The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Moving geroscience from the bench to clinical care and health policy
Abstract
Geriatricians and others must embrace the emerging field of geroscience. Until recently geroscience research was pursued in laboratory animals, but now this field requires specialized expertise in the care of vulnerable older patients with multiple chronic diseases and geriatric syndromes, the population likely to benefit the most from emerging therapies. While chronological aging measures the inevitable passage of clock time that occurs equally for everyone, biological aging varies among individuals, and importantly, it is modifiable. Advances in our understanding of biological aging, the discovery of strategies for modifying its rate, and an appreciation of aging as a shared risk factor for chronic diseases have jointly led to the Geroscience Hypothesis. This hypothesis states that interventions modifying aging biology can slow its progression—resulting in the delay or prevention of the onset of multiple diseases and disorders. Here we wish to report on the Third Geroscience Summit held at National Institutes of Health on November 4–5, 2019, which highlighted the importance of engaging other disciplines including clinicians. Involvement by scientists with expertise in clinical trials, health outcomes research, behavioral and social sciences, health policy, and economics is urgently needed to translate geroscience discoveries from the bench to clinical care and health policy. Adding to the urgency of broadening this geroscience coalition is the emergence of biological aging as one the most important modifiable factors of COVID‐19, combined with the inability of our society to once again recognize and confront aging as a priority and opportunity when facing these types of public health emergencies.
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A barrier to advancing translation of therapies through human trials is that intervention studies run for months or years, but human aging takes decades to cause disease.
“A barrier to advancing translation of these therapies through human trials is that intervention studies run for months or years, but human aging takes decades to cause disease46–48.”
From Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial (2023) · cites this paper as [47]
The section on behavioral and social science perspectives in geroscience says disease diagnosis or death may be too distant to serve as trial endpoints and that waiting many years to judge a therapy is unreasonable. This supports the claimed barrier, but our copy does not specify that intervention studies run for months or years or that aging takes decades to cause disease. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe PhenoAge and GrimAge clocks were developed to predict mortality risk at a single timepoint in mixed-age and older adults.
“The PhenoAge and GrimAge clocks were developed to predict mortality risk at a single timepoint in mixed-age and older adults.”
From Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial (2023) · cites this paper as [47]
The section on behavioral and social science perspectives discusses measuring the pace of biological aging, and the References name the DunedinPoAm DNA-methylation algorithm. Searches for PhenoAge, GrimAge, and mortality-predicting epigenetic clocks found no passage in our copy addressing how those two clocks were developed or the populations used. (LLM, conf=0.75)
Experimental — accuracy not yet measuredThe GrimAge clock was based on analysis of eight plasma protein markers, smoking pack years, age, sex and mortality data from the Framingham Heart Study Offspring and Gen3 Cohorts.
“The GrimAge clock was based on analysis of eight plasma protein markers, smoking pack years, age, sex and mortality data from the Framingham Heart Study Offspring and Gen3 Cohorts (n = 2,751 participants aged 24–92 yr)47–49.”
From Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial (2023) · cites this paper as [47]
The section on behavioral and social science perspectives discusses measuring biological aging but does not describe how GrimAge was developed. Searches for GrimAge, plasma protein markers, smoking pack years, and the Framingham cohorts found no passage in our copy addressing the claim, including its participant count or age range. (LLM, conf=0.73)
Experimental — accuracy not yet measured
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Citations
Cites
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BackgroundGeroscience: Linking Aging to Chronic Disease
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Self-citationmTOR is a key modulator of ageing and age-related disease
Johnson, S. C., Rabinovitch, P. S., & Kaeberlein, M. (2013) · Nature · doi:10.1038/nature11861 · Cited by 1,676 · cited 1×
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BackgroundDevelopment of clinical trials to extend healthy lifespan
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Self-citation
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Cited by
Sorted by citations
Waziry, R., Ryan, C. P., Corcoran, D. L., Huffman, K. M., Kobor, M. S., Kothari, M., Graf, G. H., Kraus, V. B., Kraus, W. E., Lin, D. T. S., et al. (2023) · Nature Aging · doi:10.1038/s43587-022-00357-y · Cited by 217
The New Frontier of Ageing: Innovations and Insights in Gerontology
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Metadata
- Authors
- Sierra, F., Caspi, A., Fortinsky, R. H., Haynes, L., Lithgow, G. J., Moffitt, T. E., Olshansky, S. J., Perry, D., Verdin, E., & Kuchel, G. A.
- Venue
- Journal of the American Geriatrics Society
- Publisher
- Wiley
- Published
- 2021-06-19
- Volume
- 69
- Issue
- 9
- Pages
- 2455-2463
- ISSN
- 0002-8614
- 1532-5415
- PMC
- PMC10202082
- Cited by
- 92
- References
- 7
- Language
- en
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