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Accelerated Aging: Animal Models - Experimentally Induced Models, Gene-modified Models, Selection Models, Spontaneous Models

genetic diseases normal pathologies senescence

Animal models have been used to study accelerated aging, accelerated senescence, premature aging, premature senescence, and progeria-like syndromes. These models may be grouped into four classes: (1) experimentally induced models, (2) gene-modified models, (3) selection models, and (4) spontaneous models. There has been much debate over the connection between accelerated aging and disease status in animal models. Investigators interested in the basic mechanisms of normal aging have had to be prudent in their choice of animal models because early diseases leading to reduced life spans usually result from certain defects unrelated to mechanisms associated with normal aging, as suggested by David E. Harrison. In actuality, however, it is fairly difficult to discriminate between accelerated aging due to acceleration of the normal aging process and that due to the manifestation of diseases or pathologies. Thus, it might be important to check the pathologies or diseases an animal model manifests throughout its lifetime. In this context, species such as the nematode and fruit fly have disadvantages, in spite of their usefulness for genetic studies, because of a scarcity of information on diseases and pathologies.

Accelerated Aging: Human Progeroid Syndromes - Progeroid Syndromes As Models Of Aging, Down Syndrome, Adult Progeria (werner Syndrome), Progeria (hutchinson-gilford Syndrome) [next] [back] Outline of Contents

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over 5 years ago

ACCELERATED AGING: ANIMAL MODELS http://whatisencyclopedia.com/encyclopedia-of-aging/accelerated-aging-animal-models/

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almost 10 years ago

This entry betrays an entirely inappropriate bias against nonmammalian models of aging!
Largely it sins by omission, saying nothing of the huge contributions of these systems to gerontological knowledge, e.g., the clear association of insulin-like signaling to life extension discovered first in worms, but subsequently confirmed in flies, yeast and mice. Care to wager about its eventual importance to clinical geriatrics?
What does the article include? After two general and uninformative sentences, it embarks on a diatribe about accelerated aging! Trust me, we who do work with animal systems are fully aware of limitations of studies based on phenomena of accelerated aging, and we don't do those studies. What we do study are mechanisms underlying verifiable extensions of life spans of wild type animals that themselves are the longest lived 'normal' varieties available, e.g. in the worm, the 'DRM' isolate of the N2 normal (wild-type) strain. No one believes that DRM is hampered by a disease that invalidates it as an aging model, and those who actually DO the experiments observe quite different morphologies in worms upon their death, just as David Harrison would want to see in a mouse aging study in the C57Bl/6 strain. This is a specious argument, arguably not worthy of comment, certainly not worthy of 80% of your encyclopedia entry!

That author bias should either be made overt, or edited out, and the article should be given some balance!

John Thaden
Research Assistant Professor of Geriatrics
University of Arkansas for Medical Sciences
Little Rock AR, USA.

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almost 4 years ago

difference in antibody response to sheep red-blood cells, which was reached after fifteen successive generations of selective breeding. The life span of the H line and L line is 612 days and 346 days, respectively. Interpopulation correlation between life span…

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over 4 years ago

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over 4 years ago

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