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Review
. 2000 Mar;55(3):B117-23.
doi: 10.1093/gerona/55.3.b117.

Principles of animal use for gerontological research

R A Miller  1 , N L Nadon
Affiliations
Review

Principles of animal use for gerontological research

R A Miller et al. J Gerontol A Biol Sci Med Sci. 2000 Mar.

Abstract

This essay presents some practical advice and suggestions for those who wish to use mice and rats in experiments on the biology of aging. Ten principles set forth guidance on choice of ages, choice of stocks, the importance of specific pathogen-free status, the uses of necropsy data, the dangers of pooling samples from different individuals, planning ahead for loss of aged mice to death and disease, the use of cost-adjusted power calculations, and the dangers of inferring causal associations from correlated age effects.

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Figures

Figure 1.
Figure 1.
Some reasons to include middle-aged animals in a survey experiment. Panel A shows the hypothetical results of a study looking at three interleukins in the blood of young and old rats. The authors conclude that all three interleukins decline in parallel with aging—perhaps they share some common control mechanism on which one could base a Program Project application? Panel B shows a more comprehensive survey of the same topic conducted at another laboratory: IL-X drops early in adult life (a maturational effect), IL-Y shows a progressive decline through the life span, and IL-Z drops only when the animals get ill in very old age. Panel C shows three hypothetical reports of age effects on Ig-X levels in serum. Lab 1 says there's no change; Lab 2 says the levels go down; Lab 3 says the levels go up. Panel D shows the real hypothetical data set from which each lab drew its misleading conclusion: use of a wider and higher resolution set of age groups would have avoided much embarrassment and needless confusion.
Figure 2.
Figure 2.
Misleading inferences from age-confounded correlations. This hypothetical data set represents an attempt to test the idea that the low levels of IL-2 production seen in old mice contribute to poor antibody production in these mice. Unsophisticated investigators might conclude, from the left panel, that there is indeed a strong correlation between IL-2 production (already known to decline with age) and antibody production, and thus claim that their hypothesis is supported. The right panel, showing old and young individuals separately, reveals the fallacy: the correlation results from the high age-sensitivity of both measured traits. Any two traits strongly influenced by aging would generate a similar correlation, even if neither trait had any direct mechanistic relation to the other.
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