Warner came to this conclusion after analyzing human case of Hutchinson's Gilford syndrome and mouse models of accelerated aging.
According to their findings, it is possible to track male GSCs labeled with lacZ gene in Drosophila model by inducing recombination with heat shock and observe the decrease in GSC number with aging.
In order to mark GSCs with lacZ gene, flip recombinase (Flp)-mediated recombination is used to combine a ubiquitously active tubulin promoter followed by an FRT (flip recombinase target) site with a promotorless lacZ ORF (open reading frame) preceded by an FRT site.
Heat shock is used to induce Flp recombinase marker gene expression is activated in dividing cells due to recombination.
Findings of the study indicate that diabetes leads to premature myocyte senescence and death and together they result in the development of cardiomyopathy due to decreased muscle mass.
[9] DNA ligase 4 (Lig4) has a highly specific role in the repair of double-strand breaks by non-homologous end joining (NHEJ).
Also, some diseases related to hematopoietic system, such as aplastic anemia and complete bone marrow failure, are not especially age-dependent.
Aplastic Anemia is often an adverse effect of certain medications [17] but as such it cannot really be considered as evidence against the stem cell theory of aging.
[18] A dog study published by Zaucha J.M, Yu C. and Mathioudakis G., et al. also shows evidence against the stem cell theory.
Experimental comparison of the engraftment properties of young and old marrow in a mammal model, the dog, failed to show any decrement in stem cell function with age.
The system theories include the immunologic approach to ageing, rate-of-living and the alterations in neuroendocrinal control mechanisms.