Aging is an important challenge for all societies. With the world’s population aging rapidly, some predict that by 2050, for the first time on Earth, there will be as many elderly people as there are children under the age of 15. In this case, it is predicted that the economic and health burden that age-related diseases impose on societies will increase in the next few decades. However, based on research conducted last year, it is possible to slow down the aging process in the future.With their studies on the aging of the body, researchers claim that it may be possible to slow down the aging process in the future. So can the aging process be slowed down?
Can the aging process be slowed down?
Harvard Medical School (HMS) scientists have investigated the cause of aging and identified a possible way to reverse it. In experiments on mice, they showed that problems with epigenetics trigger the signs of aging and that a reboot can reverse them and perhaps extend life.
Our genome contains a complete map of the DNA found in every cell in our body, but this is not the complete picture, but an additional layer of information called the epigenome, which controls which genes are turned on and off in different cell types. It’s as if all the cells in our body work based on an operating manual, which is the genome, but the epigenome is like a list of contents that directs different cells to different chapters, which are genes. After all, lung cells need instructions that are very different from heart cells.
Environmental and lifestyle factors such as diet, exercise, and even childhood experiences can alter epigenetic expression throughout our lives. Epigenetic changes have been linked to the rate of biological aging, but whether they represent signs of aging or are themselves symptoms is not yet clear. In this project, researchers conducted experiments on mice to find out the answer. Using a system called “Induced Changes in the Epigenome” (ICE), they sped up the natural process of DNA damage and repair in mice to test whether this accelerated the signs of aging. but whether they show signs of aging or are a symptom itself is not yet clear.
In mammalian cells, chromosomes undergo a million DNA breaks per minute, and epigenetic factors rapidly coordinate the repairs before returning to their original sites. The research group engineered mice that underwent DNA breakage at a rate three times faster than normal.
Over time, researchers discovered that epigenetic factors become increasingly disturbed and do not return home after repairing DNA breaks. This leads to epigenome scrambling. At six months of age, the mice showed physical signs of aging and appeared to be in significantly worse health than age-matched unedited mice.
Testing a possible treatment to reverse the aging process
Researchers say that with this research, they have confirmed the role of epigenome in aging. The next step was to test whether something could be done about the problem. Researchers tested a gene therapy combination of three genes named “Oct4”, “Sox2” and “Klf4”. These genes are active in stem cells, and researchers found in their previous study that they could be used to restore vision to mice with age-related glaucoma.
These two mice are the same age, but the mouse on the right has undergone an epigenetic experiment and its aging is accelerated.
In this case, the ICE mice experienced a dramatic reduction in biomarkers of aging. Their epigenome was torn apart, restoring their tissues and organs to a youthful state. David Sinclair, the project’s lead researcher, said: “It’s like restarting a broken computer and it sets off an epigenetic program that directs cells to restore the epigenetic information they had when they were young.” This is a permanent reset.
Researchers believe that this discovery is very big. By tackling aging, many diseases caused by this natural process can be treated more effectively. Sinclair wrote in a tweet: “If the result obtained is correct, it means that cancer, diabetes, and Alzheimer’s may have the same underlying cause.” In this way, the cause can be reversed to treat age-related diseases.
Although there is still much research to be done before such lofty goals can be realized, research is being done. A preprint paper, which has not yet been reviewed, applied the same gene therapy combination to aged mice, which are the equivalent of 77 years in humans. These mice lived 9% longer than untreated mice.
A combination that can slow down the aging process
In their new study, Tokyo Metropolitan University researchers have shown the significant effect of a particular compound in slowing down the process of muscle loss associated with aging.
Researchers have shown that a combination of 5-aminolevulinic acid (5-ALA) hydrochloride and sodium ferrous citrate (SFC) slows down aging-related muscle loss in fruit flies and slows the decline in locomotor activity and length. It leads to more life. In tests, this combination was associated with better preservation of muscle structure and mitochondrial function. This research is the first of its kind in animals and may help provide treatment options to slow muscle aging.
Healthy muscles are vital to a healthy life, but they don’t last forever. Age-related frailty can lead to problems such as slower walking, decreased strength, increased falls, and injuries, some of which may be fatal. An important part of age-related muscle loss is due to a decrease in mitochondrial function. Mitochondria are considered to be the factory for the production of a very important chemical substance called “adenosine triphosphate” (adenosine triphosphate), which is an essential source of chemical energy for various biochemical processes. However, the exact mechanism of how aging affects mitochondria is still not fully understood. An important part of age-related muscle loss is due to a decrease in mitochondrial function.
