Maybe you heard about telomeres in biology class? They are like the protective caps on shoelaces and help DNA to keep its shape. What is exciting is that these protective caps are constantly being dismantled and rebuiltFor the discovery of this mechanism, Australian researcher Elisabeth Blackburn was awarded the Nobel Prize and the telomere attrition was added to the repertoire of 12 molecular mechanisms that we have identified as Hallmarks of Aging describe.
As a first indicator we have already identified the genomic instability This accumulation of DNA damage with age seems to affect our genetic information almost randomly. Depending on where the damage occurs, different conditions arise.
So what do telomeres have to do with aging? Quite a lot, as it turns out, and we'll show you the details here. But first, let's take you back to biology class and explain the basics.
What is a telomere?
In almost every cell in our body, DNA is located in the cell nucleus. DesoxyriboNukleinSAcid, as it is spelled out, is viewed in a very simplified way as a book in which the genetic information is written down. However, a book is not enough for this analogy – our DNA is rather a whole libraryIn healthy people, this library contains 23 books – the so-called chromosomes.
Telomere attrition – the best comes last
The last chapter of these books is special and is called Telomere. Here, no information for proteins is encoded or stored, but the telomeres act as a degradation protection for the DNAEvery time the DNA is duplicated during cell division, the telomeres shorten. The reason for this is very complex and would go beyond the scope of this article. What is important is that the shortening of telomeres 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 upThis situation leads to the cessation of cell function and the inability to divide. Leonard Hayflick discovered this threshold and since then it has been called "Hayflick limit“.
The exhaustion of telomeres thus 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 divided about 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 extend telomere length in humansIn contrast, other publications have shown that low magnesium levels coupled with high homocysteine levels lead to shorter telomeres.
Telomerase as the key to immortality?
But what about the remaining cells that are not affected by this telomere shortening? Well, they have an enzyme called telomerase, which can lengthen the telomeres again. This enzyme practically gives a cell immortality. Aha! Then researchers only have to manage to introduce this telomerase into every cell? As always in science, it is not that simple; after all, nature had a reason for not equipping all cells with it.
Let us think back to the first hallmark – genomic instability. A constant drizzle of external and internal influences rains down on our genetic information, threatening the integrity of DNAAs a result, mutations and DNA changes occur every second throughout our bodies, most of which, but not all, can be repaired by the very extensive repair system.
If cells with unrepaired genetic mutations now possessed the enzyme telomerase, the altered cell would be able to continue dividing. The result is an increasingly large pile of completely degenerated cells, better known as cancer - a double-edged sword.
Stem cells – the royal class among cells
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 well as possible from harmful influences on their DNA by 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 major works 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 cared for chronically ill children), had shorter telomeres and telomerase activity was lower than in the comparison groups.
DNA repair – well-intentioned, badly executed
Our understanding of telomeres must now be expanded to include another factor, or rather, another protein. We already know that DNA is not a continuous strand, but is divided into chromosomes, at the end of which are the telomeres. Telomeres are, if you look at it this way, DNA strand breaks – places where the DNA ends.
As we know, our repair system usually immediately recognizes this in its attempt to prevent any loose DNA ends and repairs them. Well-intentioned, but in the case of telomeres, a bad idea. The repair mentioned must not take place at telomeres under any circumstances, as this could potentially lead to two chromosomes being connected to each other.
If this happens and the cell wants to divide later, harmful “chromosome breaks” occur – the genetic material is distributed unevenly among the daughter cells.Both too much and too little genetic information impairs cell function.
Shelterin – is the name misleading?
As is so often the case, nature is there to help, because we humans and some other organisms have shelter. shelter is a complex of six proteins that binds to telomeres and protects them from the repair system (shelter). This solves the major problem of chromosome breaks and the threat of cell degeneration – assuming that shelterin is functioning.
However, telomeres are not immune to DNA damage, such as that experienced in the context of genomic instability. Since shelterin makes telomeres invisible to DNA mechanics, actual DNA damage cannot be repairedThis does not sound good at first, as the above-mentioned circumstance leads to more and more damage, which over time leads to senescence (intermediate state, a kind of “zombie cell”) or cell death.
However, DNA damage in the area of the telomeres is not particularly serious, since this is a non-coding region, meaning that no information is read for the construction of proteins.
Short Telomeres and Diseases
Shelterin protects us from the greater evilThe 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 diseasesSpecifically, 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, combined studies have shown a link between short telomeres and risk of death, especially at a young age.
Can we stop telomere attrition?
Initial successes have already been achieved in mouse experiments with telomere therapies. For example, telomerase was successfully genetically reactivated in prematurely aged mice with a telomerase deficiency. Another experiment showed a delay in normal aging, without an increase in the occurrence of cancer, through pharmacological activation.
The next few years and decades will show whether our future in terms of telomere research is as bright as that of mice. In the meantime, we can take a look at what is proven to work 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 to ALA, DHA and EPA. Scientists spent 6 years looking at whether there was a connection between the Omega-3 index and telomeres. And indeed there was. Patients who consumed little DHA and EPA (and consequently had a low Omega-3 index), showed 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 impact 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 of it is beneficial, too much seems to accelerate aging. A plant-rich Diet rich in secondary plant substances seems to promote this balance and thus indirectly contributes to longer telomeres.
Sirtuins and telomeres – two partners for longevity
If we take a closer look at the molecular relationships between telomeres and secondary plant substances, you come across the sirtuinsSirtuins are often described as longevity genes, since Sirt-1 and Sirt-6 in particular are associated with better health.
The Sirtuins can be particularly effective through Fast be activated, but also some secondary plant substances such as 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 all you had to do was extend it to live forever. 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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