Maybe you heard about telomeres in biology class? They are like the protective caps on shoelaces and help the DNA keep its shape. What's exciting is that these protective caps are constantly being dismantled and reassembled. For the discovery of this mechanism, the Australian researcher Elisabeth Blackburn received the Nobel Prize and Telomere abrasion was included in the repertoire of the 12 molecular mechanisms that we call Hallmarks of Aging describe.
The first characteristic we have already learned about is genomic instability . This accumulation of DNA damage with age appears to influence our genetic information almost randomly. Depending on where damage occurs, different conditions arise.
So what do telomeres have to do with aging? A lot, as it turns out and we'll show you the details here. But first, let's take you to biology class and clarify the basics.
What is a telomere?
In almost every cell in our body there is DNA (in German: DNA) in the cell nucleus. DesoxyriboNukleinSacid, as it is spelled out, is viewed very simply as a book in which the genetic information is written down. However, one book is not enough for this analogy - our DNA is rather an entire library. In healthy people, this library includes 23 books - the so-called chromosomes.
Telomere abrasion – the best comes last
The last chapter of these books is special and is called Telomere. There is no longer any information for proteins encoded here. stored, but the telomeres act as a protection against degradation for the DNA. Every time DNA is duplicated during cell division, telomeres shorten. The reason for this is very complex and would go beyond the scope at this point. The only important thing is that telomere shortening is a normal physiological process that occurs in most cells in all people.
Over time, the following happens: Once a certain number of DNA duplications have occurred, a threshold is reached and the telomeres are used up. This circumstance leads to the cessation of cell function and the inability to divide. Leonard Hayflick discovered this threshold and since then it has been called the “Hayflick Limit”.
The exhaustion of the telomeres explains the limited ability of cells to divide and thus also partly the limited regeneration potential of tissues. In Hayflicks' experiment, an average human cell grew approx. Shared 52 times.
Did you know? Magnesium metabolism plays an important role for telomeres. Magnesium is needed in many places in our body, but is particularly involved in energy production and electron balance. We need both to maintain healthy telomeres. Magnesium supplementation has been shown to increase telomere length in humans. In return, other publications have shown that low magnesium levels coupled with high homocysteine levels lead to shorter telomeres.
Telomerase as the key to immortality?
However, what about the remaining cells that are not affected by this telomere shortening? Well, these have an enzyme called Telomerase, which can lengthen the telomeres again. This enzyme essentially gives a cell immortality. Aha! Then researchers just have to manage to introduce this telomerase into every cell? As always in science, it's not that simple, after all, nature has it Something was thought about not equipping all cells with it.
Let's think back to the first characteristic - genomic instability. A constant drizzle of external and internal influences rains down on our genetic information and thus threatens the integrity of the DNA. As a result, mutations and DNA changes occur everywhere in our body every second, most of which, but not completely, can be repaired by the very extensive repair system.
If cells with unrepaired genetic mutations now had the enzyme telomerase, then the modified cell would be able to continue dividing. The result is an increasingly larger pile of completely degenerated cells, better known as cancer - definitely a double-edged sword.
Stem cells – the royal class among cells
The telomerase-privileged cells include, for example, stem cells or bone marrow cells, which are usually located in protected places in the body. In addition, they are protected as best as possible from harmful influences on their DNA through a variety of properties and mechanisms - much better than the majority of other cells. Accordingly, the risk of degeneration is significantly reduced.
Did you know? The discoverer of telomerase, Elisabeth Blackburn, is still working on the topic today. One of her larger papers looked at the connection between chronic stress and telomere length. Here she was able to show that chronically stressed people (in her case, mothers who looked after chronically ill children), had shorter telomeres and telomerase activity was lower than in the comparison groups.
DNA repair – well-intentioned, badly hit
Our idea of telomeres must now be expanded by another factor, or better yet, another protein. We already know that DNA is not a continuous strand, but is divided into chromosomes with telomeres at the end. If you look at it that way, telomeres are DNA strand breaks - places where the DNA ends.
As is well known, our repair system usually immediately recognizes this in its attempt not to allow any loose DNA ends and repairs them. Well-intentioned, but in the case of telomeres, poorly taken. The repair mentioned must under no circumstances take place in telomeres, as in this way two chromosomes can be connected to one another.
