Review compares six mouse model categories for aging research
This review compares six broad categories of laboratory mouse aging models, noting that no single model fully captures organismal aging and that model choice should match the aging mechanism and research aim. [1]
Automatic summary · not editorially reviewed
The key findings
The review states that no single mouse model fully recapitulates the complexity of organismal aging. [1]
Natural aging models such as C57BL/6, BALB/c, FVB/N and SAMP8 mice are said to most closely recapitulate physiological aging. [1]
The authors present these models as a toolkit for aging research and as platforms for anti-aging drug development. [1]
The source at a glance
- Study type / format
- Review abstract
- Population / context
- Laboratory mouse models of aging described in a review
- Summary based on
- Study abstract
- Original publication
- September 28, 2026
Why mice and why model choice matters
The review describes aging as a complex biological process with progressive decline of physiological and cognitive function, greater vulnerability to disease and eventual mortality. Laboratory mice have been used in aging research because of their genetic tractability, short lifespan and physiological similarities to humans. The authors state that no single mouse model fully recapitulates the complexity of organismal aging, and that individual models differ substantially in the biological processes, aging hallmarks and translational relevance they represent. Selecting a model therefore requires careful consideration of the specific aging mechanisms and research objectives.
Supporting source [1]
Six model categories and their reported uses
The review gives a comparative overview of six broad categories. Natural aging models such as C57BL/6, BALB/c, FVB/N and SAMP8 mice are said to most closely recapitulate physiological aging. Accelerated models such as Klotho⁻/⁻, Ercc1⁻/Δ and Lmna are described as offering mechanistic insights into genetic pathways of senescence. Chemically induced models using D-galactose and paraquat are presented as rapid, cost-effective ways to mimic oxidative stress-related aging phenotypes. Telomere and senescence models such as Terc⁻/⁻, p16-reporter and INK-ATTAC mice allow visualization and direct manipulation of cellular senescence. Metabolic and mitochondrial models (Polg mutant and Sod mice) link mitochondrial DNA instability and oxidative stress to conditions associated with aging, including sarcopenia, presbycusis, anemia and reduced fertility. Dietary and environmental models cover high fat diets, irradiation, dietary restriction and chronic stress exposure.
Supporting source [1]
Toolkit framing and abstract-only scope
The authors describe these models together as a versatile toolkit for investigating cellular, organismal and systemic aspects of aging, and as platforms for anti-aging drug development. This is a review abstract; the full text was not reviewed here. The abstract does not report sample sizes, follow-up periods, outcome measures or effect estimates for any model, and it does not present new experimental results. Statements about translational relevance and drug development are the authors' framing, not demonstrated human lifespan benefits.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract reports no sample sizes, follow-up, outcome measures or effect estimates, and presents no new experimental data. Statements on translational relevance and drug development are the authors' framing, not demonstrated human benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Coleman C, Thomas H, Qiu S, Murphy EA, Fan D. · europepmc.org · September 28, 2026