Comparison of mice with accelerated aging caused by distinct mechanisms

• Published in: Experimental gerontology 2015-08, Vol.68, p.43-50
• Main Authors: Gurkar, Aditi U., Niedernhofer, Laura J.
• Format: Article
• Language: English
• Subjects: Aging, Premature - etiology; Animals; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Cell Cycle Proteins - physiology; Disease Models, Animal; DNA Damage - physiology; DNA Repair - physiology; DNA, Mitochondrial - physiology; DNA-Binding Proteins - deficiency; DNA-Binding Proteins - physiology; Endonucleases - deficiency; Endonucleases - physiology; Heterozygote; Humans; Mice; Mitochondria - genetics; Mitochondria - metabolism; Mutation - genetics; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Protein-Serine-Threonine Kinases - physiology; Reactive Oxygen Species - metabolism
• ISSN: 0531-5565; 1873-6815
• DOI: 10.1016/j.exger.2015.01.045

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. •Mouse models of progeroid syndromes can be exploited to accelerate aging research.•The majority of diseases with accelerated aging are linked to genomic instability.•Mice with very diverse causes of genomic instability have similar aging features.•No one progeria model mimics all aspects of mammalian aging.