Why Clinuvel Stock Could go Extremely $$$$ Up
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But aside from Scennese causing melaingenisis (tanning of skin) it appears in various unrelated research that all leads to Melanocyte stimulating hormone (Scennese)
at MCR1 will dramatically increase telemere repair.
Keeping in mind what happens with the telemere repair in the previous link in telemere repair in the worms. Think what appears to be happening when a human is medically implanted with Scennese.
Natural Melanocyte stimulating hormone that could cause what Scennese does is very short half life in blood stream, and even the keraticyte cells produce very little natural msh and it is localized very close to them in the skin.
So Scennese will be massively more effective by many factors and better at binding longterm with all the mcr1s. (melanocortin receptors)
So we all have an idea of what age and time does to skin and how it looks. But if Scennese is reaching the P53 gene transcription factor by way of the MCR1's in all the skin cells, and the MCR1's in all the Fibroblast cells in the skin (the collagen and connective tissue) just below the surface of and in the skin. And if Scennese is reaching the MCR1s in the adiopyctye fat cells in the skin................then Scennese will by several times cause more telemere repairs.
Relative to the worms (and many other study's) this would indicate that Scennese would cause the skin and supporting tissue to remain younger and more youthful much longer in actuality and not just appearance. Scennese would give a tan
and slow the aging look several factors, and prevent and slow down cancers in these cells/tissues and promote apoptosis, scenescene and overall homeostasis in the skin.
In theory here with valid science corroborating (but alot not known yet) a beautiful women whom starts getting sagging skin, wrinkles, and deepening furrows, and less elasticity, and less moisture in her late 30's or early 40's would have all this tissues or cells or telemeres repaired replaced and hold onto her youthful appearance much longer.
I do not think a method exists whereby Clinuvel could measure in a control group and where it could indicate how much Scennese quantatively increases telemere repair and increases longevity of youth very easily.
Scennese has scientific basis all I have connected too, but there could be other implications or reasons Scennese may not do all the above, but so far they are not there.
I have given reasons of why I think Scennese could do all this by way of telemere repair, but it is beyond comprehension of how valuable Clinuvel could go.
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Msh and Scennese till new research Clarifys more distinctly or changes the overall inter relations of genes and protiens thru mainly P53 recognize bad deoxynucleicacids or bad daughter cells replicated after splitting from one
cell to two.
Although it may snip and clip and reconnect and
shorten and then when so short after the granddaughter cells and then great granddaughter cells and up to 60 to 180 cell divisions (mitosis differs in different people and different to various body cells in differing people)
it will push the cell into Senescenne (cell can live and function but no more splitting to make it's daughter cells) or kill the cell when the deoxynucleicacid is deemed to have shortened to a too damaged state.
A very old person in an age of 100 or abouts would have an enormous number of cells in
Senescenne. Soon after this so many cells would not be replaced in organs, and diminished function of that organ or group of cells not functioning to maintain the organ or capability of immune cells will not be enough. Death.
From just this aspect of only one small and simplistic view, leaving out counter chain reactions and other expressed protiens and genes, it would appear that Scennesewould not help an extremely old person from Ageing, but would help cells and organs with mcr1 use their P53 genes to fend off cancer.
But scennese introduced into a about 20 year old, whom has completed puberty and bones have connected and hardened and whom has avoided as much electromagnetic waves and radiation as possible, avoided as many viruses as possible, and avoided as many inorganic chemicals and the known bad elemental metals could have a tremendous affect in living a longer life by exponentially slowing down the inevitable shortening of alot of their cells deoxyribonucleicacid (DNA)
It would be the very first cell division that first has it's DNA copy not perfect that would have an affect most integral. Msh and therefore Scennese per abstract would increase the nucleatoid excision repair threefold relative to no msh (repair is not really what they do, that's telomerase protiens)
The better the original cell the better the copy
cell. If the radiation, viruses, insults and free radicals are lessened as Scennes will do, that will lead to fewer P53 cells with mcr1
Making fewer DNA repairs because there will be less DNA damaged.
And when the cells finally do get DNA damage, it will be snipped out and recoupled more frequently and efficously. Perhaps this would lead to more successful and less missed damaged cell divisions and better daughter cells with better DNA. And cell senescene and apoptosis could be put off longer and more cell divisions befor the telomerers got to short.