In major research conducted over the past decade, scientists found that mitochondrial decay in cultured cells could be reduced by adding a combination of two chemicals, 5-ALA and SFC. 5-ALA is known in biochemistry as the starting point of the porphyrin cycle that leads to the production of “heme”. Heme is a key precursor compound of hemoglobin; A molecule that is responsible for carrying oxygen in the body.
The research group, led by Kanae Ando, an associate professor at Tokyo Metropolitan University, hypothesized that the 5-ALA/SFC combination could be used in a therapeutic setting to help slow the process of age-related muscle wasting. They have shown in this research that this compound can affect the muscle health of Drosophila. By mixing chemicals with fly food, they found that flies fed the compound showed less decline in locomotor performance over time and lived longer.
By looking at the muscles of the flies under the microscope, the researchers found that the structure of the myofibers that make up the muscle tissue of older flies is more similar to the muscle tissue of younger flies.
Most importantly, by examining how this compound affects mitochondrial function, the researchers found that it is not necessarily the activity or dynamics of the flies that are directly affected; Rather, it is the electrical potential across the membrane that physically surrounds the mitochondria. It was found that this electrical potential is directly related to the production of active oxidative species that can damage muscle tissue.
Surprisingly, 5-ALA/SFC was found to be a common dietary supplement for health maintenance. The research group’s findings not only reveal a key mechanism that underlies the onset of aging and frailty but also provide a therapeutic option to help slow the process of age-related muscle loss.
Slowing down the cell aging process with the help of oxidants
The researchers of “Chalmers University of Technology” in Sweden have stated in their recent study that oxidants can slow down the process of cell aging. Oxidants, like reactive oxygen species, can damage the cells of living organisms and are related to aging. The researchers of “Chalmers University of Technology” in Sweden have stated in their recent study that oxidants can slow down the process of cell aging.
However, a recent study by Swedish scientists has shown that low levels of the oxidizing agent hydrogen peroxide, or hydrogen peroxide, can stimulate an enzyme that slows the aging process of yeast cells. Antioxidants, despite being neutralizing oxidants, may react with essential body molecules and disrupt their biological functions.
Large amounts of oxidants can cause severe damage to DNA, especially cell membranes and proteins. So our cells have developed powerful defense mechanisms to get rid of these oxidants. Previously, only the harmful side of oxidants was known, but now scientists are beginning to understand the positive functions of oxidants as well.
In a new study, scientists have shown that the oxidizer hydrogen peroxide or hydrogen peroxide can slow down the aging process of yeast cells. During this study, scientists investigated the enzyme “Tsa1”, which is part of a group of antioxidants called peroxiredoxin.
Peroxiredoxins are hydrogen peroxide or hydrogen peroxide inhibiting enzymes that also perform signaling and hydrogen peroxide or hydrogen peroxide chaperone work. In yeast, large amounts of cytosolic peroxiredoxin Tsa1 are required for resistance to hydrogen peroxide and longevity under calorie restriction. Chaperone is a protein that helps the folding of other proteins.
“Mikael Molin” (Mikael Molin), the leader of the research group of the Faculty of Biology and Biological Engineering of Chalmers University, said: Previous studies on these enzymes have shown that they participate in the defense of yeast cells against harmful oxidants. But peroxiroxins also help cells live longer when calories are restricted.
The mechanisms behind these functions are not yet fully understood. Researchers have also shown that stimulating peroxiredoxin activity slows cell aging in organisms such as yeast, flies, and worms, especially when they consume fewer calories than normal in their diet.
Cecilia Picazo, the post-doctoral researcher of this study, said: Now we have found a new function of Tsa1. Previously, we thought that this enzyme neutralizes reactive oxygen species. But now we have shown that Tsa1 is stimulated by a specific amount of hydrogen peroxide to participate in the slow aging process of yeast cells.
Scientists are now closer to understanding the mechanisms by which oxidants can slow the aging process, which could lead to further studies in the development of peroxiredoxin-stimulating drugs and testing whether age-related diseases can be prevented by other drugs that have the positive effects of oxidants in the body. increase, decrease, or not, lead to
Researchers at University College London (UCL), the University of Kent (UKC), and the University of Groningen (UG) have discovered that inhibiting an enzyme common to all mammals has anti-aging potential and can extend lifespan. By inhibiting this enzyme in the body of flies and worms, they were able to increase their lifespan. This enzyme exists in all kinds of mammals, including humans.
