Scientists at the University College London have discovered a group of genes that builds components of our cells. These genes can potentially extend the human lifespan.
In a past study, the same set of genes extended lifespan in tiny organisms. They extend fruit flies’ lives 10% longer. For the first time, scientists demonstrated the effect of these genes on humans as well.
Co-lead author Dr. Nazif Alic (UCL Institute of Healthy Ageing) said: “We have already seen from extensive previous research that inhibiting specific genes involved in making proteins in our cells can extend lifespan in model organisms such as yeast, worms, and flies. However, in humans, loss of function in these genes has been seen to cause diseases, such as developmental disorders known as ribosomopathies.”
“Here, we have found that inhibiting these genes may also increase longevity in people, perhaps because they are most useful early in life before causing problems in late life.”
The genes are involved in the synthetic protein machinery of our cells. This machinery is essential for our life. But, according to scientists, we do not need as much of its effect late in life.
The genes are an example of antagonistic pleiotropy, where genes that shorten our lives are selected for evolution if they help us early in life and through our child-bearing years.
For the study, scientists reviewed data from previous studies, which involved more than 11k patients who lived an exceptionally long life. They found that people with reduced activity of specific genes tend to live longer.
The genes are linked to two RNA polymerase enzymes (Pols) that transcribe ribosomal and transfer RNAs, namely Pol I and Pol III, and the expression of ribosomal protein genes.
More specifically, scientists found that the genes’ effects were linked to their expression in specific organs, including abdominal fat, liver, and skeletal muscle. The impact of longevity went beyond just associations with any specific age-related diseases.
Professor Karoline Kuchenbaecker (UCL Genetics Institute) said: “Ageing research in model organisms, such as flies, and humans are often separate efforts. Here we are trying to change this. In flies, we can experimentally manipulate aging genes and investigate mechanisms. But ultimately, we want to understand how aging works in humans. Bringing the two fields together using methods such as Mendelian Randomisation has the potential to overcome the limitations of both fields.”
Journal Reference:
- Sara Javidnia et al. Mendelian randomization analyses implicate biogenesis of translation machinery in human aging. DOI: 10.1101/gr.275636.121