Of course cells with no mcr1 would age likely at the same with or without Scennes.
In general only a few human cells divide an unlimited number of times, including cancer cells.
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Identical Twins, one living a year in space, have unexplained telomere length compare, that quickly changes upon return to earth.
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Longevity research always reminds me of the parable of blind men and an elephant. A group of blind men, who’ve never seen an elephant before, each touches a different part of the elephant’s body to conceptualize what the animal is like. Because of their limited experience, each person has widely different ideas—and they all believe they’re right.
Aging, thanks to its complexity, is the biomedical equivalent of the elephant. For decades, researchers have focused on one or another “hallmark” of aging, with admirable success. For example, we now know that energy production in aging cells goes haywire. Immune responses ramp up, stewing aging tissue in a soup of inflammatory molecules. Dying cells turn into zombie-like “senescent cells,” where they abdicate their normal functions and instead pump out chemicals that further contribute to inflammation and damage.
Yet how these hallmarks fit together into a whole picture remained a mystery. Now, thanks to a new study published in Nature Metabolism, we’re finally starting to connect the dots. In mice, the study linked up three promising anti-aging pathways—battling senescent cells, inflammation, and wonky energy production in cells—into a cohesive detective story that points to a master culprit that drives aging.
Spoiler: senolytics, the drug that wipes out senescent cells and a darling candidate for prolonging healthspan, may also have powers to rescue energy production in cells.
Let’s meet the players.
From Metabolism to Zombie CellsIndividual cells are like tiny cities with their own power plants to keep them running. One “celebrity” molecular worker in the process of generating energy is nicotinamide adenine dinucleotide (NAD). It’s got a long name, but an even longer history and massive fame.
Discovered in 1906, NAD is a molecule that’s critical for helping the cell’s energy factory, the mitochondria, churn out energy. NAD is a finicky worker that appears on demand—the cell will make more if it needs more; otherwise, extra molecules are destroyed (harsh, I know). As we age, our cells start losing NAD. Without the critical worker, the mitochondria factory goes out of whack, which in turn knocks the cell’s normal metabolism into dysfunction.
At least, that’s the story in mice. Although yet unproven for slowing aging or age-related disorders in humans, NAD boosters are already making a splash in the supplement world, raising even more need to understand how and why NAD levels drop as we age.
Giving NAD a run for its anti-aging fame are senolytics, a group of chemicals that destroy senescent “zombie” cells. These frail, beat-up cells are oddities: rather than dying from DNA damage, they turn to the dark side, staying alive but leaking an inflammatory cesspool of molecules called SASP (senescence associated secretory phenotype) that “spread” harm to their neighbors.
A previous study in ancient mice, the equivalent of a 90-year-old human, found that wiping out these zombie cells with two simple drugs increased their lifespan by nearly 40 percent. Others using a genetic “kill switch” in mice found that destroying just half of zombie cells helped the mice live 20 percent longer, while having healthier kidneys, stronger hearts, luscious fur, and perkier energy levels. Similar to NAD supplements, pharmaceutical companies are investigating over a dozen potential senolytics in a race to bring one to market.
But what if we can combine the two?
A Hub for AgingThe new study, led by aging detectives Drs. Judith Campisi and Eric Verdin at the Buck Institute for Research on Aging in Novato, California, asked if we can connect the line between NAD and zombie cells, like suspects on an evidence board.
Their “lightbulb” clue was a third molecule of interest, highlighted in a 2016 study. Meet CD38, a molecule that plays double roles as an aging culprit. It wreaks havoc as an immune molecule to boost inflammation, while chewing up and destroying NAD. If CD38 is a new drug flooding the streets, then the team’s goal is to hunt down where it came from.
Using tissue from both mice and humans, the team traced CD38 to a type of immune cells. These cells, called M1 macrophages (literally, “big eaters”) are well known to increase inflammation in the body and cause DNA damage with age. When comparing fat tissue isolated from young and old mice, the team realized that these over-hyper immune cells pump out CD38 like crazy as the cells age—which, in turn, breaks down the good-for-you molecule, NAD.
One mystery in aging, explained Verdin, is whether NAD levels drop because of a faucet problem—our ability to make NAD—or leaky sink problem, where aging cells break down NAD too fast. “Our data suggests that, at least in some cases, the issue stems from the leaky sink,” he said.
