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#61 RE: Junges Blut von lupor 15.04.2020 16:25

Zitat von Prometheus im Beitrag #60

Und vor allem: Basierend auf dem aktuellen Wissensstand werden auch Ansätze zur Verjüngung geschildert. Interessiert?

Schön, dass auch DNA-Reperaturmechanismen angesprochen werden. Nicht selten führt die Reperatur eines DNA-Bruchs zu irreversiblem Informationsverlust:
Wenn man dann mit zunehmendem Alter immer mehr solcher DNA-Schäden akkumuliert, ist das sicher nicht so toll... Hat jemand einen Lösungsvorschlag?

#62 RE: Junges Blut von Prometheus 15.04.2020 17:13


Zitat von lupor im Beitrag #61

Schön, dass auch DNA-Reperaturmechanismen angesprochen werden. Nicht selten führt die Reperatur eines DNA-Bruchs zu irreversiblem Informationsverlust:
Wenn man dann mit zunehmendem Alter immer mehr solcher DNA-Schäden akkumuliert, ist das sicher nicht so toll... Hat jemand einen Lösungsvorschlag?
Die Autoren des Papers erklären, dass im Laufe der Alterung zwei Signalwege herunterreguliert werden: NER (nucleotide excision repair) und NHEJ (nonhomologous end-joining) Diese beiden Signalwege müssen aktiviert werden!

Dafür haben wir schon ein paar Ideen gesammelt: DNA-Reparatur aktivieren

#63 RE: Junges Blut von Prometheus 05.05.2020 12:38


Eine Senolyse funktioniert auch über hormonelle(?) Faktoren im Blut:

Heterochronic parabiosis regulates the extent of cellular senescence in multiple tissues.

#64 RE: Junges Blut von Scout 11.05.2020 09:25

Age Reduction Breakthrough
by Josh Mitteldorf
If you eschew hyperbole and hang in for the long haul, maintaining a discipline of understatement in the midst of a flashy neon world, you may be offered a modicum of credence when you make an extraordinary announcement. No one is entitled to this courtesy twice. If the news that you trumpet to the moon does not pan out, your readers will be justified in discounting everything you say thereafter.

Here goes.

I believe major rejuvenation has been achieved in a mammal, using a relatively benign intervention that shows promise of scaling up to humans. I’m going to stake my reputation on it.

Cartoon by Maddy Ballard

In the race to effect substantial, system-wide rejuvenation, Harold Katcher is a dark horse. He has the right academic credentials and a solid history of research. In fact, in earlier life he was part of a team that discovered the breast cancer gene, brca1. I asked Harold for a biographical sketch, and have printed it in a box at the end of this posting.

But Katcher has no research grants or university lab or venture capital funding, no team of grad students mining databases and screening chemicals in the back room.

One thing Katcher has going for him is the correct theory. Most of the explosion in aging research (and virtually all the venture capital startups) are looking to treat aging at the cellular level. Their paradigm is that aging is an accumulation of molecular damage, and they see their job as engineering of appropriate repair mechanisms.

The truth, as Katcher understands it, is that, to a large extent, aging is coordinated system-wide via signal molecules in the blood. It was our common realization of this vision that brought Katcher and me together more than a decade ago. Katcher briefly describes his 2009 epiphany below. It was the source of his 2013 essay (it took a few years to get it into print) on the significance of parabiosis experiments for the future of aging science.

Of course, Katcher was not the only one to get the message about the power of signal molecules in the blood to reprogram tissues to a younger state throughout the body. The problem is that there are thousands of constituents represented in tiny concentrations in blood plasma, but conveying messages that cells read. Which of these are responsible for aging? A small number of labs, including the Conboys at Berkeley, Amy Wager at Harvard, and Tony Wyss-Coray at Stanford have been searching for the answer over the last decade and more.

Katcher has been able to guess or intuit or experimentally determine the answer to this question. With seed funding from Akshay Sanghavi, he set up a lab in Bangalore two years ago, and tried to rejuvenate old lab rats, using a fraction extracted from the blood of younger rats. The first round of experiments were encouraging, published in this space a year ago. He obtained the next round of funding from a reader of this blog, and had enough rats to titrate dosages experimentally, and to see if treated rats who aged again over time could be re-treated successfully.