“Pol III” is an enzyme that is essential for cell growth and is present in almost all cells among all mammals. After the immunosuppressive drug rapamycin, known to inhibit Pol all, increased the lifespan of several animal models, including mice, researchers have begun investigating the role of this enzyme in aging.
The study that first showed the benefits of ADHD
In a new study, it has been hypothesized that some genetic traits associated with attention deficit hyperactivity disorder (ADHD) can actually be beneficial by increasing exploratory behaviors.
The study that first showed the benefits of ADHD
While current diagnostic definitions of attention-deficit/hyperactivity disorder (ADHD) are relatively new, the condition has been recognized and defined by clinicians under various names for centuries.
According to NA, recent genetic studies have shown that this disease is highly hereditary, which means that most people with this disease genetically inherited it from their parents.
Depending on the diagnostic criteria, between 2% and 16% of children can be classified as having ADHD. In fact, the increase in diagnosis rates in recent years has led some doctors to argue that the disease is overdiagnosed.
What is relatively clear, however, is that the behavioral traits that underlie ADHD have potentially been genetically present in human populations for a long time, leading some researchers to speculate on the evolutionary advantages of this What could be the conditions?
Imagine you are part of a wandering tribe of early humans. Your group comes across a field full of one type of fruit and everyone is faced with one big question. Do you settle on a farm and exploit its fruit supply until it’s all gone, or do you quickly pick up what you can and continue exploring for more diverse foods?
This opposition to exploitation or exploration is fundamental to the survival of all animals. At what point does the risk of staying in one place outweigh the risk of moving to find what’s next?
In the early 2000s, a team of scientists studied the genetics of a unique tribe of people in northern Kenya. This tribe, known as Ariaal, has traditionally been incredibly nomadic and nomadic since ancient times, and they have continued to live in this way. Some members of the Arial tribe settled down during the 20th century and adopted modern farming methods, while others continued to live as nomadic herders.
Scientists compared the genetic and health differences between these two groups of the Arial tribe and discovered something incredibly interesting. In general, all people of the Arial tribe carry a unique genetic mutation called DRD4/7R. This genetic trait has previously been commonly identified in people with ADHD.
This genetic mutation in today’s children who have been diagnosed with ADHD is generally associated with restlessness and distraction, and in those children of the Ariel tribe who were used to the behaviors of staying still settling down, and avoiding moving, this gene was associated with health. Poor and disruptive behaviors in class were related. But in Aryalees who still lived a traditional nomadic life, this gene mutation was associated with better nutritional health and strength.
The DRD4/7R mutation is associated with increased food and drug cravings, novelty seeking, and ADHD symptoms, explained Dan Eisenberg, lead author of the 2008 study. It is possible that in a nomadic environment, a boy with this gene mutation would be able to more effectively defend livestock against invaders or find water and food sources, but these same tendencies may be limited to fixed jobs such as setting up a school, farming, or selling goods. not useful
So an interesting hypothesis emerged. Whether the genetic traits of ADHD can be somewhat beneficial to a tribe, as it predisposes some individuals to “exploration” What appears in modern times as unrest and restlessness could actually have been beneficial to tribes that were looking for food.
David Barak from the University of Pennsylvania along with a team of colleagues tested this hypothesis experimentally. They produced a unique game where players were given eight minutes to collect as many berries as possible by hovering over a bush. Each time they picked berries from a bush, the player’s harvest was reduced slightly, but if they went to a new bush, there was a time penalty.
So what did most players do? Did they stick to the original bush? Or risk wasting time trying another plant to see if it bears more fruit? The same basic question, exploration or exploitation?
About 450 people participated in this experiment and all were simultaneously screened for ADHD symptoms. Not surprisingly, the researchers found that people with higher ADHD scores reached out to new plants sooner than others, but more importantly, people with ADHD tended to collect a larger volume of berries overall.
In a recently published study, Barak and his colleagues noted that participants without ADHD traits tended to overeat individual plants.
Finally, looking at the optimal withdrawal strategy for this game, it was found that players with high ADHD scores were more successful overall.
“We found that participants who screened positive for ADHD gave up the bushes more easily and achieved higher rates of reward than participants who screened negative,” the researchers wrote in their conclusion. Given that participants stayed more on a plant in general, those with high ADHD scores made more exploratory decisions, consistent with the predictions of optimal search theory, and thus behaved more optimally.
It should be noted that these findings do not represent a definitive verdict on the possible evolutionary benefits of ADHD, but they provide compelling and plausible reasons why a small percentage of humans still have these traits.
In the 21st century, we may have pathologized ADHD as a negative disorder, but this could simply be because these characteristics no longer fit the world we have constructed. So in a different context, a person with ADHD may be the savior of a society with their restless exploration of new fields.
