Abstract
Understanding the molecular basis of the aging process is a daunting problem, given the complex genetic and physiological changes that underlie human aging and the lack of genetically amenable primate model systems. However, analysis of mouse models exhibiting aging phenotypes reminiscent of those observed in elderly humans has enhanced our understanding of the biological mechanisms underlying mammalian aging. In particular, these mouse models have brought to light the importance of the DNA damage pathway during the aging process. Increased genomic instability is associated with accelerated cellular decline and manifestation of premature aging phenotypes in mice. Here I discuss how one form of genomic instability, initiated by critically short telomeres in the telomerase knockout mouse, perturb normal mammalian aging. Insights into the molecular pathways of the aging process may offer unprecedented opportunities to delay the deleterious effects of the aging process.
Keywords: double strand breaks (dsbs), dna-damage, hematopoietic system, chromosomal variants, metaphases, cytogenetically, dyskeratosis, phenotypes, mammalian aging, werner syndrome (ws)
Current Molecular Medicine
Title: Modeling Premature Aging Syndromes with the Telomerase Knockout Mouse
Volume: 5 Issue: 2
Author(s): Sandy Chang
Affiliation:
Keywords: double strand breaks (dsbs), dna-damage, hematopoietic system, chromosomal variants, metaphases, cytogenetically, dyskeratosis, phenotypes, mammalian aging, werner syndrome (ws)
Abstract: Understanding the molecular basis of the aging process is a daunting problem, given the complex genetic and physiological changes that underlie human aging and the lack of genetically amenable primate model systems. However, analysis of mouse models exhibiting aging phenotypes reminiscent of those observed in elderly humans has enhanced our understanding of the biological mechanisms underlying mammalian aging. In particular, these mouse models have brought to light the importance of the DNA damage pathway during the aging process. Increased genomic instability is associated with accelerated cellular decline and manifestation of premature aging phenotypes in mice. Here I discuss how one form of genomic instability, initiated by critically short telomeres in the telomerase knockout mouse, perturb normal mammalian aging. Insights into the molecular pathways of the aging process may offer unprecedented opportunities to delay the deleterious effects of the aging process.
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Cite this article as:
Chang Sandy, Modeling Premature Aging Syndromes with the Telomerase Knockout Mouse, Current Molecular Medicine 2005; 5 (2) . https://dx.doi.org/10.2174/1566524053586662
DOI https://dx.doi.org/10.2174/1566524053586662 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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