Translating the Science of Aging into Therapeutic Interventions
Open accessAbstract
Life and health span have been extended in experimental animals using drugs that are potentially translatable into humans. Considerable effort is needed beyond the usual steps in drug development to devise the models, and realistic preclinical and clinical trial strategies are required to advance these agents into clinical application. It will be important to focus on subjects who already have symptoms or are at imminent risk of developing disorders related to fundamental aging processes, to use short-term, clinically relevant outcomes, as opposed to long-term outcomes, such as health span or life span, and to validate endpoint measures so they are acceptable to regulatory agencies. Funding is a roadblock, as is shortage of investigators with combined expertise in the basic biology of aging, clinical geriatrics, and investigational new drug clinical trials. Strategies for developing a path from the bench to the bedside are reviewed for interventions that target fundamental aging mechanisms.
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The geroscience hypothesis predicts that targeting fundamental ageing mechanisms, such as cellular senescence, could have a large impact on increasing health span and decreasing chronic disease burden.
“The geroscience hypothesis leverages the fact that ageing is the major risk factor for most chronic diseases, including diabetes, and predicts that targeting fundamental ageing mechanisms, such as cellular senescence, could have a large impact on increasing health span and decreasing chronic disease burden.”
From Cellular senescence: at the nexus between ageing and diabetes (2019) · cites this paper as [6]
Primary aging processes include chronic low-grade non-microbial inflammation, cellular senescence, accumulation of damaged macromolecules, and stem/progenitor cell dysfunction.
“Cellular and molecular processes that account for primary aging include chronic, low-grade, non-microbial inflammation, cellular senescence (see Glossary), accumulation of damaged macromolecules (DNA, proteins, carbohydrates, lipids), as well as stem and progenitor cell dysfunction [1].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [1]
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References 123 · Cited by 78
- Authors
- Kirkland, J. L.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Kirkland, James L.
- ORCID
- Kirkland, James L.
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2016-03
- Volume
- 6
- Issue
- 3
- Pages
- a025908
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC4772076
- OpenAlex
- W2291642348
- Cited by
- 78
- References
- 123
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 10 · 2023: 7 · 2022: 8 · 2021: 5 · 2020: 17 · 2019: 6 · 2018: 2 · 2017: 8 · 2016: 2
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG13925)
- National Institute on Aging (R24AG044396, AG-41122, P01AG041122, AG 13925)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- aging, anti-aging drugs, drug development, preclinical models, clinical trials, healthspan, lifespan extension, clinical trial endpoints, regulatory validation, translational research, aging mechanisms, geriatrics, funding barriers
- MeSH terms
- Aging, Animals, Drug Evaluation, Preclinical, Humans, Biomarkers, Randomized Controlled Trials as Topic, Biomedical Research
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