34 replies to this topic

[Kentavr]

I come to the conclusion that senolytics are the wrong directions in life extension. And I have arguments for this.

 

There are many cancer cells in the body of a 30-year-old person, but the immune system effectively destroys them.

With increasing age, the immune system is getting worse at its job, and as a result, the likelihood of cancer increases.

 

I am not suggesting that cancer growth is only caused by a decrease in the function of the immune system. There is evidence that the likelihood of cancer is also closely related to an increase in the rigidity of the extracellular matrix.

 

You can read it here: https://nestarenie.r...nye-metody.html

 

 

As a result of aging, the extracellular matrix becomes more rigid, which creates a favorable environment for the survival and growth of cancer cells [ncbi.nlm.nih.gov/pubmed/25415508]. In the rigid extracellular matrix, constant signals of stiffness can cause cancer cells to no longer respond to possible contact with other cells and continue to grow, and the tumor invades other tissues of the body [ncbi.nlm.nih.gov/pubmed/32540391] [ncbi .nlm.nih.gov / pubmed / 21953606]. Therefore, in old age, cancer is more common.

 

However, simply killing senescent cells will not give you the ability to beat cancer the way you do at a young age. Even if you take senolytics every day, cancer cells will form every minute. You simply won't be able to maintain a critical concentration of senolytic drugs to kill cancer all the time. And even if you take senolytics, you will be crushed by the extracellular matrix. Read carefully the information that is on the link.

 

It was recently discovered that senescent cells of the immune system are potentially some of the most damaging of all senescent cells, as they spread tissue damage and rapid aging to other organs and systems in the body:

https://www.nia.nih....hout-aging-body

 

That is, even if you destroy senescent cells with senolytics, most likely, you will not be able to significantly affect the aging cells of the immune system. One of the reasons for this is that neutrophils play a crucial role in tumor growth and progression:

https://www.ncbi.nlm...les/PMC6659000/

 

Even if you take senolytics, eventually the aging immune system and extracellular matrix will squeeze you. Unfortunately, there is no solution for the extracellular matrix yet, but we can already improve the functioning of the immune system. This is at least something.

 

Based on the foregoing, a more correct strategy would be to rejuvenate your own immune system in order for it to cleanse the body of aging cells by itself, as it did in youth. This strategy will cleanse senescent cells, reduce mortality from infectious diseases and cancer "in one shot." This is a better option.

 

Has anyone, analyzing scientific research, discovered substances that do several things at once: destroy aging cells and reverse the aging of the immune system? Or is there a decrease in the number of senescent cells along with an improvement in the functioning of the immune system?

 

P.S.: Since we are discussing this article in the context of decreasing the number of senescent cells, I posted this topic here.

 

Edited by Kentavr, 07 October 2021 - 05:42 PM.

[cinnabar]

Wouldn't Greg Fahy's work on thymus rejuvenation be the sort of thing you are looking for?

 

 

[Kentavr]

Yes, thymus rejuvenation is an approach that can show remarkable results.

 

Importantly, the rejuvenation of Thymus can eliminate the need to consume senolytics every time. This is a more correct approach.

 

Another approach that may prove very promising is vaccination against senescent cell formation:

 

https://medicalxpres...lls-immune.html

[BrentS]

"Has anyone, analyzing scientific research, discovered substances that do several things at once: destroy aging cells and reverse the aging of the immune system? Or is there a decrease in the number of senescent cells along with an improvement in the functioning of the immune system?"

 

From the below video:

 

 

Hyperbaric Oxygen may be the answer you, and the rest of us, are seeking.  I will be trying that next IF I can do so as a cost effective solution.  38% increase in telomere length and similar reduction in senescent cells is a very good start.

[Kentavr]

Another important reason that senolytics are not really life-prolonging is the following statement. I mean increasing the maximum lifespan.

 

It is important to understand the following statement: 

If you take senolytic drugs, but your extracellular matrix becomes more rigid, you will die.

 

Dmitry Veremeenko, a Russian biohacker, described it in a very interesting and detailed way. You can read his main article on this at this link:

 

https://nestarenie.r...nye-metody.html

 

Indeed: you can destroy old cells as much as you like, but if your extracellular matrix is rigid, it will not save you. In addition to senolytic drugs, you need to increase the elasticity of the extracellular matrix.

 

Otherwise, your body may be beautiful at the funeral, but still lifeless.