This new study is published in the journal Proceedings of the Royal Society B.
Flu-killer cells have been discovered in the lungs
A hidden army of flu-killer cells has been discovered in the lungs. A group of “University of California Riverside” researchers in their new research have discovered a group of virus-eating cells in the lung that can fight influenza.
A hidden army of flu-killer cells has been discovered in the lungs
Scientists have long thought of the fluid-filled sac around our lungs as merely a barrier to external damage, but new research shows that this sac also contains powerful virus-eating cells that enter when an influenza infection occurs.
According to ScienceMag, these cells should not be confused with phages that infect bacteria. These cells, called macrophages, are immune cells produced in the body.
“Juliet Morrison” (Juliet Morrison), a virologist at, “The University of California Riverside” (UC Riverside) and head of this research said: Macrophages swallow bacteria, viruses, cancer cells, and dying cells. They grab and destroy anything that looks alien. We were surprised to find them in the lungs because no one had seen anything like that before.
In this research, it is explained how macrophages leave the external cavity and enter the lungs during influenza. They reduce inflammation there and lower the level of disease. “This research shows that it’s not just what happens in the lung that matters, but what happens outside the lung as well,” Morrison said. Cells not normally associated with the lung can have important effects on lung disease and health.
He added: Since this structure contains liquid, it prevents the lungs from collapsing. Despite this, researchers haven’t thought much about the fact that it might contain an entire organ. Our research may change this perception.
Researchers initially sought to answer a more general question. The question was which type of cells are present in the lung when you get influenza? They obtained existing data on lung-related genes from research on mice that either died or survived the flu. Then, they mined the data using an algorithm to predict the types of cells that change in the lungs during influenza. “We analyzed the data to determine which immune cells were present in the lung tissues,” Morrison said. That’s when I realized that maybe we have an unknown external source of cells in the lung.
Then, using a laser-based method, the researchers tracked the macrophages entering the mice’s lungs and found out what would happen if they took these cells out. “When you take them out of the mouse lung, you see disease progression and increased lung inflammation,” Morrison continued.
Morrison hopes the research will encourage other scientists to re-evaluate data sets from older studies. He added: Our method was to make a new use of the available information and finally we were able to see something new.
In their future research, the research group hopes to understand which protein tells the macrophages to move into the lungs. Once the protein signals are identified, it may be possible to discover drugs that increase macrophage numbers or activity.
A strategy to strengthen the human defense system against infection rather than developing another antiviral drug could provide a treatment for influenza that is effective for a longer period of time. Morrison is interested in host therapy because antibiotic and antiviral drug resistance is a growing problem.
This problem occurs when microbes, such as bacteria and fungi, gain the ability to defeat drugs designed to kill them. Improper use and overdose of drugs accelerate this problem. According to the report of the “American Center for Disease Control and Prevention” (CDC), more than 2.8 million drug-resistant infections occur in this country every year, and as a result, more than 35 thousand people die.
“If we can boost what’s killing the infection in us, we’re probably going to have a better outcome and be less likely to become resistant to the drug,” Morrison said. The immune system is very complex, but our best long-term job is to work with what we have instead of chasing treatment-evasive viruses.
This research was published in the journal “PNAS”.
Why do we get old?
Aging is an inevitable fate for all living organisms and many scientists are trying to reverse this process by discovering effective factors. Now a new study shows that DNA damage may be the main cause of aging. So why do we get old?
Why do we get old?
Processes and pathways that run smoothly in our youth begin to fail as we age. Over time, these breaks build up and lead to symptoms like loss of muscle mass, weakened immune systems, memory problems, and more that we will all experience in the future.
According to Forbes, what we see on the skin is reflected at the genetic level, creating obvious differences between young and old adults, but the exact reasons for these age-related genetic changes have not been well understood. A new study suggests that DNA damage may be to blame for aging. So why do we get old?
The genetic fingerprint of aging
Genes make the world go round. It sounds like an exaggeration, but it’s true. Each of the processes we depend on for life is somehow shaped by genes. Remember that genes serve as blueprints for protein production. Without proteins, everything stops, and ultimately, they are molecules that perform functions.
Whether a protein is produced when, where, and how much it is produced is precisely regulated by a process called gene expression. Gene expression is essentially a genetic on/off switch. For example, when a person becomes ill due to a viral infection, their body begins to turn on genes related to the immune response, thereby mobilizing the appropriate immune cells to help defend against the threat. When gene expression is properly regulated, cell function proceeds smoothly, but if the balance is disturbed, genes that should be off may remain on, and vice versa. Also, too much or too little protein may be produced.