There is a hole in this story that awaits the resolution of intellectual property rights. Katcher and Sanghvi have not applied for patents and have not yet found a suitable partner to provide financing for human trials. They have not revealed any details of the treatment, besides the fact that it is in four intravenous doses, and that it is derived from a fraction of blood plasma. Katcher thinks that the molecules involved will not be difficult to manufacture, so that when a product is eventually commercialized, it will not require extraction from the blood of live subjects, rodent or human.

We’re still waiting for longevity curves of these treated rats. In the meantime, the best available surrogate measure of age comes from methylation clocks, as developed by Steve Horvath at UCLA, and other scientists as well. Crucially, Katcher found an ally in Horvath, who didn’t just test his rejuvenated rats, but did the needed statistical analysis to develop a set of six methylation clocks specialized to rats. FIve of the clocks are optimized for different tissues, and one is calibrated across species, so that it can measure age in humans as well as corresponding age in “rat years” (about 1/40 human year). The two-species clock was a significant innovation, a first bridge for translating results from an animal model into their probable equivalent in humans.

In a paper posted to BioRxiv on Friday, Katcher and Horvath report results of the methylation measurements in rejuvenated rats. “Crucially, plasma treatment of the old rats [109 weeks] reduced the epigenetic ages of blood, liver and heart by a very large and significant margin, to levels that are comparable with the young rats [30 weeks]....According to the final version of the epigenetic clocks, the average rejuvenation across four tissues was 54.2%. In other words, the treatment more than halved the epigenetic age.”

Human-rat clock measure of relative age defined as age/maximum species lifespan.

Besides the methylation clock, the paper presents evidence of rejuvenation by many other measures. For example:

IL-6, a marker of inflammation, was restored to low youthful levels
Glutathione (GSH), superoxide dismutase (SOD), and other anti-oxidants were restored to youthful levels
In tests of cognitive function (Barnes maze), treated rats scored better than old rats, but not as well as young rats.
Blood triglycerides were brought down to youthful levels
HDL cholesterol rose to youthful levels
Blood glucose fell toward youthful levels
A major question in blood plasma rejuvenation experiments has been how often the cure must be administered. Many of the components of blood plasma are short-lived, secreted into the blood and absorbed continuously throughout the day. The good news from Katcher’s results is that it seems only four injections are needed in order to achieve rejuvenation.

A second question which these experiments resolve is whether rejuvenation requires both adding and removing molecular species from the blood plasma. For example, pro-inflammatory cytokines are found in old blood at much higher levels. Irina and Mike Conboy, people who I regard as most credible in the field, have said that removing bad actors from the blood is probably more important than restoring youthful levels of beneficial signals. They were grad students at Stanford 15 years ago, when the modern wave of parabiosis science was initiated, and have pursued the subject continuously ever since. Katcher’s experiments have achieved their results only by adding blood components, not by removing or even neutralizing others.

In Katcher's experiments, molecular species were added, but nothing was removed. This suggests that he has found the necessary formula for re-programming epigenetics, so that lower levels of the bad actors occur as a result. But it remains to be seen whether even better results can be obtained if some plasma constituents are removed.

A question that remains unresolved concerns the location and mechanism of the aging clock. I have been undecided over the years between two models:

There is a central aging clock, perhaps in the hypothalamus, which keeps its own time and transmits signals throughout the body that coordinate methylation state of dispersed tissues
Information about epigenetic age is dispersed through the body, and the body's clock is a feedback loop that is continually updating methylation age locally in response to signals received about the methylation age globally.
There is a suggestion in the data that the hypothalamus may be more difficult to rejuvenate than other tissues. Does it play a more important role than other tissues in coordinating the age of the entire body? Horvath (personal communication) counsels caution in drawing this inference until measurements are corroborated and more experiments are done.

The Bottom Line

These results bring together three threads that have been gaining credibility over the last decade. Mutually reinforcing, the three have a strength that none of them could offer separately.

The root cause of aging is epigenetic progression = changes in gene expression over a lifetime.
Methylation patterns in nuclear DNA are not merely a marker of aging, but its primary source. Thus aging can be reversed by reprogramming DNA methylation.
Information about the body’s age state is transmitted system-wide via signal molecules in the blood. Locally, tissues respond to these signals and adopt a young or an old cellular phenotype as they are directed.

