‘Accelerated aging’: a primrose path to insight?
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Summary: Organism envy afflicts most researchers who work on aging in mice; how frustrating it is to see the worm and fly biologists nail down milestone after milestone, citation after citation! Surely genetic trickery can produce mice that age in a comparable jiffy? Alas, our near‐total ignorance of what times the aging process makes it hard to guess what genes to tweak, if indeed aging can be mimicked a presto. Building a case that a given short‐lived mutant ages quickly is a steep and thorny path, requiring more than just plucking a symptom here and there from a list of things that sometimes go wrong in old people or old mice. The hallmark of aging is that a lot goes wrong more or less at the same time, in 2‐year‐old mice, 10‐year‐old dogs and 70‐year‐old people. Finding ways to damage one or two systems in a 6‐week or 6‐month‐old mouse is not too hard to do, but the implications of such studies for improved understanding of aging per se are at best indirect and at worst imaginary and distracting.
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Premature aging models fail to recapitulate all aspects of aging but are instead "segmental progerias".
“A related difficulty is that premature aging models fail to recapitulate all aspects of aging but are instead “segmental progerias” (Hasty and Vijg, 2004; Miller, 2004”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Miller, 2004
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Lamming, D. W., & Salmon, A. B. (2019) · The Journals of Gerontology Series A · doi:10.1093/gerona/glz212 · Cited by 6 · see citing works
“Lastly, while it is still unclear how relevant genetic mouse models of “accelerated aging” are to “normal” aging (28,29), progeroid mouse models are clearly appropriate as models of specific age-related diseases.”
BackgroundWerner Syndrome as a Model of Human Aging
Monnat, R. J. (2006) · Elsevier eBooks · doi:10.1016/b978-012369391-4/50081-3 · Cited by 6 · see citing works
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Tail Tendon Break Time: A Biomarker of Aging?
Sloane, L. B., Stout, J. T., Austad, S. N., & McClearn, G. E. (2010) · The Journals of Gerontology Series A · doi:10.1093/gerona/glq196 · Cited by 5 · see citing works
“It is worth noting that the rationale for viewing animal models with shortened life span with some suspicion is that life span can be shortened in many ways that have little or nothing to do with fundamental aging processes (47,48).”
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Genes, rates of aging, and duration of human life
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2006 Kent Award Lecture: Is Cell Death and Replacement a Factor in Aging?
Warner, H. R. (2007) · The Journals of Gerontology Series A · doi:10.1093/gerona/62.11.1228 · Cited by 5 · see citing works
“Increasing life span has become the well-accepted standard for showing that any gene and its protein product play a role in longevity regulation ( 11 ).”
BackgroundWerner Syndrome as a Model of Human Aging
Oshima, J., Hisama, F. M., & Monnat, R. J. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811353-0.00001-4 · Cited by 4 · see citing works
Aging, p53 and the ‘24 gene mutant’: getting it right A reply to Vijg and Hasty
Venkatachalam, S. (2005) · Aging Cell · doi:10.1111/j.1474-9726.2005.00182.x · Cited by 3 · see citing works
“…is time the scientific community takes a cautionary note about the wholesale categorization of such mutants as ‘aging’ models (Lombard et al. , 2005; Miller, 2004). p53 may not be the sole contributor of the p53 +/m phenotypes: bending the rules of genetics In the final part of the discourse,…”
Backgroundp53, longevity assurance and longevity suppression
Donehower, L. A. (2006) · Drug Discovery Today Disease Mechanisms · doi:10.1016/j.ddmec.2006.02.001 · Cited by 3 · see citing works
Research on Hutchinson-Gilford Progeria Syndrome
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“This syndrome was first described over 120 years ago by Hutchinson (2), and although the phenotype does include some aging-like changes, biogerontologists have questioned whether it is a viable model for studying accelerated aging (3).”
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Nuclear Architecture and Disease
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“However, identification of the defective gene is only a first step, and even though this has not yet led to general acceptance of HGPS as an example of premature aging ( 5 ), with the help of NIH funding Dr. Gordon has developed a clinical and research database to facilitate research on HGPS in the future.”
Cardiac Metabolism and Energetic Control
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“This controversy, which has recently flared again in relation to the use and applicability of mutant mouse strains in aging research [18-21], is based on two opposing theories of aging.”
BackgroundApoptosis in Cardiovascular Pathogenesis
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“The variety of phenotypes observed in Hq mice resembles those in experimental models with premature-aging syndromes: increased oxidative stress, accelerated progression to heart failure in response to stress, neurodegenerative changes, kyphosis, age-related skin changes, growth retardation, and short life span ( 66 ).”
BackgroundDoes Oxidative Stress Limit Mouse Life Span?
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LONGEVITY REGULATION AND AGING IN ANIMAL MODELS
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A data mining-based approach for investigating the relationship between DNA repair genes and ageing
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Genes, Aging, and Parkinson’s Disease
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van de Ven, M., Andressoo, J., Holcomb, V. B., Lindern, M. V., Jong, W. M. C., Zeeuw, C. I. D., Suh, Y., Hasty, P., Hoeijmakers, J. H. J., van der Horst, G. T. J., et al. (2008) · PLoS Genetics · doi:10.1371/annotation/31502636-9bdf-4cb1-b995-4a30a607e316
- Authors
- Miller, R. A.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Miller, Richard A.
- ORCID
- Miller, Richard A.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2004-03-22
- Volume
- 3
- Issue
- 2
- Pages
- 47-51
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- OpenAlex
- W2021587119
- Cited by
- 87
- References
- 25
- Citations by year
- 2023: 2 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 9 · 2015: 3 · 2014: 1 · 2013: 4 · 2012: 3
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG013711, AG13711)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Social Sciences › Psychology › Neuropsychology and Physiological Psychology › Aging and Gerontology Research
- Keywords
- accelerated aging, mouse models of aging
- MeSH terms
- Aged, Animals, Humans, Life Style, Longevity, Aging, Premature, Models, Animal, Mice
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