A study in C. elegans worms found that a type of small RNA molecule is essential for slowing the rate of aging and prolonging the lives of animals with a damaged reproductive system
The physiological function of most living things decreases with time, as part of the aging process. Over time, the body's cells and proteins are exposed to more damage and thus age-related diseases develop (especially neurodegenerative - which cause the death of nerve cells - such as Alzheimer's and Parkinson's), and the quality of life is impaired. Many researchers are trying to find ways to slow down the rate of aging to reduce or delay these diseases.
Prof. Sion Hannis-Kornblit from the Laboratory of Molecular Genetics for the Study of Aging and Age-Dependent Diseases at Bar Ilan University studies genes and processes that regulate the rate of aging. She believes that the main factor that causes age-related diseases, especially neurodegenerative ones, is the loss of the ability of proteins to fold correctly (proteins are made up of chains of hundreds of amino acids, and in order for these chains to function they need to fold into a three-dimensional structure). According to her, "If we understand the change that occurs with age and affects the folding of proteins, we may be able to delay many age-related diseases, slow down aging, and gain a life expectancy that is not only longer but also healthier."
Prof. Hannis-Kornblit and her team use in their research the roundworm (nematode) C. elegansC. elegans) - a convenient organism for genetic research that contains many of the basic physiological mechanisms that exist in humans. It was found that genes and mechanisms that control the rate of aging in this worm also exist in mammals, including humans. "It's convenient to use C. elegans to ask questions about aging and genetic elements that slow it down," says Prof. Hannis-Kornblit, "she lives two weeks on average, during which she also ages. In addition, her genome is similar to the human genome."
The latest research by Prof. Hanis-Kornblit and her team, which won a research grant from the National Science Foundation, sought to examine the role of small RNA molecules of the endo-siRNA type (which do not code for proteins), in the control of aging. These molecules determine the breakdown rate of genes and their role is to regulate expressions to control the level of expression of the proteins they produce. Prof. Hannis-Kornblit says that to date these molecules have hardly been studied in the context of aging.
The researchers used C. elegans worms whose lives were extended using one of four manipulations. The types of manipulations were: damage to the signaling pathway of the hormone insulin, damage to the reproductive system (lack of sex cells - eggs and sperm), caloric restriction, and damage to the activity of the mitochondria (an intracellular organelle that produces a significant part of the chemical energy needed by the body's cells). Prof. Hannis-Kornblit says that these vulnerabilities contribute to life extension in diverse mechanisms; It is possible that their damage leads to the development of compensatory mechanisms, which contribute to dealing with stressful conditions and thus to prolonging life. The researchers damaged the endo-siRNA molecules of each group of worms (prevented them from forming or functioning) through mutations. That is, they turned off the worms' ability to produce active endo-siRNA and asked to see if they still lived longer.
This is how they discovered that most of the worms lived longer (exceeded the normal average age - two weeks) despite the cancellation of the endo-siRNA. The only group of worms that did not prolong life after the endo-siRNA was removed was the one whose reproductive system was damaged. Since endo-siRNA is known to destabilize genes, the researchers used genomic methods to examine gene expression in the same group of worms; They identified genes whose expression decreased and genes whose expression increased following the elimination of the endo-siRNA. The genes whose expressions decreased were those that code (translate) for chaperone-type proteins (umbrella protein) - whose role is to help protein folding. In other words, it was found that when there is damage to the endo-siRNA of animals with a damaged reproductive system - the folding of the proteins goes wrong.
The genes whose expression increased following endo-siRNA cancellation were diverse. The researchers wanted to check which of them was critical to life expectancy, so each time they silenced one of them (using genetic methods) and checked when the worms lived longer as a result. They found one gene whose silencing made the worms resistant to protein folding problems and longer life. From this, the researchers concluded that the production and function of endo-siRNA is necessary for slowing down the rate of aging and prolonging the life of animals with a damaged reproductive system. Prof. Hannis-Kornblit says that it is possible that in the future these findings could help to slow down aging and increase the healthy life expectancy of humans, especially those with a lack of sex cells (eg women who have undergone oophorectomy or men who have undergone castration).
Life itself:
Prof. Sion Hanis-Kornblit is an independent researcher at Bar Ilan University, mother of three daughters (9, 15, 19) and lives in Gani Tikva. Between the family at home and the family in the laboratory, she doesn't have much free time ("I like to research and work in my hobby. It's very rewarding on a spiritual level").
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