Harold Katcher, Biographical Sketch

So, you might consider me a late bloomer. While I have thousands of citations in the literature, with publications ranging from the discovery of the human ‘breast cancer gene’, to protein structure, bacteriology, biotechnology, bioinformatics, and biochemistry, there was no center or direction to my work as I had given up my personal goal of solving/curing aging when I learned that ‘wear and tear’ was the cause of it. Yet something happened in year 1985 when I was in California working with Michael Waterman and Temple Smith (fathers of bioinformatics) that is inexplicable: I found myself in Intensive Care with a tube inserted into my trachea and the knowledge that I might not live. And then I had a dream: I dreamed that somehow in the far future (and on another world), I was being feted for ‘bringing immortality to mankind’. Clearly, I survived that incident (started with an infected tooth). I lived a wonderful life – becoming a computer programmer (which I loved), leaving that for the University of Maryland’s Asian division, becoming a full professor and then the Academic Director for the Sciences, in Tokyo, Japan. By the time I left Japan in 2004, (my daughter Sasha was a fourth-grader, (yonensei), in the Japanese school system), I was teaching for U of M online – somewhat retired, and looking forwards to writing computer programs for fun and profit. Yet I never ever forgot that dream. It was clearly impossible; I had no lab – and really, there was no way to repair all damaged cells – it’d be like sweeping back the ocean. And then, in 2009, I read an old paper from 2005, a paper written by the Conboys, (Michael and Irina), Tom Rando and others, coming from Irv Weisman’s lab, that completely changed my life; that showed me that everything I believed about aging was wrong – that aging occurred at the organismic level, not at the cellular level and could be reversed. Well, the rest of the story is about persistence and the blessed intervention of Akshay Sanghvi who too saw there was another way and provided the structural, monetary, and emotional support (and some good ideas) that had me start a new career at age 72 in Mumbai, India. I feel twenty years younger than I did three years ago, I guess that’s another hint about aging. Now the ‘mystical’ dream? It wouldn’t be the first time in history that that happened – take that as a datum.

#65 RE: Junges Blut von Prometheus 11.05.2020 15:48


Ich bin begeistert - da ist endlich mal genau in die richtige Richtung geforscht worden!
Die vorab publizierten Daten sehen wirklich SEHR VIELVERSPRECHEND AUS!

Trotzdem ein paar kritische Anmerkungen von mir dazu:

-Es hat noch kein Peer Review Verfahren stattgefunden.
-Die Autoren haben finanzielle Intressen deklariert (muss nicht verkehrt sein, könnte aber durchaus dazu motivieren, die Daten "aufzuhübschen")
-Unklar ist außerdem, ob das Epigenom wirklich DAUERHAFT verjüngt bleibt im Vergleich zur Kontrollgruppe.
-Die Etablierung der epigenetischen Uhr wird ausführlich geschildert, aber bei Material und Methoden wird die eigentliche "Verjüngungskur" nur sehr unscharf beschrieben:

We used a unique plasma fraction "Elixir" developed by Nugenics
Research. The necessary dose of plasma fraction treatment was prepared and injected
intravenously using sterile saline as vehicle. The calculated doses were administered
intravenously to the animals of old treated group; 4 injections every alternate day for 8 days,
and a second dosing starting from the 95th day consisting of 4 injections every alternate day
for 8 days, as shown in Supplementary Figure 4.

Klar, dass sich die Firma hier nicht in die Karten schauen lassen möchte. Allerdings ist das der zentrale Baustein der Story!

Die Vorab-Publikation zum Nachlesen:

#66 RE: Junges Blut von Scout 08.06.2020 06:51

Out With the Old Blood
Posted on June 8, 2020
There is great promise in 2020 that we might be able to make our bodies young without having to explicitly repair molecular damage, but just by changing the signaling environment.

Do we need to add signals that say “young” or remove signals that say “old”?

Does infusion of biochemical signals from young blood plasma rejuvenate tissues of an old animal? Or are there dissolved signal proteins in old animals that must be removed?

For a decade, Irena and Mike Conboy have been telling us removal of bad actors is more important. But just last month, Harold Katcher reported spectacular success by infusing a plasma fraction while taking away nothing. Then, last week, the Conboys came back with a demonstration of the rejuvenating power of simple dilution.
[Link to their new paper]

Dilution procedure

They simply replaced half of the blood plasma in 2-year-old mice with a saline solution containing 5% albumin. What is albumin? Blood plasma is chock full of dissolved proteins, about 10% by weight. About half of these are termed albumin. Albumin is the generic portion. It doesn’t change through the lifetime. It doesn’t carry information by itself. But albumin transports nutrients and minerals through the body.