 

This is important to understand.

 

None of the senolytics extended the lifespan of long-lived strains of mice more than diet.

 

The mice are dying. At the same time, the mice themselves look great, they have a shiny coat, there is no cataract, etc.

Senolytics appear to only increase average lifespan and do not affect maximum lifespan.

Aging (like the reduced risk of dying with age) lies in other things. Perhaps the extracellular matrix is the key reason (or it is one of the key parameters of aging).

I ask everyone who reads this post to read the full text of the link that I published in this post.

 

You can spend $ 200 million reprogramming cells in anticipation of an increase in maximum lifespan, but if you do not increase the elasticity of the matrix, then the effect will be ZERO!

Edited by Kentavr, 22 December 2021 - 08:21 PM.

[kurt9]

How do we increase the elasticity of the extracellular matrix?

[BrentS]

How do we increase the elasticity of the extracellular matrix?

 

From the above link:

 

Dill extract in vitro increased the expression of the type 1 lysyl oxidase-like extracellular enzyme gene in skin fibroblasts, and also increased skin elasticity in women compared with placebo. This is important because a type 1 lysyl oxidase-like extracellular enzyme initiates covalent crosslinking of elastin precursor molecules (tropoelastin), which is a critical step in the normal maturation of elastin. In 2020, French researchers Vassim Feili and Quentin Bethe and colleagues published the result of an experiment with C57BL6 / J mice. The animals were treated for 3 months with an extract of dill seed powder, which was bred in the drinking water of the animals. Compared with control animals, treatment with dill seed powder extract yielded the following results:

• significant decrease in blood pressure by 11-12%
• reversing age-related heart hypertrophy
• additional newly synthesized elastic fibers in the aortic wall of old mice
• approximately twofold increase in the expression of genes tropoelastin and lysyl oxidase-like extracellular enzyme type 1
• increasing the extensibility of the tissues of the aorta
• decreased modulus of elasticity (Incremental elastic modulus) of the aorta
• Dill polyphenols dose-dependently reduce the activity of elastin-degrading enzymes belonging to the families of serine proteinases, cysteine ​​proteinases and metalloproteinases. Polyphenols reverse age-related elastic fiber calcification by inhibiting alkaline phosphatase activity.

pubmed.ncbi.nlm.nih.gov/31979322

 

[BrentS]

I am unable to edit the above post, I wanted to add:

 

Is there any known lab in the USA or Europe that can measure the elasticity of the extracellular matrix?  In order to experiment, we need to be able to measure.

 

I found this study:

 

https://arxiv.org/ft.../1801.00374.pdf

 

But they are not yet positive that extra cellular matrix is being measured, also the samples were not living.  That is a beginning, but a very long ways to go.

[sensei]

Senolytics are a bit more complex than what your theory allows for.

The main target of senolytics is, by definition, senescent cells.

Senescent cells are old, function poorly, secrete inflammatory cytokines that make other cells act old or even become old. Cancer cells are not considered senescent per se.

The reason most senolytics are actual anti-cancer drugs, or have anti-cancer actions, is because senescent cells use the same pathways as cancer cells to avoid apoptosis.

Senolytics are needed because MTORC1 signaling leads to reduced/dysfunctional autophagy which leads to senescent burden and greater inflammation in a feedback loop.

MTORC1/P3IK pathway inhibition rescues autophagy, reduces inflammation and rejuvenated stem cells.

However, senolytics are needed to clear senescent, and autophagic avoiding abnormal cells.

[sensei]

Senolytics increase the lifespan of OLD mice.

And : "Transplanting small numbers of senescent cells is sufficient to induce physical dysfunction in young mice"

So basically, old cells make young mice old.

https://www.ncbi.nlm...les/PMC6082705/

[sensei]

Real world senolytics show positive effect in humans for age related disease (pulmonary fibrosis)

"Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal cellular senescence-associated disease."

"Physical function evaluated as 6-min walk distance, 4-m gait speed, and chair-stands time was significantly and clinically-meaningfully improved (p < .05)."


https://pubmed.ncbi....h.gov/30616998/

It's not conclusive, yet.

[Castiel]

 

 

Indeed: you can destroy old cells as much as you like, but if your extracellular matrix is rigid, it will not save you. In addition to senolytic drugs, you need to increase the elasticity of the extracellular matrix.