The Zombie ConnectionHere’s the evidence so far: aging triggers a type of immune cells to pump out CD38, a nasty chemical from immune cells that eats up NAD. But why? More importantly, how can we stop it?
In an unexpected twist of events, the connection seemed to be zombie cells.
Remember, zombie cells leave a chemical evidence trace of inflammatory chemicals called SASP. They also change their “molecular look” so it’s possible to tease them out from a sea of healthy cells (think zombies versus humans in any zombie movie). In fatty tissue from aged mice, the team identified zombie cells and found that their “toxic waste” massively increased the amount of CD38 floating around. Going back to the drug analogy, if CD38 is a drug, then the specific immune cells are the manufacturers pumping it out to eat up NAD and wreck the cell’s energy production. Here, zombie cells are the drug kingpin, and their SASP molecules direct immune cells to make more CD38.
Frozen in TimeIf zombie cells are the kingpin, then getting rid of them should reduce the inflammatory CD38 “drug,” and in turn, preserve good guy NAD. To test it out, the team used a genetically engineered mouse, which allows scientists to identify zombie cells and selectively kill them off.
The team injected the mice with a drug that damaged their DNA. This mimics aging, in the sense that it increased zombie cells and CD38. Killing zombie cells lowered CD38 levels—like clearing a drug off the streets—and preserved NAD.
Voilà—case solved!
“We are very excited to link two phenomena which have been separately associated with aging and age-related disease,” said Verdin.
For now, zombie cells seem to be a master-level culprit that drives inflammation, decreases NAD levels, and breaks the cell’s energy production. This suggests that senolytics, which selectively kills off zombie cells, could as a secondary effect also increase NAD—something we didn’t know previously.
To Verdin, however, that doesn’t mean NAD supplements are useless or that senolytics are the one-and-only silver bullet against aging. “Ultimately I think supplementation will be part of the equation, but filling the sink without dealing with the leak will be insufficient to address the problem,” he said. In other words, for NAD supplementation to better work, we may need to also use senolytics to decrease zombie cells and CD38 levels, thus “plugging the leak.”
If all this makes your head spin—yup, same here! Our bodies run multiple “aging programs,” and we’ve just begun linking all these disparate culprits together. But the rewards could be great for creating therapies that slow or even reverse aging. After all, if we can find several masters that drive aging, why go after the little guys when you can target the boss?
Image Credit: Arek Socha from Pixabay
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In November we spoke to Anar Isman, the Co-founder & CEO of AgelessRx, about PEARL, the company’s IRB-approved human trial of rapamycin, a drug that has performed positively for aging in animal trials. Today we’re digging a little deeper into the company’s online anti-aging platform which promises “longevity prescriptions delivered right to your door.”
Longevity.Technology: Longevity through personalised medicine is the future; there is no point rattling with supplements that won’t target your personal aging needs. AgelessRx is hoping to use the data it collects from its supplements and prescriptions platform to analyse what products – and what combinations of products – pay the best dividends in terms of slowing and stopping aging.
AgelessRx has its foundation in something that has interested and puzzled Isman since he was a teenager – no-one wants to get old and die, but there is not as much interest and research into slowing down aging as there should be. His epiphany moment was when he encouraged his mother to begin taking metformin after learning of its anti-aging properties, but her doctor demurred, arguing that why on earth would he prescribe metformin for a non-diabetic.
“I realised there really is an opportunity to provide access to longevity therapies to people that are having a hard time accessing them – and that’s how AgelessRx came about,” Isman explains. “Our goal is to provide access to longevity products, or therapies, that require a prescription to people in an accessible and affordable manner.”
Anar Isman, the Co-founder & CEO of AgelessRx with his team“Metformin targets a number of age-related mechanisms and is heavily researched, but it’s not a magic pill, by any means,” he explains. “With continuing efforts, in the next 5 to 10 years, there will be some really powerful products that will help with longevity. The problem is that aging is not considered a disease, so it’s not going to be labelled ‘buy this for longevity’ because the science has been proved for other diseases, such as atherosclerosis or arthritis.
“If you are not suffering from those, the doctor won’t prescribe the drugs. That’s why I think our platform will fill in that gap. You don’t have to have an ‘on-label’ disease to benefit from our product; our doctors are knowledgeable about the benefits and the safety of certain drugs, and if appropriate, they’ll prescribe them to you – even without your having that particular disease, because they view the onset of age related damage itself as a disease.”