The Conboys took care to show that albumin has no rejuvenation power on its own, and had nothing to do with their experimental results. Rather, they had to replenish albumin in diluting blood, because the animals would be sickened if half their albumin were removed. Replacing the albumin in a transfusion is akin to replacing the volume of water or maintaining the salinity.

In preparation for this experiment, the Conboys have invested years in miniaturizing the technology for blood transfusions, so that mice can be subjected to the same procedures that are commonplace in human hospitals.


The Conboy lab replaced 50% of mouse blood plasma. They got spectacular results with a single treatment, based on a lucky guess. They have not yet experimented with 30% or 70%. They don’t know yet how long the treatment will last and how long it needs to be repeated.

Evidence of rejuvenation

As with previous papers from the Conboy lab, the group focused on repair and stem cell activity as evidence of a more youthful state. Three separate tissue samples were taken from liver, muscle, and brain.

“Muscle repair was improved, fibrosis was attenuated, and inhibition of myogenic proliferation was switched to enhancement; liver adiposity and fibrosis were reduced; and hippocampal neurogenesis was increased.”

They measured nerve growth factors in the brain, and detected a more robust response, typical of young mice
They lacerated muscles and showed repair rates typical of much younger animals
They examined microscope slides of liver tissue, and showed that it is less fatty and striated than is typical of older mice

Figure 2. Rejuvenation of adult myogenesis, and albumin-independent effects of TPE. One day after the NBE, muscle was injured at two sites per TA by cardiotoxin; 5 days later muscle was isolated and cryosectioned at 10 µm. (A) Representative H&E and eMyHC IF images of the injury site. Scale bar = 50 µm. (B) Regenerative index: the number of centrally nucleated myofibers per total nuclei. OO vs.ONBE p = 0.000001, YY vs ONBE non-significant p = 0.4014; Fibrotic index: white devoid of myofibers areas. OO vs ONBE p = 0.000048, YY vs YNBE non-significant p = 0.1712. Minimal Feret diameter of eMyHC+ myofibers is normalized to the mean of YY [9]. OO vs. ONBE p=3.04346E-05, YY vs. YNBE p=0.009. Data-points are TA injury sites of 4-5 YNBE and 5 ONBE animals. Young and Old levels (detailed in Supplementary Figure 1) are dashed lines. Representative images for YY versus YNBE cohorts are shown in Supplementary Figure 6. (C) Automated microscopy quantification of HSA dose response, as fold difference in BrdU+ cells from OPTI-MEM alone (0 HSA). There was no enhancement of myogenic proliferation at 1-16% HSA. N=6. (D) Meta-Express quantification of BrdU+ cells by automated high throughput microscopy for myoblasts cultured with 4% PreTPE versus PostTPE serum and (E) for these cells cultured with 4% of each: PreTPE serum + HSA or PostTPE serum + HSA. Significant increase in BrdU positive cells is detected in every subject 1, 2, 3, and 4 for TPE-treated serum (p=0.011, <0.0001, <0.0001, 0.0039, respectively), as well as for TPE-treated serum when 4%HSA is present (p<0.0001, <0.0001, <0.0001, =0.009 respectively). N=6. (F) Scatter plot with Means and SEM of all Pre-TPE, Post-TPE, +/- HSA cohorts shows significant improvement in proliferation in Pre TPE as compared to and Post TPE cohorts (p*=0.033), as well as Pre+HSA and Post+HSA cohorts (p*=0.0116). In contrast, no significant change was observed when comparing Pre with Pre+HSA (p=0.744) or Post with Post+HSA (p=0.9733). N=4 subjects X 6 independent assays for each, at each condition. (G) Representative BrdU IF and Hoechst staining in sub-regions of one of the 9 sites that were captured by the automated microscopy. Blood serum from old individuals diminished myogenic cell proliferation with very few BrdU+ cells being visible (illustrated by one positive cell in Pre-TPE and arrowhead pointing to the corresponding nucleus); TPE abrogated this inhibition but HSA did not have a discernable effect.