 

 

 

I've heard that white tea can increase the amount of elastin in the extracellular matrix, that should increase elasticity

[timedilation]

I've heard that white tea can increase the amount of elastin in the extracellular matrix, that should increase elasticity

 

Do you have a source on that?  I was looking for ways to increase elastin formation a while back and didn't find very much.

Edited by timedilation, 17 March 2022 - 07:38 PM.

[Mind]

Even if senolytics do NOT increase maximum lifespan, if they increase average lifespan, that's HUGE!

 

Current senolytics are cheap and effective. If they make me more healthy while I wait for better rejuvenation treatments, I will take them.

Edited by Mind, 17 March 2022 - 07:56 PM.

[Castiel]

Do you have a source on that?  I was looking for ways to increase elastin formation a while back and didn't find very much.

 

 

Results showed white tea prevented the activities of the enzymes which breakdown elastin and collagen which can lead to wrinkles that accompany ageing. These enzymes, along with oxidants, are associated with inflammatory diseases such as rheumatoid arthritis

https://www.scienced...90810085312.htm

   I've heard that elastin and collagen breakdown increases with age. 

Edited by Castiel, 18 March 2022 - 03:46 AM.

[timedilation]

Dill extract in vitro increased the expression of the type 1 lysyl oxidase-like extracellular enzyme gene in skin fibroblasts, and also increased skin elasticity in women compared with placebo. This is important because a type 1 lysyl oxidase-like extracellular enzyme initiates covalent crosslinking of elastin precursor molecules (tropoelastin), which is a critical step in the normal maturation of elastin. In 2020, French researchers Vassim Feili and Quentin Bethe and colleagues published the result of an experiment with C57BL6 / J mice. The animals were treated for 3 months with an extract of dill seed powder, which was bred in the drinking water of the animals.

 

Interesting work!  Are there any reputable dill extract products available, or are people mainly making their own from dill seeds?  Also, I'm curious if dill weeds have benefits as well.

[Kentavr]

If you go to the longevity technology website and go to the "research" section, you will find a report called "Senotherapeutics. If you look at Figure 4 (page 25), you will see the main diseases associated with aging cells. 

 

https://longevity.te...peutics-report/

 

After taking a close look at the figure (it illustrates the point very well), I realized the following:

 

1. It is important to avoid diseases caused by aging cells. But! Read point 2.

2. But eliminating even ALL of the diseases listed in the picture is only a very small part of what can be called rejuvenation.

 

Hence point 3.

3. Removing aging cells is not enough to prolong life. By removing senescent cells from the body, we can only avoid the diseases shown in the figure, and reduce the risk of death from those diseases (which is a lot!) but we cannot significantly prolong life with senolytics.

 

Just look at the picture and think about what limited set of diseases we can cure with them!

 

Yes, it will improve our lives, but it won't extend them much. Of course, I am not talking about cases where a person dies as a result of a disease caused by senolytics (for example, a person loses mobility due to sarcopenia or osteoarthritis, and dies more quickly because of it).

 

Yes, I understand that sarcopenia is among the top 5 diseases that cause death in old age. If all people, starting at a certain age, cleared the body of senescent cells, then in a few years the person would die of a disease unrelated to the accumulation of senescent cells.

 

This would affect the Gompertz curve (it would curve out). And the person would have been able to live even to the age of 90. But after that, he would have died just as quickly (e.g. due to the increase in the stiffness of the extracellular matrix).

 

So, senolytics are not a tool for radical life prolongation, but just a medicine. Yes, it is good, yes, it is necessary. But just a medicine.

 

So we need not only senolytics, but something else as well. 

 

 

With the help of senolytics, a person can simply be buried later. He will look prettier with it. Like a mouse that also died: with nice hair and a moustache and no cataracts.

But she still became a corpse.

 

Edited by Kentavr, 29 July 2022 - 10:16 AM.

[johnhemming]

I prefer the approach of fixing senescent cells if that is possible (and it is for quite a few).  The key to this is making the cells capable of producing a bigger range of proteins.  Now I would assume this would also affect the ECM the proteins for which come from cells.  However, only experimentation can give the answer.

[Mind]

 

If you go to the longevity technology website and go to the "research" section, you will find a report called "Senotherapeutics. If you look at Figure 4 (page 25), you will see the main diseases associated with aging cells. 

