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Young Blood Reverses Signs of Aging in Old Mice


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#31 Mind

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Posted 01 April 2013 - 05:38 PM

Avatar of Horus, I look forward to your project idea!

#32 daouda

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Posted 01 April 2013 - 08:06 PM

Do the beneficial properties of actovegin have anything to do with this ? ("highly purified hemodialysate extracted from vealer blood by ultrafiltration.")?
http://en.wikipedia.org/wiki/Actovegin
It's widely available, some even use it as a nootropic, or to recover from injury, or before an athletic event to boost endurance...
Just google and pubmed it...

To book this BIOSCIENCE ad spot and support Longecity (this will replace the google ad above) - click HERE.

#33 Gerald W. Gaston

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Posted 05 April 2013 - 11:46 PM

As best as I can tell from researching the subject of plasma for dollars, in the U.S., it is not now, nor has it been for a long time, permissible to pay for blood or plasma (a personal pet peeve of mine for a long time). For plasma donation, this rule is side stepped slightly by reimbursing people for the time it takes for them to donate the plasma (I have not donated plasma personally, but understand it takes a few hours for the filtering).


90 minutes on average, and up to $300/mth from this company:

http://www.cslplasma.com/plasma-donation-FAQ



How long does it take to donate plasma?

If you are a return (repeat) donor, it normally takes about 90 minutes. A first time donor can expect to be at the center for about 2 to 3 hours.


Compensation

How much do you receive from donating plasma?
Donation fees vary by location, but plasma donors can earn up to $300 a month.



#34 Logic

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Posted 06 April 2013 - 10:35 PM

I am heading way out of my depth here again, but:

It seems that the chemokines mentioned by Avatar of Horus are "implicated in the resolution of allergic inflammation, an essential protective mechanism."
http://www.ncbi.nlm....les/PMC2771179/

This study points to bad gut bacteria as the reason for the increase in chemokines.
Cryptosporidium parvum, Bacteroides fragilis, and Nocardia brasiliensis are mentioned.
http://www.ncbi.nlm....les/PMC2728352/

Again; I have not studied this study well at all and am way out of my depth here, but it seems that the eradication of bad bacteria in the gut and good intestinal health in general may reduce chemokines?
Perhaps some of the positive effects of fasting, like those mentioned by xEva, has a lot to do with decreased chemokines due to the starvation of bad bacteria in the gut?

Other bacterial, fungal and viral infections are also mentioned as leading to an increase in inflammation and thus chemokines:
http://www.nature.co.../ni0201_95.html
http://www.ncbi.nlm..../pubmed/9299399

It seems that perhaps old blood differs from young blood in that its adapted to prevent inflammation etc. from a lifetime of collected low level infections?
Infections that can be eradicated...
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#35 xEva

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Posted 10 April 2013 - 11:24 PM

It seems that perhaps old blood differs from young blood in that its adapted to prevent inflammation etc. from a lifetime of collected low level infections?
Infections that can be eradicated...



Ahh Logic.. this is my favorite aging theory. In it, various microbes that colonize us, starting in utero***, act as agents of biological entropy. The microbiota is the dust from which life arises and into which it returns, both on the evolutionary and individual levels.

*** Re the colonization in utero part: this may be news for most here. And it does not refer to some pathology. The fact is that we are born already colonized with gut microbes (and not only). You can get the refs by googling latest research on meconium (=newborn's first poop). And the rest of our tissues are far from sterile either, as it was believed not that long ago. We are used to associating infections with an acute process, while slow growing, barely smoldering ones escape our attention.. But if you compare an old cell with an infected cell, there is hardly any difference..

#36 Avatar of Horus

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Posted 11 April 2013 - 12:46 PM

I am currently formulating a detailed research project in the Project Ideas thread, in which these and similar things would be researched and tested, so if anyone has any further ideas, please don't hesitate to tell it.

Avatar of Horus, I look forward to your project idea!

it is here:
Human and Mouse Life Extension DIYBio Stem Cells Experiment
http://www.longecity...lls-experiment/

Click HERE to rent this BIOSCIENCE adspot to support LongeCity (this will replace the google ad above).

#37 Logic

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Posted 11 April 2013 - 01:27 PM

Ahh Logic.. this is my favorite aging theory. In it, various microbes that colonize us, starting in utero***, act as agents of biological entropy. The microbiota is the dust from which life arises and into which it returns, both on the evolutionary and individual levels.

*** Re the colonization in utero part: this may be news for most here. And it does not refer to some pathology. The fact is that we are born already colonized with gut microbes (and not only). You can get the refs by googling latest research on meconium (=newborn's first poop). And the rest of our tissues are far from sterile either, as it was believed not that long ago. We are used to associating infections with an acute process, while slow growing, barely smoldering ones escape our attention.. But if you compare an old cell with an infected cell, there is hardly any difference..


Am I correct in understanding that an infected in-utero cell is very similar to an old cell!?

