Comparison of mice with accelerated aging caused by distinct mechanisms

Aditi U. Gurkar, Laura J. Niedernhofer

Research output: Contribution to journalReview articlepeer-review

42 Scopus citations


Aging is the primary risk factor for numerous chronic, debilitating diseases. These diseases impact quality of life of the elderly and consume a large portion of health care costs. The cost of age-related diseases will only increase as the world's population continues to live longer. Thus it would be advantageous to consider aging itself as a therapeutic target, potentially stemming multiple age-related diseases simultaneously. While logical, this is extremely challenging as the molecular mechanisms that drive aging are still unknown. Furthermore, clinical trials to treat aging are impractical. Even in preclinical models, testing interventions to extend healthspan in old age are lengthy and therefore costly. One approach to expedite aging studies is to take advantage of mouse strains that are engineered to age rapidly. These strains are genetically and phenotypically quite diverse. This review aims to offer a comparison of several of these strains to highlight their relative strengths and weaknesses as models of mammalian and more specifically human aging. Additionally, careful identification of commonalities among the strains may lead to the identification of fundamental pathways of aging.

Original languageEnglish (US)
Pages (from-to)43-50
Number of pages8
JournalExperimental Gerontology
StatePublished - Aug 1 2015
Externally publishedYes

Bibliographical note

Funding Information:
A.U.G. is supported by NIH/NIA K99 AG049126 . L.J.N. is supported by NIH/NIA P01 AG043376 . In addition, the Niedernhofer lab is supported in part by a sponsored research agreement between the Scripps Research Institute and Aldabra Biosciences LLC, of which she is a co-founder. We acknowledge the contribution of Dr. Amanda Beck, D.V.M., D.A.C.V.P., to early drafts of this manuscript.

Publisher Copyright:
© 2015 Elsevier Inc.


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