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What Are Telomeres?

As our cells divide (a process known as mitosis), our cells replicate the long strands of DNA located within the nucleus of our cells (known as chromosomes). This process however is imperfect, and due to the mechanics of how this is carried out by the body, the DNA is shorted ever so slightly during each replication cycle. I will not get into the details on how exactly this happens in this article, but if you are interested then this video should give you a better understanding of this process. In order to prevent important parts of the DNA being lost through the replication process, areas of what is mostly blank DNA at the end of the chromosomes are used as a sort of sacrificial buffer, allowing for the DNA to be replicated without the loss of genetic information. These areas of the chromosomes are known as telomeres. In addition to providing a buffer zone for DNA replication, telomeres also prevent broken strands of DNA attaching themselves to the ends of chromosomes, which both prevents chromosomes from becoming conjoined, as well as allowing for the opportunity for the broken strand of DNA to be repaired.

Do longer telomeres correspond to longer lifespans?

Calico has made some important discoveries about Yamanaka factors.


In a preprint paper, scientists from Calico, Google’s longevity research behemoth, suggest that contrary to our previous understanding, transient reprogramming of cells using Yamanaka factors involves suppressing cellular identity, which may open the door to carcinogenic mutations. They also propose a milder reprogramming method inspired by limb regeneration in amphibians [1].

Rejuvenation that can give you cancer

In 2006, a group of scientists led by Shinya Yamanaka developed a technique for reprogramming somatic cells back into pluripotent stem cells by transfusing them with a cocktail of transcription factors [2]. These four pluripotency-associated genes, Oct4, Sox2, Klf4, and c-Myc (OSKM), became known as the Yamanaka factors. This breakthrough made it possible to produce patient-specific stem cells from their own somatic cells.

A team of researchers from the University of Sydney, the ARC-Plant Protection Research Institute and York University, has found that workers in a species of honeybee found in South Africa reproduce by making near-perfect clones of themselves. In their paper published in Proceedings of the Royal Society B, the group describes their study of the bees and what they learned about them.

Prior research has found that some creatures reproduce through parthenogenesis, in which individuals reproduce without mating. This form of reproduction has the advantage of not wasting time and energy on mating and the gene pool remains undiluted. The downside, of course, is loss of genetic diversity, which helps species survive in changing conditions. Prior research has also shown that for most species, parthenogenesis is a less-than-perfect way to produce . This is because some tiny bit of genetic material is generally mixed wrong—these mistakes, known as recombinations, can lead to birth defects or non-productive eggs. In this new effort, the researchers have found a kind of honeybee that has developed a way to avoid recombinations.

The researchers found that South African Cape honeybee queens reproduce sexually, but the workers reproduce asexually. They then conducted a small experiment—they affixed tape to the reproductive organs of a queen, preventing males from mating with her, and then allowed both her and the worker bees in the same hive to reproduce asexually. They then tested the degree of recombination in both. They found that offspring of the queen had approximately 100 times as much recombination as the worker bees. Even more impressive, the offspring of the worker bees were found to be nearly identical clones of their parent. More testing showed that one line of worker bees in the hive had been cloning themselves for approximately 30 years—a clear sign that workers in the hive were not suffering from birth defects or an inability to produce viable offspring. It also showed that they have evolved a means for preventing recombination when they reproduce.

While DNA provides the genetic recipe book for biological form and function, it is the job of the body’s proteins to carry out the complex commands dictated by DNA’s genetic code.

Stuart Lindsay, a researcher at the Biodesign Institute at ASU, has been at the forefront of efforts to improve rapid DNA sequencing and has more recently applied his talents to explore the much thornier problem of sequencing molecules, one molecule at a time.

In a new overview article, Lindsay’s efforts are described along with those of international colleagues, who are applying a variety of innovative strategies for protein sequencing at the single-cell, and even single-molecule level.

Preliminary results from young blood plasma transfusions in mice are showing some really promising results!


For organisms like us, survival is a team sport. I do not mean in the sense of being a pack animal that forms mutually beneficial relationships with others in order to increase the likelihood of acquiring protection and resources (although this is certain true), but instead to the fundamental functions of our biology. The cells which make up our body are all in essence working towards the goal of survival, and in turn work with one another in a variety of different ways. As anyone who has ever worked in a team will tell you, communication is key, and without it a team is doomed to failure. However, often poor or incorrect communication can be even worse than no communication at all.

Immortal gut biome o.o


Our genetic material is stored in our cells in a specific way to make the meter-long DNA molecule fit into the tiny cell nucleus of each body cell. An international team of researchers at the Max Planck Institute for Biology of Aging, the CECAD Cluster of Excellence in Aging Research at the University of Cologne, the University College London and the University of Michigan have now been able to show that rapamycin, a well-known anti-aging candidate, targets gut cells specifically to alter the way of DNA storage inside these cells, and thereby promotes gut health and longevity. This effect has been observed in flies and mice. The researchers believe this finding will open up new possibilities for targeted therapeutic interventions against aging.

Our lies in the form of DNA in every cell nucleus of our body . In humans, this DNA molecule is two meters long—yet it fits into the cell nucleus, which is only a few micrometers in size. This is possible because the DNA is precisely stored. To do this, it is wound several times around certain proteins known as histones. How tightly the DNA is wound around the histones also determines which genes can be read from our genome. In many species, the amount of histones changes with age. Until now, however, it has been unclear whether changes in cellular levels could be utilized to improve the aging process in living organisms.

A well-known anti-aging compound with a new target

David Sinclair is a geneticist at Harvard and author of Lifespan.

Nature – Reversal of biological clock restores vision in old mice

Sinclair and his team restored vision in old mice and in mice with damaged retinal nerves by resetting some of the thousands of chemical marks that accumulate on DNA as cells age. They are now working to rejuvenate the brains of old mice. This work is so promising that Sinclair believes he can get to human trials within two years. Sinclair is using three genes to reset the age of cells.

New research suggests age-related changes in blood cell chromosomes are a marker of impaired immunity.

A person’s risk of severe infections increases dramatically as they grow older, but scientists do not yet understand how age might be linked to weakened immunity. Now, research shows that certain age-related changes in are associated with a higher risk of a range of severe infections including severe COVID-19, other pneumonias, and sepsis.

Researchers analyzed genetic and clinical data from nearly 800000 patients from around the world. They discovered that people with a specific type of acquired rearrangement in the chromosomes of their cells, called mosaic chromosomal alterations (mCAs), were nearly three times more likely to develop sepsis and two times more likely to get pneumonia than those without mCAs. These genetic changes accumulate in blood cells with age and often indicate a common condition in the elderly called clonal hematopoiesis.

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For all the cool regenerative tricks the human body can do, it’s kind of weird that we only have one shot at tooth enamel with no way to get it back. That may be about to change, as researchers at the University of Washington have developed a lozenge that rebuilds this precious protective coating a few microns at a time and are taking it to the trial stage. Could it really work? It’s certainly something to chew on.