Jan Van Deursen: How Clearing Clutter Can Boost Life Span?
Jan Van Deursen is not a researcher and famous scientist for humans only, but for animals as well. Being a universal researcher, Jan Van Deursen is the one who thoroughly examined and presented an idea to the table – clearing cellular clutter can boost the life span of mice. Jan Van Deursen further concludes that zombie drugs can kill COVID-19’s long-haul syndrome.
Alike this, many other studies have been carried by Jan Van Deursen. Let’s have a close look into his research of clearing cellular senescence to boost life span in mice.
How Removing Cellular Clutter Work in Boosting Mice’s Life Span?
When researchers eliminated a specific type of cell that builds up in the body with aging, mice had significantly better health and were expected to live a bit longer. Furthermore, the loss of the mice’s so-called “senescent cells” didn’t appear to negatively impact them.
Although it’s not always the case, these cells no longer divide simply because they are old. According to Jan van Deursen, who researches senescent cells at the Mayo Clinic College of Medicine in Rochester, Minnesota, “it’s a normal cell that underwent an unusual degree of stress and decided to stop dividing?”
These cells are much more prevalent in older organisms than in young ones. Even if the cells aren’t dividing, they are still active because they emit a combination of chemicals that can cause inflammation, contributing to almost all of the leading age-related diseases.
Jan Van Deursen and his associates so desired to know:
What would happen if senescent cells were just eliminated?
Although difficult for humans, it might be possible for mice when senescent cells were treated with a drug, the mice that the researchers genetically manipulated committed suicide. Some of the mice received the medication when they reached middle age.
The removal of senescent cells didn’t seem to have much impact. But as the mice grew older, the research team noticed that the medicated mice appeared in better physical shape.
Jan Van Deursen said: “when we started to record the animals’ life spans, we discovered that there was around a 25% extension in animals whose senescent cells were removed from 1 year of age on.”
In addition, the mice who received the treatment had a higher renal function, hearts that could withstand stress better, and fewer cataracts. The researchers wrote in the journal Nature on Wednesday that losing the cells didn’t appear to have any adverse effects.
Overall, “it seems like we’re amassing a cell type that we really don’t need for anything and that makes us unhealthier and shortens the length of our good lives,” says Jan Van Deursen.
Researchers are already looking for medications that could kill these cells in people. Of course, that won’t occur tomorrow, and good medications might never exist. However, the results in mice provide researchers with a fresh angle to consider.
Unity Biotechnology, a young business with some promising candidates in San Francisco, currently employs Jan Van Deursen. Additionally, Unity collaborates with Judith Campisi, a researcher on senescent cells at the independent Buck Institute for Research on Aging.
She considers the most recent study’s findings to be necessary. The remarkable thing, according to Campisi, is the mice not only lived longer but also were healthier.However, she warns that eliminating these cells won’t be a panacea for aging. She notes that:
“Even in the Nature publication, the mice got old and perished.”
Additionally, some study suggests that these cells might serve a purpose in our bodies. Senescent cells, for instance, have been shown to aid in the healing of wounds and offer cancer prevention benefits.
According to Dominic Withers, a researcher at the MRC Clinical Sciences Centre, Imperial College London, “One must proceed cautiously while attempting to purge senescent cells under the presumption that doing so will be entirely helpful.”
Jan Van Deursen claims that while it’s too early to decide what should be done with these cells, they appear to contribute to aging.
Withers states, “I believe that the time is still early.” There is still a lot to learn about whether you should try to eliminate senescent cells or take care of the ones already there, like preventing them from secreting this mix of possibly harmful compounds.
Jan Van’s Research on Mice Cellular Cells During His Tenure in Unity Technology
During his doctoral studies, Jan Van Deursen developed strategies to inhibit the production of endogenous genes in mice. These methods have shown to be particularly effective in revealing the physiological role of mammalian genes necessary for cell division or viability.
Jan Van Deursen discovered that BubR1, a crucial mitotic gatekeeper protein that maintains faithful chromosomal segregation, is causally associated with cancer, progeria, and aging while using these technologies to answer the age-old question of whether aneuploidy is a cause or a consequence of cancer.
The first in vivo proof that p16-positive senescent cells cause aging and age-related disease is credited to studies that grew out of his desire to comprehend these mechanisms. This establishes cellular senescence as a prospective target for therapeutic intervention.