TY - CHAP
T1 - Mouse Models of Accelerated Aging
AU - Vijg, Jan
AU - Hasty, Paul
N1 - Funding Information:
The authors are grateful for support from NIH grants AG 17242, AG20438, ES11044 (JV), and R01 CA76317–05A1 (PH). We thank Drs. Yousin Suh, Judith Campisi, Jan Hoeijmakers, and Harry van Steeg for stimulating discussions, and John David Garza for creating Figure 49.5 and for his help with the manuscript.
Publisher Copyright:
© 2006 Elsevier Inc. All rights reserved.
PY - 2006/1/1
Y1 - 2006/1/1
N2 - 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.
AB - 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.
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U2 - 10.1016/B978-012369391-4/50050-3
DO - 10.1016/B978-012369391-4/50050-3
M3 - Chapter
AN - SCOPUS:84882814675
SP - 601
EP - 618
BT - Handbook of Models for Human Aging
PB - Elsevier
ER -