If this happens and the cell wants to divide later, then harmful “chromosome breaks” occur – the genetic material is distributed unevenly among the daughter cells. Both too much and too little genetic information then hinders cell function.
Shelterin – the name is deceptive?
As is so often the case, nature is there because we humans and some other organisms have shelter. Shelterin is a complex of six proteins that binds to telomeres and protects them from the repair system. “shelter”). This means that the big problem of chromosome breaks and the impending degeneration of cells – assuming functioning shelterin – has been solved for the time being.
However, telomeres are not immune to DNA damage, as we have come to know in the context of genomic instability. Since shelterin makes telomeres invisible to DNA mechanics, actual DNA damage cannot be repaired. That doesn't sound good at first, as the circumstance mentioned leads to more and more damage, which over time leads to senescence (intermediate state, a kind of “zombie cell”) or can contribute to cell death.
DNA damage in the telomere area is not particularly serious because it is a non-coding region, i.e. no information is read for the construction of proteins.
Short telomeres and diseases
So Shelterin protects us from the greater evil. The loss of a few cells is a smaller problem than that of degenerated cells and chromosome breaks. If Shelterin or parts of it are missing, a rapid decline in regenerative capacity and accelerated aging have been observed - a phenomenon that occurs even when telomeres are actually of normal length.
In addition to shelterin deficiency, telomerase deficiency also leads to premature development of diseases. In particular, this refers to hardening of the lungs (technical term: pulmonary fibrosis), anemia with a reduction in all blood cells (technical term: aplastic anemia) and a rare skin disease called dyskeratosis congenita.
All three diseases result in the loss of the regenerative capacity of various tissues. In addition, summarized studies have shown a connection between short telomeres and the risk of death, especially at a young age.
Can we stop telomere attrition?
The first successes with telomere therapies have already been achieved in mouse experiments. For example, telomerase was successfully genetically reactivated in prematurely aged mice with telomerase deficiency. Another experiment showed a delay in normal aging, without increasing cancer incidence, through pharmacological activation.
The next few years and decades will show whether our future in terms of telomere research looks as bright as that of mice. In the meantime, we can take a look at what works reliably in humans. How can we lengthen our telomeres?
Did you know? Omega-3 fatty acids are an important part of a healthy diet. They occur in nature mainly in three forms, abbreviated ALA, DHA and EPA. Scientists have been looking for 6 years to see whether there is a connection between the Omega-3 index and telomeres. And indeed. Patients who consumed little DHA and EPA (and consequently had a low omega-3 index), showed a much faster telomere attrition.
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Plant-based diet lengthens telomeres
The publications on telomere research are sometimes confusing and contradictory. This is also due to how the studies are structured and which telomeres are measured. The simplest way is to measure the telomere length of leukocytes (white blood cells). But this may not always be the best measurement method.
To understand the influence of diet, we need to look at the bigger picture. In the context of genomic instability, we have already seen that our DNA is constantly exposed to oxidative stress. A little bit is beneficial, too much seems to accelerate aging. A diet rich in plants , rich in secondary plant substances seems to promote this balance and thus indirectly contributes to this longer telomeres.
Sirtuins and telomeres – two partners for longevity
If you take a closer look at the molecular connections between telomeres and secondary plant substances, you come across the sirtuins. Sirtuins are often described as longevity genes because Sirt-1 and Sirt-6 are associated with better health.
The Sirtuins can be activated particularly effectively by Fasting , but also some secondary plant substances like that Resveratrol are potent Sirt activators. High sirtuin levels help us protect DNA from damage, support telomeres and affect epigenetics.
Conclusion on telomere attrition
Telomeres play an important role in the aging process. For a while, telomeres were even the “stars” in aging research. It was believed that in order to live forever you just had to extend it. It's not quite that simple and despite a few setbacks, we now know a lot more about this important structure in our cells, thanks in part to Elisabeth Blackburn. As part of the Hallmarks of Aging, they are a building block on our path to slowing down aging.
The next article in this series is about the third hallmark of aging: Epigenetic changes.
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