What’s missing? They did not test any measures of physical or cognitive performance at the level of the organism.
Evidence of behavioral changes (learning and memory, endurance, strength)
Inflammatory markers
Blood lipids
Methylation clock (Horvath, UCLA) or proteomic clock (Lehallier, Stanford)
Some of this is planned for future research. Mike and Irina plan to submit tissue samples for analysis by the Horvath mouse methylation clock.


I am a committed enthusiast for the methylation and proteomic clocks that are the best surrogates we have for aging. These technologies can tell us whether anti-aging interventions have been effective without having to wait for animals (or humans) to die before reporting results. But the Conboys still regard these technologies as unproven, and they bristle at the word “clock”. The closest they come is to catalog the entire proteome of treated mice, comparing it to untreated young and old mice.

Multi-dimensional t-SNE analyses and Heatmapping of these data revealed that the ONBE proteome became significantly different from OO and regained some similarities to the YY proteome. Supplementary Figure 4 confirms the statistical significance of this comparative proteomics through Power Analysis, and shows the YY vs. OO Heatmap, where the age-specific differences are less pronounced than those between OO vs. ONBE, again emphasizing the robust effect of NBE on the molecular composition of the systemic milieu.

Translation: As controls, they had mice that underwent plasma exchange with mice of similar age. YY were young, positive controls, and OO were old, negative controls. Treated mice were ONBE=”Old—Neutral Blood Exchange”. Rather than relying on “clock” algorithms that compute an age from the proteome, they compared the entire proteomes of test animals with those of old and young animals, and foud that they resembled the young animals more closely.

Aging and epigenetics

I was an early advocate of the theory that aging is driven primarily by changes in epigenetics. Other proponents include Johnson, Rando, and Horvath. This theory is now mainstream, though its acceptance is far from universal. (The main reason people have difficulty with the idea is the question, “why would the body evolve to destroy itself?” I present a comprehensive answer in my popular book and my academic book.)

On the face of it, the new Conboy result is powerful evidence for the epigenetic theory. They have shown that there are proteins in the blood that actively retard growth and healing. Remove half theses proteins and the animals are able to grow youthful tissues and to heal better. The obvious conclusion is that, with age, there are signaling changes in the blood that weaken the animal and inhibit repair.

There are, however, other ways to interpret the changes. Aubrey de Grey has said (personal communication)

“When everything in the blood except the cells and the albumin is replaced by water, the body will definitely respond by synthesising and secreting everything that it detects a shortage of, whereas the bad stuff will not be so rapidly replaced, since by and large it was only there in the first place as a result of impaired excretion/degradation.”

The Conboys don’t embrace the programmed aging perspective, but neither is their understanding of what they see the same as Aubrey’s. The way Irina explained it to me is that the age of the biological of the body is simply a measure of how much damage has accumulated, but that cycles of epigenetics and catalysis are self-reinforcing.

“Epigenetic, mRNA, and protein are steps of one process, regulation of gene expression. And none of these steps are permanent they all actively and constantly respond to cell environment — tissue and systemic milieu…With aging there is a drift which is re-calibrated by a number of rejuvenation approaches…When an auto-inductive age-elevated ligand is diluted, it cannot activate its own receptor and induce its own mRNA, so ligand levels diminish to their younger states for prolonged time.”

The Conboys theorize that these harmful proteins are part of a positive feedback loop, in other words, a cycle that is self-sustaining

epigenetic state ⇒ gene expression ⇒ translation to circulating proteins ⇒ feedback that alters the epigenetic state

With age, the body has slipped into a dysfunctional, self-sustaining cycle, and with the shock of disruption, they are able to nudge it back into a more robust and youthful cycle, also self-sustaining.

Figure 6. Model of the dilution effect in resetting of circulatory proteome. System: A induces itself (A, red), and C (blue); A represses B (green), C represses A. A dilution of an age-elevated protein (A, at D1: initial dilution event), breaks the autoinduction and diminishes the levels of A (event 1, red arrow); the secondary target of A (B, at event 2 green arrow), then becomes de-repressed and elevated (B induces B is postulated); the attenuator of A (C, at event 3 blue arrow), has a time-delay (TD) of being diminished, as it is intracellular and was not immediately diluted, and some protein levels persist even after the lower induction of C by A. C decreases (no longer induced by A), and a re-boot of A results in the re-induction of C by A (event 4 blue arrow) leading to the secondary decrease of A signaling intensity/autoinduction, and a secondary upward wave of B (events 5 red arrow and 6 green arrow, respectively). alpha = 0.01, kc = 0.01, beta = 0.05, epsilon = 0.1, ka = 0.1. Protein removal rates from system: removalA = 0.01, removalB = 0.1, removalC = 0.01, Initial values: initialA = 1000, initialB = 400, initialC. = 700

