Research suggests that it may be possible to eliminate the correlation between age and diseases.
ISB is working to leverage systems biology approaches to understand the mechanistic links among the processes that accompany and/or lead to aging.
“Aging isn’t inevitable, but it is the key to slowing all diseases.”
– ISB Co-founder Dr. Lee Hood
Humans have grown accustomed to the hallmarks of aging: increased mortality, decreased fitness, loss of function, damage accumulation, and the general process of becoming old. The incidence rates of heart disease, cancer, Alzheimer’s and nearly every other chronic disease increase sharply as we age.
However, controlling aging is surprisingly less complex when compared to most biological processes, and researchers have uncovered a few key regulators that control the hallmarks of aging.
WHAT ISB IS DOING
ISB researchers have learned to harness deep molecular and physiological information to determine a person’s biological age. Unlike your chronological age (the number of birthdays you’ve celebrated), researchers have found that biological age can serve as an effective and reliable predictor of overall health, and they are getting to the root of aging and determining ways to slow its progression. We do this by working to understand how aging processes, the immune system, the gut microbiome, and other systems affect our ability to modify aging.
We are exploring the use of longitudinal multi-omics to translate discoveries from model organisms to human clinical trials and mitigate varied responses to different anti-aging interventions.
ISB is a core member of the National Institute on Aging’s (NIA) Longevity Consortium. NIA was set up by the National Institutes of Health to lead a broad scientific effort to understand the nature of aging and to extend the healthy, active years of life. NIA is also the primary federal agency supporting and conducting Alzheimer’s disease research.
Our aging research is built on the foundation of P4 medicine. P4 is predictive, preventive, personalized and participatory, and its two major objectives are quantifying wellness and demystifying disease by identifying transitions into disease before they even occur. This approach is the clinical face of systems medicine, provides new approaches to drug target discovery, and will continue to drive profound economic, policy and social changes.
WATCH A CONVERSATION WITH DRS. LEE HOOD AND DAVID SINCLAIR
- Wilmanski, T., Diener, C., Rappaport, N. et al. Gut microbiome pattern reflects healthy ageing and predicts survival in humans. Nat Metab 3, 274–286 (2021). https://doi.org/10.1038/s42255-021-00348-0
- Baloni, Priyanka, Cory C. Funk, Jingwen Yan, James T. Yurkovich, Alexandra Kueider-Paisley, Kwangsik Nho, Almut Heinken, et al. 2020. “Metabolic Network Analysis Reveals Altered Bile Acid Synthesis and Metabolism in Alzheimer’s Disease.” Cell Reports Medicine 1 (8). https://doi.org/10.1016/j.xcrm.2020.100138.
- Wainberg, Michael, Andrew T. Magis, John C. Earls, Jennifer C. Lovejoy, Nasa Sinnott-Armstrong, Gilbert S. Omenn, Leroy Hood, and Nathan D. Price. 2020. “Multiomic Blood Correlates of Genetic Risk Identify Presymptomatic Disease Alterations.” Proceedings of the National Academy of Sciences of the United States of America 117 (35): 21813–20. https://doi.org/10.1073/pnas.2001429117.
- Earls, John C., Noa Rappaport, Laura Heath, Tomasz Wilmanski, Andrew T. Magis, Nicholas J. Schork, Gilbert S. Omenn, Jennifer Lovejoy, Leroy Hood, and Nathan D. Price. 2019. “Multi-Omic Biological Age Estimation and Its Correlation With Wellness and Disease Phenotypes: A Longitudinal Study of 3,558 Individuals.” The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences 74 (Supplement_1): S52–60. https://doi.org/10.1093/gerona/glz220.
- Wilmanski, Tomasz, Noa Rappaport, John C. Earls, Andrew T. Magis, Ohad Manor, Jennifer Lovejoy, Gilbert S. Omenn, Leroy Hood, Sean M. Gibbons, and Nathan D. Price. 2019. “Blood Metabolome Predicts Gut Microbiome α-Diversity in Humans.” Nature Biotechnology. https://doi.org/10.1038/s41587-019-0233-9.
HOW YOU CAN HELP
We aim to harness the findings from our aging research to decrease the incidence rates of nearly every chronic disease, but we need your support.
For more information, please contact:
Renee Duprel | 206.732.1287 | email@example.com