 

https://longevity.te...peutics-report/

 

After taking a close look at the figure (it illustrates the point very well), I realized the following:

 

1. It is important to avoid diseases caused by aging cells. But! Read point 2.

2. But eliminating even ALL of the diseases listed in the picture is only a very small part of what can be called rejuvenation.

 

Hence point 3.

3. Removing aging cells is not enough to prolong life. By removing senescent cells from the body, we can only avoid the diseases shown in the figure, and reduce the risk of death from those diseases (which is a lot!) but we cannot significantly prolong life with senolytics.

 

Just look at the picture and think about what limited set of diseases we can cure with them!

 

Yes, it will improve our lives, but it won't extend them much. Of course, I am not talking about cases where a person dies as a result of a disease caused by senolytics (for example, a person loses mobility due to sarcopenia or osteoarthritis, and dies more quickly because of it).

 

Yes, I understand that sarcopenia is among the top 5 diseases that cause death in old age. If all people, starting at a certain age, cleared the body of senescent cells, then in a few years the person would die of a disease unrelated to the accumulation of senescent cells.

 

This would affect the Gompertz curve (it would curve out). And the person would have been able to live even to the age of 90. But after that, he would have died just as quickly (e.g. due to the increase in the stiffness of the extracellular matrix).

 

So, senolytics are not a tool for radical life prolongation, but just a medicine. Yes, it is good, yes, it is necessary. But just a medicine.

 

So we need not only senolytics, but something else as well. 

 

 

With the help of senolytics, a person can simply be buried later. He will look prettier with it. Like a mouse that also died: with nice hair and a moustache and no cataracts.

But she still became a corpse.

 

 

Senolytics are cheap, easy to use, and beneficial. I would take anything similar to keep me healthy in the short term while I wait for better rejuvenation therapies. I don't think it is beneficial denigrate this class of therapeutics. They could help a lot of people in the short term - help them survive.

[Kentavr]

Senolytics are cheap, easy to use, and beneficial. I would take anything similar to keep me healthy in the short term while I wait for better rejuvenation therapies. I don't think it is beneficial denigrate this class of therapeutics. They could help a lot of people in the short term - help them survive.

 

I understand this and by no means consider senolytic therapy unnecessary. It is necessary, and it can be very useful for many people.

 

All I'm saying is that it's not enough to prolong life. 

 

I understand the following: 

 

1. There is some "CAUSE" that increases the likelihood of dying as we age. 

 

This reason is not aging cells, because even without aging cells, you will die anyway, whether you have aging cells or not.  Only before that you will not get sick with the diseases that the aging cells are responsible for.

 

2. Because of this "CAUSE" there is a consequence: the accumulation of senescent cells.  And it is very likely that the aging cells are just collateral manifestations. 

 

3. Further, after the age of 90 is a sharp increase in mortality, from which no escape has yet been invented. This is a consequence of a "CAUSE" and it doesn't depend on how many aging cells you have.

 

After the age of 90 you will die along with all your healthy cells. You will die like a mouse that ate too many senolytics.

 

Maybe the cause is the extracellular matrix

Maybe the cause is proteins that slow down cell and tissue repair

It could be due to gradual depletion of microRNA, which causes a person to simply "shut down". Shut down like a biological machine. No programs - no work.

 

Maybe it's all of the above. But from what I understand, this cause is not senescent cells.

Edited by Kentavr, 29 July 2022 - 07:41 PM.

[johnhemming]

My view is that "the cause" is a system that prevents cells from differentiating properly.  Senescent cells are part of this cause in that they secrete SASP which includes IL-10 which engages with the Janus Kinase of other cells which reduces NF Kappa B which cuts SLC25A1 which results in less Acetyl-CoA in the nucleus so the histone is inadequately acetylated and cells become senescent.  This causes a number of the diseases of aging (osteoporosis, sarcopenia - good evidence, NAFLD, Diabestes - hypothesis neither proven or disproven).,

 

This results in increasing mortalitty as people get older (Gompertz).

[Kentavr]

My view is that "the cause" is a system that prevents cells from differentiating properly.  Senescent cells are part of this cause in that they secrete SASP which includes IL-10 which engages with the Janus Kinase of other cells which reduces NF Kappa B which cuts SLC25A1 which results in less Acetyl-CoA in the nucleus so the histone is inadequately acetylated and cells become senescent.  This causes a number of the diseases of aging (osteoporosis, sarcopenia - good evidence, NAFLD, Diabestes - hypothesis neither proven or disproven).,

 

This results in increasing mortalitty as people get older (Gompertz).