For me, the surprising thing in Irina’s account is that there is no hysteresis in this system. The reprogramming responds to changes in the blood levels of signals within minutes. There is no homeostasis in such a system. I wonder how that can be. Life is all about homeostasis, and intuitively, we all imagine that negative feedback loops are more common than positive feedback loops. (Negative feedback loops lead to homeostasis; positive feedback loops lead to runaway, exponential change.)

Is there a clock somewhere? Is the brain special?

In the Conboy view, signals in the blood are emitted from all over the body, and not especially from the hypothalamus. If brain tissue responds in a seemingly exceptional way to proteins in the blood, it is because of selective passage of those proteins by the blood-brain barrier.

The authors remind us that in past parabiosis experiments (where blood is exchanged between old and young mice), the brain tissue of the young mice grew older but brains of the old mice didn’t get younger. This was an indication that brain aging is caused by affirmative action of “bad actors” in the plasma, and that these are able to penetrate the blood-brain barrier. This observation was part of the inspiration for the current experiments.

The corresponding procedure in humans is already FDA approved

Therapeutic Plasma Exchange (TPE) is a well-established medical procedure, and has already been performed on an experimental basis by co-author Dobri Kiprov. There is anecotal history of suggestive results, which I will write about in my next post.

Comparison with Katcher’s Elixir

This week’s announcement from the Conboys and last month’s preprint from Katcher/Horvath come from the same school of thought: that aging is coordinated through the body by signal molecules in the blood. Both demonstrated dramatic rejuvenation in rodents based on a short-term intervention, and both have plans for commercialization and human trials to begin ASAP.

So it is curious that in other ways, the programs of Katcher and Conboy are so different.

While both approaches are rooted in differing compositions of blood plasma between young and old, the Conboys focus exclusively on removing species that are inhibiting youthful regeneration, while Katcher’s approach is to add back the proteins that formerly kept the animal young.
The Conboys have fully disclosed all aspects of their experimental protocol, whereas the content of Katcher’s elixir remains a trade secret.
Katcher is on the fringe of academic research, and the Conboys’ lab is at one of the premier academic institutions in the world.
Katcher is a year further along, having experimented with different dosages and timings. Neither Katcher nor the Conboy lab has yet demonstrated life extension.
The Conboys demonstrate rejuvenation with wound healing, tissue structure, and renewal of nerve growth. Katcher’s claim is based on physiology (especially inflammation), cognitive performance, and methylation clock algorithms.
In fact, Katcher regards restoration of youthful methylation patterns as the best evidence he could offer for rejuvenation (I agree), while the Conboys are reserving judgment about the importance of methylation, and bristle at the language of a methylation “clock”.
Katcher understands the effects of plasma transfusions in terms of a broad theory (which I support). Aging is an epigenetic program, governed and enforced by a “clock” that operates via a feedback loop between circulating proteins that govern gene expression and gene expression that generate those proteins. The Conboys recognize they are working this feedback loop (their Fig 6) but they resist the theory that it is the essential cause of aging.
My guess is that a combination of their two approaches will be necessary for full remediation of aging, and that a combination of their resources, credibility, theoretical foundations, and contacts would be a transformative event for medical science, for biotech industry, and for biological theory. It is my fervent hope that Katcher and the Conboys might work together.

#67 RE: Junges Blut von Prometheus 08.06.2020 13:44



Ich finde das Thema absolut genial!
Wir sollten hier gemeinsam dringend auch mal ein paar praktische Aspekte diskutieren!

#66 Grob zusammengefasst:
Der gesamte Organismus kann sich verjüngen, wenn das Plasma verdünnt wird!

Und das beste daran: Dieser Effekt ist nicht nur temporär, sondern offenbar sogar länger anhaltend!

#68 RE: Junges Blut von Prometheus 09.06.2020 17:50


Gut, dann diskutiere ich hier mal alleine weiter...

These: Im Blutplasma existieren Signalstoffe, die den Zellen signalisieren, wie alt sie sich zu verhalten haben.

