In a recent study, scientists describe their findings and how they contribute to existing data on aging.
“Long genes that become less active with age may simply be the central cause of our body’s aging,” said correspondent Thomas Stoeger, an assistant professor of pulmonary and critical care medicine at Northwestern University Feinberg School of Medicine and a member of the Potocsnak. Longevity Institute. ” Our discovery advances the identification of a unique phenomenon that connects much of the existing wisdom about aging and makes this underlying phenomenon measurable. “
The paper, which highlights the joint findings of four foreign study teams, was published in Trends in Genetics on March 21. The teams are the first to conclude that the maximal aspects of biological aging are similar to the length of genes.
Conditions that are known to accelerate aging minimize the activity of long genes. This includes oxidative stress and ultraviolet irradiation. Conditions known to slow aging increase the activity of long genes, such as calorie restriction. In addition, very short or very long genes encode cellular processes that are known to be replaced with aging, such as cellular energy formation, protein synthesis, and neuronal signal transmission.
“Gene regulation is one of the most central processes in life, and our four studies study why the activity of long genes, in particular, adjusts with aging,” Stoeger said. “In addition to aging, we show that the same outcomes occur in patients with Alzheimer’s disease, an age-associated disease. Our findings help us reconsider the reasons for neurodegenerative diseases such as Alzheimer’s disease. Because genes with neuronal functions are unusually long, we hypothesize that the reduced activity of cells with long genes fails to produce enough biomaterials to maintain neuronal function well.
The cause of aging is a physical phenomenon similar to the lifespan of genes and not to the expressed genes in question or the function of those genes, the scientists report. The original effects were based on a body of molecular knowledge from humans, mice, and rats. , killifish, C. elegans, D. melanogaster and experiments with mice. Previously, clinical trials sought to identify the genes responsible for aging. This new view differs from conventional biological approaches that examine the effects of single genes.
Long genes simply have more potential genes that can be damaged. Scientists liken this to a road trip: the longer the trip, the more likely it is that something will go wrong. And because the physiological functions of some mobile types depend on longer during aging, genes are damaged when the DNA strands involving them are broken. This prevents mobiles from reading the data and activating the data in the gene. The longer the gene, the more likely it is that at least one of the DNA damages exists and stops the gene from activating.
Since neuronal cells are known to rely on long genes and divide slowly or not at all, they are sensitive to this phenomenon. Many of the genes involved in brain loss, aging, and related to Alzheimer’s disease are exceptionally long. Pediatric cancer patients, cured through DNA-damaging chemotherapy, then suffer premature aging, adding neurodegeneration. (ANI)