 

I have already published a post on how the extracellular matrix acts on cells and how gene expression changes due to this interference.

 

If you think very carefully, then this is logical: the cell has neither eyes nor ears, and it somehow needs to understand what tissue it is in. The cell in the tissue is guided by the degree of rigidity of the environment and adapts to it.

 

Watch this video, I will also post a translation from Russian here (because I am from Russia):

 

https://www.youtube....h?v=2mNyV6tCPsw

 

(0:00 – 0:21) «Our bodies are made up not only of cells, but also of a special environment surrounding cells called the extracellular matrix. The structures of the extracellular matrix - such as muscles, or blood vessels - are largely formed by elastin and collagen fibers, which mechanically press on the surface of the cells. 

 

(0:21 – 0:29) And there are various receptors on the surface of the cells - for example, integrins (which are marked here in yellow).

 

(0:30 – 0:43) When the cell moves along the fiber, these receptors eventually bind to the fibers of the extracellular matrix. And the cell, which thanks to these receptors gets hooked on the fiber, begins to change its shape - to stretch.

 

(0:44 – 1:23) As a result of such tension, signal proteins inside the cell are activated, through which these tension signals are transmitted by the outer cell membrane to the very center of the cell, where the nucleus with the genetic code recorded in DNA is located. 

 

(1:24 – 1:40) If the extracellular matrix is young, elastic, soft, and the matrix fibers are easy to stretch, it does not cause a lot of tension in the cell itself (you will soon see this).

 

(1:41 – 1:49) Here, it shows how when the extracellular matrix is young, the fibers stretch quite easily and the cell itself can deform.

 

(1:50 – 2:13) However, in a rigid matrix (even more so in a matrix with a suboptimal amount of collagen fibers) this interaction with the cell receptors leads to more tension. As a result, the cell adequately responds to the stiffer properties of the matrix, and the stiffness signals are also transmitted via signaling molecules to the cell nucleus, where the DNA code is located.

 

(1:50 – 2:13) Also, depending on the stiffness of the extracellular matrix, the throughput of the ion channels, through which various ions of the intercellular medium enter the cell, also affects the work of the cell's signaling molecules. 

 

(2:28 – 2:24) Stiffness signals from the cell surface and signals of ions entering the cell affect transcription factors located in the cell nucleus - these are the factors that affect the operation of DNA. They, in turn, change how our genes work. 

 

(2:45 – 3:06) Thus, the elasticity and rigidity properties of the extracellular matrix directly and rigidly govern the work of genes, govern the entire fate of the cell. How the DNA molecules are read depends very much on the extracellular matrix.

 

(3:07 – 3:34) If the extracellular matrix is too rigid and inelastic, cell can start to "not feel good", divide slower and slower, produce proteins that don't work properly, age, and lose its ability to divide at all (like the one in the video now)».

 

That is, the extracellular matrix itself directly affects gene expression! This connection is very powerful, because it helps cells navigate where they are and behave accordingly.

 

If the environment in the tissues of the vessels is more rigid, then the genes begin to work in such a way that the cells of the vessels become not smooth muscle cells, but cartilage tissue cells. There is a study on this:

 

https://pubmed.ncbi....h.gov/30581820/

 

The problem of aging lies in a completely different plane, you know?

 

The growth of calcium deposits depending on age (growth is associated mainly with an increase in the rigidity of the extracellular matrix):

 

 

 

Do you see how bad it is?

 

Read all of this text with comments:

 

https://nestarenie.r...nye-metody.html

 

Pay special attention to the fact that it is not possible to extend life after 90 years even in states with developed medicine (because the main problem is not solved: the increase in the rigidity of the extracellular matrix). You will simply die with all your healthy cells. Like a lab mouse that's gorged on senolytics.

 

The simple removal of senescent cells is an improvement in one's own health. But, apparently, it has nothing to do with real life extension.

 

Senolytics will simply increase the average life expectancy, and nothing more. After 90 years people will still die like flies. Even if they overeat with senolytics. Because they will be compressed by "steel cables" of the extracellular matrix penetrating every organ and every vessel.

 

This is a very terrible truth. But if you really want to defeat AGING, then it seems that you need to lead the direction of research towards the extracellular matrix.

Edited by Kentavr, 01 August 2022 - 08:21 AM.