“Aging is malleable. It has levers, and these levers can be adjusted.”
AgelessRx sells a range of longevity therapies, including metformin, NAD+ and glutathione. Some products are taken orally, others taken dermally through patches, by an injection, or through a nasal spray. Customers complete a medical intake form which is reviewed by a licensed medical professional before the prescriptions are dispatched.
The AgelessRx platform also offers a virtual longevity consultation and a biological age assessment based research published in Aging [1]. The biological age is determined from a blood sample drawn at one of over 2000 lab locations in the US by inputting the data of nine biomarkers into AgelessRx’s online calculator.
AgelessRx sells a range of longevity therapies, including metformin, NAD+ and glutathioneAging is malleable, Isman says. “It has levers, and these levers can be adjusted.” Isman is hopeful that AgelessRx can leverage the data from its longevity products for everyone’s benefit, especially if plans for expansion outside the US come to fruition.
“We already have hundreds of healthy adults that are taking therapies for longevity,” he explains, “we just need to get more systemised data, analyse it, and we can hopefully produce useful data in the next six to twelve months. We’ll be able to analyse what works for which people, which combinations are better, and work towards providing a targeted solution for longevity.”
Use code: MET20 or LDN20 at checkout for $20 off first month & FREE online doctor consultation
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The faithful transmission of our genetic code from one generation to the next places DNA – the source of our genetic material – at the centre of two fundamental problems we must overcome. First, cells must be able to perfectly replicate at each cell division. Second, cells must be able to identify and repair any damage once it has occurred. Exogenous factors – such as chemical exposure, ultraviolet light, and ionising radiation – and endogenous factors, such as reactive oxygen species, constantly threaten the stability of DNA and must be identified and restored immediately.
In DNA Repair Communiqué I, we outlined the fundamentals of cell division and DNA repair. The phases of the cell cycle outlined therein are fundamental to our understanding of the synthesis and replication of DNA. Furthermore, knowledge of how a cell repairs its DNA proteins, specifically the nucleotide excision repair (NER) pathway, is crucial to understanding key topics outlined below. Thus, we recommend reviewing DNA Repair Communiqué I before reading further if these concepts are not well understood.
Within DNA Repair Communiqué II we delve deeper into the topic of DNA synthesis and repair. We begin with the fundamentals of how DNA is synthesised, focusing on the role of DNA polymerases. Once this foundational knowledge is established, we review how cells cope with damage to the DNA template, using translesion DNA synthesis (TLS).
As discussed in DNA Repair Communiqué I, the most basic function of the cell cycle is to duplicate human DNA into two genetically identical daughter cells through two overlapping, phases: nuclear division (mitosis) and the division of the cytoplasm to form two daughter cells (cytokinesis).
Although visually striking, the events of mitosis are only one phase of the cell cycle (Figure 1); for a typical mammalian cell, this period, known as M phase, usually lasts less than an hour. Cells spend most of their time in between divisions, a period known as Gap Phase, otherwise known as the G Phases.
Combined with S Phase and G2 Phase, this period is the longest growth period of the cell cycle, known as Interphase. During interphase, the cell is given time to grow and synthesise mRNA and protein required for the next step of the cell cycle. DNA replication occurs during S phase (S for synthesis), a part of the interphase, which requires 10–12 hours and occupies a significant part of the cell-cycle time in a typical mammalian cell.
The underlying mechanisms of DNA replication depend on the double-helical structure of DNA. In fact, a month after Watson and Crick published their now-classic paper postulating a double helix for DNA, they followed up with an equally important paper suggesting how such a base-paired structure might duplicate itself.
The model Watson and Crick proposed for DNA replication was one of the two strands of every newly formed DNA molecule is derived from the parent molecule, whereas the other strand is newly synthesised.1,2 This is called semi-conservative replication (Figure 2) because half of the parent molecule is retained by each daughter molecule. Within five years of its publication, the Watson–Crick model of semi-conservative DNA replication was tested and proved correct by Matthew Meselson and Franklin Stahl, in collaboration with Jerome Vinograd.3
According to this model, during DNA replication, each strand of the DNA double helix serves as a template for the synthesis of a new complementary strand. As biologists proceeded to unravel the molecular details of this process, it gradually became clear that DNA replication is a complex event involving numerous enzymes and other proteins—and even the participation of RNA.