Etwas korrekter formuliert: Die Epigenetik der Zellen wird von Signalstoffen aus dem Blutplasma beeinflusst. Im alten Organismus zirkulieren also Botenstoffe, die die epigenetische Uhr der Zellen auf "alt" programmieren.

Einige dieser Signalstoffe sind bereits bekannt. Josh Mitteldorf hat sie vor ca 7 Jahren mal in seinem Blog übersichtlich aufgelistet:

Molecules in the Blood that Signal Self-Destruction

Es geht also darum, diese (und möglicherweise weitere) ungewünschte Signalstoffe aus dem Blutplasma zu entfernen. Erst wenn der "Blutplasma-Taktgeber" wegfällt, haben die Zellen die Chance, sich epigenetisch auf jung umzuprogrammieren.
An verschiedener Stellen haben wir hier im Forum bereits über epigenetische Reprogrammierung gesprochen und darüber, mit welchen Biohacks man sie möglicherweise anstoßen kann.

Was aber, wenn der "Blutplasma-Taktgeber" eine effektive Umprogrammierung verhindert?

Jeden einzelnen Botenstoff spezifisch aus dem Blut herauszubekommen klingt extrem kompliziert - und ist es vermutlich auch (Man denke an irgendwelche Antikörper-Therapien oder Nanobots, die im Blutstrom mitschwimmen und den Job erledigen sollen...)

Was aber, wenn eine simple Plasmaverdünnung völlig ausreicht um den "Blutplasma-Taktgeber" vorrübergehend abzuschalten?
Was, wenn wir dann NACH einer Plasmaverdünnung (die ja an sich schon Verjüngungseffekte hat) noch zusätzlich epigenetisch reprogrammieren?
Was, wenn wir anschließend noch Signalstoffe hinzufügen, die für ein junges Körpermilieu typisch sind?

#69 RE: Junges Blut von Joker 09.06.2020 17:56

Zitat von Prometheus im Beitrag #68
Gut, dann diskutiere ich hier mal alleine weiter...

These: Im Blutplasma existieren Signalstoffe, die den Zellen signalisieren, wie alt sie sich zu verhalten haben.

Etwas korrekter formuliert: Die Epigenetik der Zellen wird von Signalstoffen aus dem Blutplasma beeinflusst. Im alten Organismus zirkulieren also Botenstoffe, die die epigenetische Uhr der Zellen auf "alt" programmieren.

Joaa, fast genau getroffen.

Im jungen Organismus/Blut sind Hormone, genauer gesagt Zellkernhormone, die den Organismus auf jung programmieren. Denen bin ich schon länger auf der Spur.

Es sind halt noch nicht alle bekannt, aber ich weiß zumindest ungefähr wie die aussehen!

Zitat von Prometheus im Beitrag #68

Einige dieser Signalstoffe sind bereits bekannt. Josh Mitteldorf hat sie vor ca 7 Jahren mal in seinem Blog übersichtlich aufgelistet:

Molecules in the Blood that Signal Self-Destruction

Klar, gibt auch negative Signalgeber, aber diese sind nicht entscheidend. Mitteldorf liegt hier falsch, nur meine Meinung.

Das entscheidende ist, was in dem jungen Blut an positiven Signalgebern drin ist, und das sind die Zellkernhormone.

Das jeweilige Zellkernhormon ist der Schlüssel, um an die (junge) Zellkerninformation zu kommen. Schlüssel-Schloss-Prinzip! Ohne den Schlüssel geht gar nichts!

Das mit dem Blut ist wurstegal. Vampirismus bringt uns auch nicht weiter, sondern nur schlimmstenfalls HIV. Es geht um die Hormone! Man bräuchte einfach eine komplette Liste aller Zellkernhormone und dann kann man ja die benötigten Mengen durch Ausprobieren an Mäusen herausfinden. Wäre easy, wenn man das Prinzip mal verstanden hat.

Diese Zellkernhormone kann man leicht synthetisch herstellen.

Ich sag's mal so, Prometheus. Wenn 2 Profis wie wir zusammenarbeiten, haben wir spätestens in 2 Jahren die wichtigsten Zellkernhormone aufgelistet und können uns an die Verjüngung machen.

