects, with the support of many collaborators and funding schemes:

• Molecular characterization of the senescence heterogeneity.
Role of senescent cells during disease.
• Clearance of senescent cells.
• Lifestyle effects on induction of cellular senescence.
• Pro-senescence therapies to improve tissue repair.

From August 1th, 2022 onwards, Folkert Kuipers PhD (1957) acts as Scientific Director of ERIBA and head of the Department of the Biology of Ageing at the University Medical Center Groningen (UMCG). Folkert studied biology/biochemistry at the University of Groningen (UoG) and recieved his PhD degree in Medical Sciences at UoG in 1987. After a research fellowship from the Royal Netherlands Academy for Arts and Sciences and an Established Investigatorship from the Netherlands Heart Foundation, he was appointed as Professor of Pediatrics in 2000 and was head of the Laboratory of Pediatrics at UMCG from 2000-2008 and from 2016-2022. His research program deals with molecular (dys)regulation of cholesterol, bile acid and lipid metabolism and transport in liver and intestine in inherited and age-related chronic metabolic diseases, including roles of the gut microbiome. He is (co-)author of >350 peer-reviewed publications and has supervised >40 PhD theses. From 2008-2016 he served as Dean of the Faculty of Medical Sciences/vice-chairman of the board of UMCG and was involved in initiation and implementation of the Healthy Ageing program at UMCG, with population cohort LifeLines and ERIBA as scientific flagship projects. He is member of the External Advisory Boards of the Robert and Arlene Kogod Center for Aging Research, Mayo Clinic, Rochester, MN, USA, and the Multidisciplinary Institute for Ageing (MIA), University of Coimbra, Coimbra, Portugal.

Senior Program Coordinator
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Dr. Diana Jurk, Ph.D. is an Associated Professor at Mayo Clinic Rochester and directs the Biology of Aging and Age-related Diseases laboratory.

Dr Jurk is originally from Germany where she graduated with a degree in Natural Sciences from the University of Freiberg in 2004. Following her degree, she conducted biomedical research at Bayer, first in Wuppertal and then in Leverkusen (where she was awarded a master's degree).

Having decided to move to academia, Dr. Jurk was first a research assistant at the Uniklinik in Freiburg, Germany (2005-2007) and then conducted her PhD studies at Newcastle University in the UK (2007-2012), in the area of liver senescence and inflammation.

In 2015, Dr. Jurk was awarded the Newcastle University Faculty fellowship and in 2018 the prestigious Springboard Award from The Academy of Medical Sciences which allowed her to direct an independent research program. In 2018 she moved her research team to Mayo Clinic, Rochester.

Diana's work has led to new insights into the mechanisms driving the process of cellular senescence in the context of liver disease and neurodegeneration. Her work, published in Nature Communications, has demonstrated a key role for senescence in Non-alcoholic fatty liver disease. More recently, her team published in Cell Metabolism the first evidence for the involvement of senescence in neuropsychiatric diseases and in cognitive decline during aging (Aging Cell, 2021).

Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown to improve brain function in mouse models of neurodegenerative diseases as well as obesity. However, it is still unknown whether senescent cell clearance alleviates cognitive dysfunction during the aging process. To investigate this, we first conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice. We observed an age-dependent increase in p16Ink4a senescent cells, which was more pronounced in microglia and oligodendrocyte progenitor cells and characterized by a SASP. We then aged INK-ATTAC mice, in which p16Ink4a-positive senescent cells can be genetically eliminated upon treatment with the drug AP20187 and treated them either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin. We observed that both strategies resulted in a decrease in p16Ink4a exclusively in the microglial population, resulting in reduced microglial activation and reduced expression of SASP factors. Importantly, both approaches significantly improved cognitive function in aged mice. Our data provide proof-of-concept for senolytic interventions' being a potential therapeutic avenue for alleviating age-associated cognitive impairment.

Marissa Schafer joined Mayo Clinic faculty as an Assistant Professor and Senior Associate Consultant in the Department of Physiology and Biomedical Engineering and the Department of Neurology in May 2020. She is an active member of the Mayo Clinic Robert and Arlene Kogod Center on Aging. Dr. Schafer's NIH-funded research focuses on identifying mechanisms that can be targeted to counteract age-dependent cognitive dysfunction. She is a member of the NIH Cellular Senescence Network Consortium. Dr. Schafer is passionate about prioritizing diversity and inclusion in research and is actively engaged in a wide range of local and international service activities focused on education and science communication.

Age is a primary risk factor for multiple chronic conditions, including cognitive decline and dementia. Dr. Schafer's research focuses on cellular and molecular mechanisms that contribute to age-related brain dysfunction, with the goal of developing strategies to prevent, slow, or reverse cognitive decline. Cellular senescence and inflammation are interconnected causes and consequences of tissue aging. Dr. Schafer and her research team synergistically investigate the brain-specific and peripheral impact of senescent cells and inflammation on brain aging and cognitive health. Researchers in Dr. Schafer's lab implement a multidisciplinary approach that spans the basic-to-translational continuum. They leverage state-of-the-art cellular, molecular, and behavioral methods in mouse and cell-based models of aging, coupled with clinical data and biomarker analyses, to discover mechanisms of dysfunction and develop therapeutics to combat age-related brain dysfunction.

Joao Passos, Ph.D., received his PhD at Newcastle University. He is a Professor in the Department of Physiology Biomedical Engineering and Associate Director of the Robert and Arlene Kogod Center on Aging. Dr. Passos investigates the role of senescent cells in aging and age-related disease, with a particular focus on the role of mitochondria and telomeres in the process. His work demonstrates how cellular senescence depends on chronic DNA-damage signaling that results from irreparable damage to telomeres. Furthermore, Dr. Passos uncovered a key role for mitochondria in the induction of cellular senescence.

The goal of Dr. Passos' current work is to develop new therapies that target mitochondrial dysfunction to counteract the detrimental impact of senescent cells with aging and age-related diseases.

Nathan LeBrasseur, PT, PhD, is a Professor and the Co-Chair of Research in the Department of Physical Medicine and Rehabilitation and has a joint appointment in the Department of Physiology and Biomedical Engineering at Mayo Clinic. Dr. LeBrasseur is the Director of the Robert and Arlene Kogod Center on Aging, the Co-Director of the Paul F. Glenn Center for Biology of Aging Research, and Scientific Director of the Office of Translation to Practice at Mayo Clinic. He is the current chair of the NIH Cellular Mechanisms in Aging and Development Study Section. Dr. LeBrasseur's research team conducts translational “bench-to-bedside” research on strategies to improve physical function, metabolism, and resilience in the face of aging and disease. Dr. LeBrasseur has received the Glenn Award for Research in Biological Mechanisms of Aging, the Nathan W. Shock Award Lecture from the National Institute on Aging, and the Vincent Cristofalo Rising Star Award in Aging Research from the American Federation for Aging Research. He is a Fellow of the Gerontological Society of America.