When the semi-conservative model of DNA replication was first proposed in the early 1950s, biologists thought that DNA replication would be so complex that it could only be carried out by intact cells. Just a few years later, however, Arthur Kornberg showed that an enzyme he had isolated from bacteria can copy DNA molecules in a test tube, work for which he received a Nobel Prize in 1959.4 This enzyme, which he named DNA polymerase, requires that a small amount of DNA be initially present to function as a template. More than a dozen different enzymes have subsequently been identified as being involved in the DNA replication and repair process.
Given the complexity of DNA replication, one might wonder how cells are able to accurately replicate DNA so often without causing errors. They cannot. About 1 out of every 100,000 nucleotides incorporated during DNA replication is incorrectly base paired with the template DNA strand, an error rate that would yield more than 120,000 errors every time a human cell replicates its DNA.5 One of the key roles of DNA polymerases is to remove incorrect nucleotides, improving the fidelity of DNA replication to an average of only a few errors for every billion base pairs replicated.
During replication, DNA synthesis stalls when replication machinery encounters a fault within the template strand. Persistent replication stalling and blockages can lead to cell death, as well as genomic instability, which may ultimately go on to form cancer if left unchecked. Thus, organisms have evolved DNA damage tolerance (DDT) mechanisms to bypass DNA lesions and enable cells to continue replication by incorporating the error into future strands of DNA.
Key to DNA replication, synthesis and repair is Proliferating Cell Nuclear Antigen (PCNA). PCNA works as a DNA clamp, encircling DNA during the replication process and acting as a scaffold in the recruitment of DNA polymerases. In this role, PCNA serves as a moving platform, recruiting various factors for replication or DDT, dependent upon which is required. Two of the most important polymerases PCNA interacts with are DNA polymerases delta (Pol δ) in DNA replication and DNA polymerase eta (Pol η) during TLS. A table of important DNA replication and repair proteins are included below for reference. More information on the specific functions of PCNA may be found in Scientific Communiqué VIII and Scientific Communiqué IX.
Protein
Main Activities and/or Functions
DNA helicase
Unwinds double-stranded DNA
DNA ligase
Makes covalent bonds to join adjacent DNA strands, including the Okazaki fragments in lagging strand DNA synthesis and the new and old DNA segments in excision repair of DNA
DNA polymerase alpha (α)
Nuclear DNA synthesis: forms complex with primase and begins DNA synthesis at the 3˜ end of RNA primers for both leading and lagging strands (also functions in DNA repair)
DNA polymerase delta (δ)
Nuclear DNA synthesis; 3˜ S 5˜ exonuclease (for proofreading); involved in lagging and leading strand synthesis (also functions in DNA repair)
DNA polymerase epsilon (ε)
Nuclear DNA synthesis; 3˜ S 5˜ exonuclease (for proofreading); thought to be involved in leading and lagging strand synthesis (also functions in DNA repair)
DNA polymerase gamma (γ)
Mitochondrial DNA synthesis
DNA topoisomerase (type I and type II)
Makes single-strand cuts (type I) or double-strand cuts (type II) in DNA; induces and/or relaxes DNA supercoiling; can serve as swivel to prevent overwinding ahead of the DNA replication fork; can separate linked DNA circles at the end of DNA replication
Initiator proteins
Bind to origin of replication and initiate unwinding of DNA double helix
PCNA
Binds core polymerase subunit and keeps it on DNA
Primase
RNA synthesis: makes RNA oligonucleotides that are used as primers for DNA synthesis
RNA endonuclease (RNase H), RNA exonuclease (FEN1)
RNase H recognises RNA/DNA strands and nicks them; FEN1 then digests the RNA
Single-stranded DNA binding protein
Binds to single-stranded DNA; stabilises strands of unwound DNA in an extended configuration that facilitates access by other proteins
Telomerase
Using an integral RNA molecule as template, synthesises DNA for extension of telomeres (sequences at ends of chromosomal DNA)
XPV/ POLη
DNA-polymerase eta (pol-eta) performing trans-lesion DNA synthesis due to UV damage
The features that give DNA polymerases their high speed and accuracy (replication, recognition, and repair) also mean that they are easily stalled by DNA damage. If DNA lesions are unable to be fixed by nucleotide excision repair (NER), DNA synthesis is blocked as DNA polymerases cannot adapt to the damage effectively. These blockages can lead to the collapse of the replication fork, compromising DNA synthesis and potentially causing severe consequences such as the formation of cancer. Considering this risk, nature has equipped the human body with several alternative pathways to tolerate (rather than fix) DNA damage using specialised DNA polymerases in a process known as translesion DNA synthesis (TLS). Within this section, we shall focus on this complex process through the lens of XPV protein, also known as DNA polymerase eta (Pol η). In humans, the XPV protein, encoded by the XPV gene, is responsible for bypassing a very common form of sunlight-induced damage, cyclobutene pyrimidine dimers (TT dimer(s)), and is deficient in patients with XP-variant. Subsequently, these patients are at a far higher risk of non-melanoma skin cancers as the body is unable to tolerate the damage as effectively, leading to severe consequences to each damaged cell.
