By P. Tarok. University of Pittsburgh at Bradford. 2019.
Basic aging research is no The Geroscience Hypothesis: Is It Possible to Change the Rate of Aging? The longevity and disease prole of mouse strains a strain is the product of at least 20 generations of brother-sister inbreeding varies considerably  cheap dipyridamole 100 mg on line heart attack 1d. Some strains should be strenuously avoided for aging research because they are particularly prone to die early of a single spe- cic disease  dipyridamole 100 mg low cost heart attack ekg, meaning that studies of those strains are useful for investigating the disease process but not informative with respect to generalized aging processes. The presumed advantage of standardization, facilitating comparison of experimental results among laboratories and between studies, is purchased at the expense of gen- erality. One never knows if a result is an idiosyncrasy of a particular genetic back- ground or is a more general phenomenon. Like many laboratory strains, they exhibit defective melatonin synthesis due to mutations in both necessary biosynthetic enzymes . So over-reliance on any single mouse strain or sub-strain limits our ability to spot cryp- tic aberrancies affecting what is classied as a healthy state. One approach to the problem of cryptic strain idiosyncrasies that combines some generality with some genetic control is the use of genetically heterogeneous mice generated in a repeatable fashion. Originally created for gene mapping studies, this stock is created by interbreeding two F1 hybrids of inbred strains. The resultant F2 mice are each genetically unique full siblings representing a broad swathe of genetic diversity within the laboratory mouse. One reason that inbred mouse strains became so popular was the belief that they would be phenotypically more uniform that outbred populations. Over-reliance on a single genetic background is not a research phenomenon con- ned to mice or to aging research. However both mice and y researchers have discov- ered that genetic background makes a dramatic difference in the impact of longevity interventions. Austad in adult y motorneurons signicantly increased longevity in both males and females, by approximately 30 % and 40 %, respectively, in a particular laboratory strain. However the same mutation introduced into ten inbred, wild-caught strain found that females lived signicantly longer in only 6 of the 10 strains and male lived longer in only 1 of the 10 strains compared to controls [36 ].
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