[johnhemming]

I would assume that the extracellular matrix is generated by the cells, however.

 

We will not necessarily agree on this issue today and I accept the ECM is important, but one has to assume it is generated by the cells.  Hence cellular improvements should result in skin improvements, the largest component of which is the ECM.

[Kentavr]

I would assume that the extracellular matrix is generated by the cells, however.

 

We will not necessarily agree on this issue today and I accept the ECM is important, but one has to assume it is generated by the cells.  Hence cellular improvements should result in skin improvements, the largest component of which is the ECM.

 

I ask you to think about the following:

 

1. The production of substances for the extracellular matrix is ​​produced by cells.

2. At the same time, the type of substances that cells produce depends on the rigidity of the extracellular matrix.

3. The rigidity of the extracellular matrix gradually increases due to the accumulation of crosslinks, destruction of elastin and a decrease in the level of hyaluronic acid.

 

As a result, the cell thinks that it enters the bone environment and begins to intensively deposit calcium compounds.

 

Rigidity increases.

 

As a result, according to the laws of system dynamics, a "feedback loop" is formed: more calcium --- more rigidity --- more calcium, etc.

 

That is, in fact, the matrix with the help of rigidity, in fact, dictates how the cells function.

 

Therefore, I see a fundamental error in your answer. In fact, it's exactly the opposite: it is the extracellular matrix that regulates what the cell will produce.

Edited by Kentavr, 01 August 2022 - 08:35 AM.

[johnhemming]

So we disagree.  I accept that as usual there are feedback systems, but in the end we start out with cells without the ECM and that develops over time.

 

The objective is to improve cells including the ECM hence experimentation can determine whether it is possible to improve the ECM by improving the cells.  That could be seen by improvements in skin following action which improves the functioning of cells.

[Kentavr]

So we disagree.  I accept that as usual there are feedback systems, but in the end we start out with cells without the ECM and that develops over time.

 

The objective is to improve cells including the ECM hence experimentation can determine whether it is possible to improve the ECM by improving the cells.  That could be seen by improvements in skin following action which improves the functioning of cells.

 

There is a cross-link in collagen called glucosepane:

 

https://en.wikipedia...iki/Glucosepane 

 

They gradually accumulate with age. Because of these stitches, the matrix becomes more and more rigid. and, believe me, these cross-links do not care what kind of cell modification you are currently carrying out. They are not destroyed by any enzyme.

 

Here the problem is fundamental. The cell will not be able to break this crosslink. Stiffness will still increase, regardless of your modifications.

 

This is PHYSICS.

Edited by Kentavr, 01 August 2022 - 08:55 AM.

[Mind]

Just wanted to highlight that this is a great LongeCity discussion. There is disagreement but everyone can learn a lot and think critically about senolytics through the data and ideas presented.

[johnhemming]

My understanding is that ECM turnover breaks down all of the ECM including Glucosepane.

[Kentavr]

How tired of the clowns in the longevity industry!

 

They deliberately shorten telomeres, after that they give a drug that increases telomeres, and write: "We have extended the life of mice by 100%!"

 

They initiate cell aging with free radicals, provide senolytics, and then shout: "We have extended life by 50% with the help of senolytics!"

 

 

Hey clowns! You are not testing drugs for aging, you are developing drugs to lengthen telomeres, drugs to kill senescent cells, and so on. But not from aging!

 

And you try to take AT LEAST a long-lived mouse and extend her life at least 20% more than a diet does! You can not???   

 

 

How rotten this industry is! HOW can you do such a bad research design, and then beat yourself in the chest that WE DEVELOPED A CURINE FOR AGING!

 

This is a lie!

 

Moreover, such drugs would not work in humans because the individual would most likely die from microglia depletion caused by aging of the extracellular matrix

(the real cause of Alzheimer's disease)

 

Test medicines at least on a chimpanzee!

 

First on body tissues (OLD BODY TISSUES!!! TOGETHER WITH THE OLD EXTRACELLULAR MATRIX!!!), and then test on chimpanzees!

 

It is necessary to clean the longevity industry from charlatans!

Edited by Kentavr, 07 August 2022 - 03:12 PM.

[Avatar of Horus]

IMHO another serious question needs to be considered in senolytics, which is rarely mentioned,

namely that the neurons - which are post-mitotic cells - also develop a senescent-like state, and if these are removed too that can have catastrophic effects in humans.