TLS is a DNA damage tolerance process that allows the DNA replication machinery to bypass damage to the DNA template strand. Whereas most translesion synthesis polymerases have a low fidelity (error prone), XPV protein is believed to have a far greater level of accuracy.
TLS is one of the most complex processes within DNA repair and is yet to be fully understood. The process may, however, be simplified as a trade-off. When a blockage occurs within the DNA strand during replication, the cell has a choice: it can stop the replication process, thus risking chromosomal stability within the cell and likely resulting in cell death. From a cellular perspective, enabling the pyrimidine dimer to remain is preferable to allowing the TT dimer to remain or attempt to repair the dimer in situ, both of which could lead to severe consequences for our genetic stability.
Because the TT lesion has not been eliminated, TLS is a damage tolerance mechanism, enabling damage to remain. This process has subsequently become known as an SOS pathway as it is only initiated once all alternative mechanisms of repair have failed.
Thus, following the presence of a TT dimer in the replication fork, TLS enables DNA replication to continue through switching normal DNA polymerase for DNA polymerase eta, which instructs the DNA strand on how to bypass the lesion and allow cell proliferation, and thus human life, to continue. Figure 3 provides a simplified visualisation of this process.
XPV and Translesional SynthesisXeroderma pigmentosum (XP) is a rare autosomal recessive human disorder that is characterised by extreme sensitivity to ultraviolet radiation. While most XP patients exhibit a defect in nucleotide excision repair, about 20% of patients, the so-called XP-variant (XPV), have a normal excision repair system but are defective in their capacity to replicate lesion containing DNA using POLη.
Although often referred to as a milder subtype, XPV patients still have a far greater risk of non-melanoma skin cancers compared to the general population. The lack of XPV protein leads to a strong blockage of the replication forks in XPV cells, thus causing severe abnormalities within the cell leading to an increased risk of cancer.
While replication can still recover through the action of other alternative DNA repair pathways and polymerases, these polymerases are less efficient in their repair and thus carry the risk of causing point mutations within cells and increasing the risk of oncogenesis. Regrettably, XPV patients are thus forced into a life of sun and ultraviolet light avoidance and systemic photoprotection as a therapy is still lacking.
All living organisms on the planet are subjected to the continual threat of DNA damage. Resultantly, nature has equipped us with a plethora of DNA repair pathways to protect ourselves from the long-term consequences of such attacks. Unfortunately, situations nevertheless arise where damage is not correctly repaired, and cells are forced to adapt and overcome.
Translesion DNA synthesis (TLS) provides an SOS pathway for tolerating irreparable DNA damage. Through specialised DNA polymerases, our body may continue cell proliferation and thus maintain homeostasis, though at a cost. Damage to template strands cannot be repaired and thus the introduction of point mutations within our body increases the collective risk of cancer, especially if the number of mutations is large, or situated next to an oncogene (such as P53).
Leveraging alternative pathways of DNA repair and assisting the body in DNA damage recognition can mitigate the required risk of using SOS pathways. Within the skin – the first line of defence against environmental threats such as ultraviolet radiation – the MC1R signalling axis has shown promise in helping to reduce the risk of oncogenesis and ultimately skin cancer; a topic we will explore further in DNA Repair Communiqué III.