Mouse Models of Accelerated Aging

Jan Vijg, Paul Hasty

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

This chapter discusses the validity of the aging phenotypes observed in the mouse models, with a focus on the possible implications with respect to DNA damage as a proximate cause of aging common to all mammals. Among biological macromolecules, the DNA of the genome is unique in view of its role in transferring genetic information from cell to cell and from generation to generation. A strong, logical argument to consider the DNA of the genome as the Achilles heel of an aging organism is the lack of a backup template. Aging differs from all human diseases by its complexity. It is the most complex phenotype currently known and the only example of generalized biological dysfunction. Its effects become manifest in all organs and tissues, it influences an organism's entire physiology, impacts function at all levels, and increases susceptibility to all major chronic diseases. One of the most prominent aging-related phenotypes occurring early in the mutants is lordokyphosis, the lateral curvature of the spine that is also present in the mutants.

Original languageEnglish (US)
Title of host publicationHandbook of Models for Human Aging
PublisherElsevier Inc.
Pages601-618
Number of pages18
ISBN (Print)9780123693914
DOIs
Publication statusPublished - Dec 1 2006
Externally publishedYes

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ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Vijg, J., & Hasty, P. (2006). Mouse Models of Accelerated Aging. In Handbook of Models for Human Aging (pp. 601-618). Elsevier Inc.. https://doi.org/10.1016/B978-012369391-4/50050-3