The study found that the tiny gene that makes the peptide Humanin is still working in almost all humans, but in many other animals the gene has become broken, which could mess up how useful those animals are for testing Humanin‑related treatments.

In the human the peptide Humanin is produced from the small <i>Humanin</i> gene which is embedded as a gene-within-a-gene in the 16S ribosomal molecule of the mitochondrial DNA (mtDNA). The peptide itself appears to be significant in the prevention of cell death in many tissues and improve cognition in animal models. By using simple data mining techniques, it is possible to show that 99.4% of the human <i>Humanin</i> sequences in the GenBank database are unaffected by mutations. However, in other vertebrates, pseudogenization of the Humanin gene is a common feature; occurring apparently randomly in some species and not others. The persistence, or loss, of a functional <i>Humanin</i> gene may be an important factor in laboratory animals, especially if they are being used as animal models in studies of Alzheimer's disease (AD). The exact reason why <i>Humanin</i> underwent pseudogenization in some vertebrate species during their evolution remains to be determined. This study was originally planned to review the available information about <i>Humanin</i> and it was a surprise to be able to show that pseudogenization has occurred in a gene in the mtDNA and is not restricted solely to chromosomal genes.