#70 RE: Junges Blut von Nurdug 09.06.2020 18:34

Ich sag's mal so, Prometheus. Wenn 2 Profis wie wir zusammenarbeiten, haben wir spätestens in 2 Jahren die wichtigsten Zellkernhormone aufgelistet und können uns an die Verjüngung machen.

Jo, Ihr Superkerle, dann legt mal los, damit wir alle noch was davon haben

Joker, warum gehst Du davon aus, dass die Zellkernhormone andere sind, als die, die wir schon kennen?
Sind es vielleicht eher die Mengen, die vorhanden sind?
Oder irgend welche Metaboliten der bekannten Hormone?

#71 RE: Junges Blut von Joker 09.06.2020 18:39

<ignore nurdug>

#72 RE: Junges Blut von Nurdug 09.06.2020 18:43

Was meinst Du damit?

#73 RE: Junges Blut von Prometheus 10.06.2020 11:26


Zitat von Joker im Beitrag #69

Klar, gibt auch negative Signalgeber, aber diese sind nicht entscheidend. Mitteldorf liegt hier falsch, nur meine Meinung.

Das entscheidende ist, was in dem jungen Blut an positiven Signalgebern drin ist, und das sind die Zellkernhormone.


Das mit dem Blut ist wurstegal. Vampirismus bringt uns auch nicht weiter, sondern nur schlimmstenfalls HIV.

Ja, es gibt negative und positive Signalgeber im Blut!

Was hier bisher uns allen allen entgangen ist: Es ist vergleichsweise leicht, sie zu beeinflussen!

Dafür muss man kein Vampir werden!

Es geht um die Methode aus Post #66. Eine simple Verdünnung des Blutplasmas, und das gesamte System stellt sich auf jünger ein. Einfacher geht es wirklich nicht!!!

Hat jemand eine Idee, von welcher einfachen Maßnahme ich spreche?


Die meisten Hormone sind gleichzeitig auch "Zellkernhormone", weil sie auch an Kernrezeptoren andocken. Darüber hinaus gibt es aber auch andere Signalmoleküle, die an Kernrezeptoren andocken.

Hier ein Überblick über die Kernrezeptoren:

Ja, ich sehe da auch ein großes Potential... Neues Thread?

#74 RE: Junges Blut von Joker 10.06.2020 11:45

Zitat von Prometheus im Beitrag #73

Hier ein Überblick über die Kernrezeptoren:

Ja, ich sehe da auch ein großes Potential... Neues Thread?

Ja, die Übersicht der Kernrezeptoren auf Wikipedia zeigt ja grundsätzlich die Vielfalt derer. Man kann hier hunderte von Hormonen oder hormonähnlichen Substanzen annehmen. Einige davon sind vermutlich gar nicht oder kaum bekannt.

Aus diesem Grund bin ich zwar für ein neues Thema, würde dies aber beschränken auf Zellkernhormone der embryonalen bzw. Stammzellenentwicklung. Die Stammzellenentwicklung und Regenerierung scheint im gealterten Organismus vor allem deshalb nicht zu funktionieren, weil die Informationen im Zellkern mangels Zellkernhormonen nicht mehr zugänglich sind. Die Information (DNA) ist in jeder Zelle, aber der Schlüssel (das Zellkernhormon) fehlt oder ist in zu geringer Dosis vorhanden!

Interessant sind in dem Zusammenhang auch die Proteohormone, insbes. auch Oligopeptide (bis Länge 10) und Polypeptide bis Länge 100.

In einem Sequenzer könnte man die auch leicht selbst produzieren bzw. produzieren lassen. Technisch ist die Herstellung solcher Peptide nicht sehr aufwendig.

Trotz der erschreckenden Vielfalt wäre es aber möglich, dass nur 1 oder 2 Substanzen bereits einen entscheidenden Unterschied machen und die Regenerationsfähigkeit des gealterten Körpers stark erhöhen.

Also bitte nicht nur über Zellkernhormone im allgemeinen, sondern speziell über den Zusammenhang Reverse Aging und Zellkernhormone diskutieren, damit es nicht ausufert. Den Titel überlasse ich dir.

#75 RE: Junges Blut von jayjay 22.06.2020 12:06


Aderlass war nicht ganz verkehrt :)
hätten halt wieder auffüllen müssen ;)

Naja, ob so eine Blutspendemaus wirklich älter wird? Mir reicht schon eine Blutentnahme und ich liege am Boden.

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