Aging is characterized by a specific pattern of gene expression. In a sense, it can be said that aging has a specific genetic fingerprint. Just like a thief leaves his fingerprints at a crime scene, age leaves its mark, and this is true of all animal species, from tube worms to humans.
Read More: Can the aging process be slowed down?
Changes in gene expression associated with aging have been known for some time, but answering what triggers these changes in the first place has been surprisingly difficult. We know what aging looks like at the genetic level, but we don’t know why it happens.
From DNA to RNA
Protein production is a complex, multi-step process, and as with any complex process that has multiple moving parts, there is room for error. In fact, the findings of this new research show that changes in gene expression with age may be related to defects in protein production. It seems that damage to DNA is associated with damage to an important step called “transcription”.
Proteins are made from RNA, but our genes are stored in the form of DNA. Therefore, DNA must first be converted into RNA. In technical language, this work is called transcription. Why is this genetic procedure needed? Our DNA is stored in the nucleus of cells and does not leave this area of the cell to minimize damage, but protein production takes place in the cytoplasm. Therefore, genetic information must reach the cytoplasm from the nucleus.
This is where mRNA, or to be more precise, “messenger RNA” (mRNA) comes into play. While DNA is used for long-term storage, messenger RNA serves as a single-use set of genetic instructions. A messenger RNA encodes a copy of a specific gene and transfers it from the nucleus to the cytoplasm; Where the gene can be converted into a protein. The process is similar to copying part of a rare book that you need but can’t get out of the library.
The body even has its own genetic photocopying machine called RNAi polymerase II, or RNAPII. Arane polymerase II is a complex of several proteins that, depending on the gene that needs to be transcribed, attaches to a specific segment of DNA and then moves along the target gene, delivering a copy of the complementary arane. The resulting RNA strand, called the transcript, is the precursor to the messenger RNA.
In this study, Akos Gyenis, Jiang Chang, and their colleagues at the Erasmus MC Medical Center in the Netherlands discovered that in older mice, RNAi polymerase II often fails when transcribing DNA into Arani starts to stop. Analyzing the livers of two-year-old mice, they found that up to 40% of all polymerase II arane complexes were stopped. Additionally, each stalled set likely blocks three others behind it, causing the DNA strands to line up until the blockage is resolved. The researchers found that larger genes were particularly susceptible to these issues, leading to a bias towards the expression of small genes.
When transcription stops, gene expression also stops. As a result, many cellular pathways begin to fail. They are deprived of the proteins they need to function properly. This includes all pathways that malfunction with age. In other words, the genetic fingerprint created by interrupted transcription is the same as that created by aging, suggesting that they are closely related. Pathways affected include those involved in nutrient sensing, cellular debris clearance, energy metabolism, immune system function, and the ability of cells to cope with injury. All of these things play a vital role in shaping longevity.
In the next step, the researchers sought to understand the cause of the arrest of Aran polymerase II in aged mice. Their suspicions led to DNA damage that was spontaneous and internal. Gene expression patterns in cells exposed to DNA-damaging agents are very similar to those seen during normal aging. Premature aging disorders such as Cockayne syndrome are also characterized by DNA damage. Normal DNA repair mechanisms malfunction and result in the stalling of polymerase II at sites of damage known as lesions. Considering these similarities, scientists speculated that DNA damage could also be involved in normal aging.
To test their hypothesis, the researchers looked at genetically modified mice that lacked the normal DNA repair system and were prone to DNA damage. These mice showed many features of premature aging; Including their life span which was significantly shortened. As expected, the transcription speed was significantly lower in these mice compared to the healthy group.
Although we have a good understanding of how gene expression changes with age, we do not fully understand what causes these genetic changes. This situation is just like looking at the symptoms of a disease without knowing the root cause. This new research suggests one possible mechanism is the DNA damage that accumulates in RNAi polymerase II as it attempts to transcribe the template strand into RNAi. When RNAi polymerase II hits a site of damage, it stalls and interferes with transcription, disrupting several important cellular pathways.
Although this research does not yet have any immediate therapeutic implications, research of this type helps us better understand the inner workings of the aging process. The deeper our understanding, the more likely it is to develop effective drug interventions. Until then, it’s best to avoid behaviors that pose a risk of DNA damage, such as smoking and exposure to UV rays. Temporary programmed caloric restriction may also help reduce transcriptional pressure.
This research was published in “Nature Genetics” magazine.
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