A group of scientists from the University of New South Wales has found something that could allow the creation of an “anti-aging” pill. The objective of the investigation is to discover how it could be possible to repair damaged DNA.
The DNA repair is one essential factor when it comes to cell survival and vitality. It’s also a key mechanism that avoids the development of cancer diseases in humans. This ability of cells to repair damaged genetic material usually declines as a person gets older, and scientists have not been able to identify the reason.
Now, the study published this week shows a never seen step in the damaged DNA reparation process, and it could explain how cells mend those damages. This publication consists on a critical insight of why the body is less efficient in repairing cells over time, as well as it includes the influence of the NAD molecule.
This NAD molecule is crucial for understanding the protein-to-protein regulation that takes place at the moment of the DNA repair natural procedure. This molecule is present in every cell of our body, and also declines in its capability as time passes by.
The team of investigators from both Wales and Harvard Medical School conducted a series of experiments on mice to determine if treatment was possible in humans.
The results showed that experts are capable of developing a treatment that avoids aging from becoming a factor in the DNA repair, as well as it wards off the cells from radiation exposure. This last feature was so impressive that even NASA showed its interest to the investigation as they think it could help to future manned missions to the planet Mars.
However, the research team warned that the effects of several therapies vary from mice to humans, for biological reasons exclusively. Many substances could be positive for mice but extremely dangerous for people.
Even though, if the researchers can prove that the experimentation on mice could function similarly in humans, it could open a whole field of new treatments oriented to the “anti-aging” of the cells and the protection of radiation exposure often provided by chemotherapy sessions in patients with cancer diseases.
The investigators stated that the experimentation in humans would begin in the next six months, as they explained how vital it is to make this process as fast as possible and to start developing potential therapeutic substances and treatments.
“Our results unveil a key mechanism in cellular degeneration and aging, but beyond that they point to a therapeutic avenue to halt and reverse age-related and radiation-induced DNA damage,” said senior author David Sinclair, professor in the Department of Genetics at HMS and professor at the University of New South Wales School of Medicine in Sydney.
Exhaustive investigation, difficult conclusions
The research team took the task to analyze different proteins involved in the DNA repair process to identify which ones were more crucial. In the study, scientists say that they know well some of these proteins, while others turned out to be enigmatic cases.
The investigation team was aware that the NAD molecule declines as the person gets older. They also knew that when it starts working organically, it boosts another molecule called the SIRT1. This protein is known for delaying the aging path of many organisms like mice, flies, and yeast. Every time the SIRT1 and the PARP1 proteins are activated, it uses NAD to function.
Another finding of the research group was the possible relation between another protein called DBC1 and the before mentioned SIRT1 and PARP1. The allegation was based on the possibility for both SIRT1 and PARP1 to have a similar function, as they also interact with the DBC1 protein.
“We thought if there is a connection between SIRT1 and DBC1, on one hand, and between SIRT1 and PARP1 on the other, then maybe PARP1 and DBC1 were also engaged in some sort of intracellular game,” said Jun Li, first author on the study and a research fellow in the Department of Genetics at HMS.
The investigators discovered that if there is plenty of presence of the NAD molecule, there are fewer chances of the body not being able of repairing damaged DNA. This is because NAD presence diminishes at older ages, and this lack of presence produces a connection between the PARP1 and the DBC1 proteins, which does not allow the PARP1 repair molecule to do its job.
Even when this is only the first step of actually developing a drug that could avoid the aging of the cells, the fact that the genetic investigation team is aware of what causes that situation makes everything easier for scientists at the time of creating new treatments and therapies.