Can we mimic Turreptosis cellular reversal in humans?

  • #1
Scientists have discovered that the deteorioration of the tightly-packed bundles of DNA that are responsible for our normal cell functioning is actually reversible, and figuring out how this process works could enable new treatments for age-related diseases like Alzheimer’s.

What I would like to brainstorm in this forum, is where to start if one would like to implement or somehow imitate the process that the turreptosis jellyfish undergoes when it renews it cellular structure to never die. I know it is very difficult or perhaps even impossible to attempt equating the way this sea creature’s biology functions in human bodies, but I would like to seriously postulate this for debate. Is immortality achievable with current date science of any relevance to this subject and how can we create a “miracle” serum for human ingestion or intravenous injection to retard, reverse and/or even nulify aging?

Researchers from the Salk Institute in the US and the Chinese Academy of Science made the discovery while studying the underlying causes of Werner syndrome - a genetic disorder that causes affected individuals to age more rapidly than normal. The team found that the genetic mutations responsible for this syndrome caused densely packed DNA - known as heterochromatin - to become destabilised, which serves to disrupt normal cellular functions and caused the cells to age prematurely.

“This has implications beyond Werner syndrome, as it identifies a central mechanism of aging - heterochromatin disorganisation - which has been shown to be reversible.” The team also observed that the deletion of this gene led to the structural breakdown of heterochromatin. This bundling of DNA, which is found inside the cell’s nucleus, controls the activity of genes and helps the molecular machinery inside cells to function normally.

I propose: Let the scientific community gear some of its efforts towards identifying which proteins, blocks or substances the Turreptosis produces, and observing at the cellular level how this creature’s cellular components behave. Perhaps that substance can be sinthezised and trialed in other living creatures for observation. Tortoises and humb back whales live up to 200 years. Let’s look into that as well, and see how their cell structure behaves compared to that of an 18, 30, 50 and 80 year old human behaves. Can it be disrupted? Or slowed down significantly enough to extend human life span?

As part of their study, the researchers also tested stem cells from the dental pulp of healthy people across a wide age range. They found that older individuals, aged between 58 and 72, had fewer genetic markers for the DNA instability than people between the ages of seven and 25. “What this study means is that this protein does not only work in a particular genetic disease, it works in all humans,” Belmonte affirms. “More broadly, it suggests that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging.

This begs the question of whether we can reverse these alterations - like remodeling an old house or car - to prevent, or even reverse, age-related declines and diseases.” Importantly, before it becomes anything close to heralding the fountain of youth we all crave, researchers will need to develop ways to specifically target, and safely edit, these genes in humans, rather than in petri dishes. End of rant.
 

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jim mcnamara
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It would help others reading your post if you could tell us where/what you read (whose article, plus title or link, for example.) Thanks.
 
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Third link fails.
 
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Ygggdrasil
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Here's a link to the paper relating heterochromatin organization to aging: http://science.sciencemag.org/content/348/6239/1160

There are very many lab looking into the "epigenetics" of aging (i.e. how DNA and histone modifications as well as chromatin state are involved in the aging process), though this is very much still an active area of research with not too many very solid results (and certainly none that I know of that are clinically actionable). Here's an example of a recent paper on the topic: https://www.cell.com/cell/abstract/S0092-8674(18)30451-3

Changes to chromatin state are likely one of very many factors contributing to aging. Aging is very likely a multi-factorial process where there are several essential biological processes involved and failure of any one of these systems contributes to aging. Thus, solving just one problem will likely not be sufficient to "solve" aging. The research on chromatin and heterochromatin is likely adding to the list of factors contributing to aging, but it is unlikely that the chromatin story will explain all of aging.

For a nice review of the biological mechanisms behind aging see the following review published in the journal Cell (abstract copied below):
Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.
https://www.cell.com/abstract/S0092-8674(13)00645-4

With regard to regeneration in other species, much work has been done to study regeneration in planaria (flatworms), which are more evolutionary related to humans than jellyfish. We have a decent idea of how planaria are able to regenerate (see https://www.nature.com/scitable/blog/accumulating-glitches/unravelling_regeneration_in_planaria), though it's not clear how applicable such knowledge is to humans as these organisms have very different biology than us. Other research is examining other interesting animals to gain clues into aging processes, such as the naked mole rat which does not seem to get cancer.

Regarding the different lifespans of various species across the tree of life, see this previous PF thread for some interesting links: https://www.physicsforums.com/threads/reason-for-different-animals-longevity.900313/
 
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