I am also more and more inclined to believe that sub-acute infection, especially of the gut, is a major reason for aging.

I don't know enough about fasting to know what pathogens are killed by it and how long a fast it takes to accomplish this?

The other options for clearing bad bacteria and other pathogens from the gut is to do so in a similar way to the way labs do so to rats etc. with a careful re-populating with pro-biotics/bacteria of one's own choice?
This would probably not work very well as other bacteria etc. would inevitably find a way in again.

The only way I can think of to be highly specific about killing off specific gut bacteria (only), and keeping them dead, is Bacteriophages.
The idea of purposefully swallowing an assortment of virii is not something the people can easily get their heads around though, even if said virus is known to only 'eat' one specific bad bacteria.
Bacteriophages are also not available at your favourite supplement shop; so most are inclined to click 'next thread' whenever the subject comes up.
It's a pity as Bacteriophages are the most useful and underappreciated anti-bacterials ever IMHO, and we would all be up to our ears in bacteria/fungi/mould if it was not for them keeping the balance in nature...

http://en.wikipedia....i/Bacteriophage

If anyone here has used Bacteriophages; please post.

#38 niner

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Posted 11 April 2013 - 04:38 PM

IThis study points to bad gut bacteria as the reason for the increase in chemokines.
Cryptosporidium parvum, Bacteroides fragilis, and Nocardia brasiliensis are mentioned.
http://www.ncbi.nlm....les/PMC2728352/

Again; I have not studied this study well at all and am way out of my depth here, but it seems that the eradication of bad bacteria in the gut and good intestinal health in general may reduce chemokines?
Perhaps some of the positive effects of fasting, like those mentioned by xEva, has a lot to do with decreased chemokines due to the starvation of bad bacteria in the gut?


In that paper, the chemokines aren't produced by the bacteria. (Bacteria can't do that AFAIK) Are these bacteria thought to somehow be responsible for the particular chemokine seen here? These were not normal guts, they were diseased, which is probably related to those chemokines.

I think we're getting way ahead of ourselves with the idea that gut microbes are responsible for aging. I don't think there's any evidence of that, and the fact that antibiotic treatment doesn't make people any more youthful suggests that bacteria aren't the problem.

#39 Mind

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Posted 11 April 2013 - 04:55 PM

I am with Niner here. Gut bacteria are a small factor in health, but are not a major cause of aging, IMO.

Other threads on this topic:

HUMAN MICROBIOME.

Hacking your body's Bacteria.

Pathogenic Microbes and Aging.
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#40 xEva

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Posted 12 April 2013 - 04:12 PM

Am I correct in understanding that an infected in-utero cell is very similar to an old cell!?


Geez no. I said our guts are colonized still in utero. But technically gut is actually outside and thus anything in it cannot be considered 'infecting' us (well, maybe worms can, but thankfully, it's not the western world problem).

When I speak of an infected cell, I mean intracellular pathogens that actually live inside a cell, such as a liver cell, a blood cell, a neuron, an immune system cell, etc. When such a cell is persistently infected, its autophagy machinery is sabotaged and its apoptosis programs are suppressed by the invaders' metabolites. This is what allows them to persist. As a result, an infected cell soon acquires the senescent phenotype: it becomes filled with junk that further compromises its function and emits toxic and inflammatory compounds into its environment (summoning up the immune sys cells for the rescue), etc.

That's what I meant by an infected cell being very similar to an old cell. I believe that we slowly acquire various such infections throughout our lives and they contribute to the gradually growing dysfunction of old age. It starts with an infection in a cell that slowly spreads to other cells, eventually affecting the function of a given organ, and then the organism as a whole.

I am also more and more inclined to believe that sub-acute infection, especially of the gut, is a major reason for aging.


Actually, this old idea was popularized back in the 19th C by Élie Metchnikoff (1908 Nobel in immunology). He went as far as advocating colectomy (= surgical removal of colon (!) I know) but later settled on the use of yogurts, sauerkraut and other fermented foods for gut health.

I don't know enough about fasting to know what pathogens are killed by it and how long a fast it takes to accomplish this?


Again, I was not talking about the gut microbes. They technically live outside us. There is a mucouid layer covering intestinal epithelium and it is completely soaked with antimicrobial peptides (=small positively charged proteins that have high affinity for the negatively charged bacterial membranes). This layer prevents the gut microbes from getting inside us (= getting access to epithelial cells and then to our plasma and blood). But blood is very inhospitable place for most microbes. Thus those who managed to get in must quickly find a niche by infecting a cell and establishing their new home in it. No cell will take such an invasion without putting up a fight. Autophagy is the usual line of defense. If the invaders manage to sabotage it with their metabolites, they will persist until a stronger signal will overcome their jamming of the cell's machinery. Starvation is one such signal.

Capisci? :)

Edited by xEva, 12 April 2013 - 04:49 PM.

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#41 xEva

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Posted 12 April 2013 - 05:23 PM

About these heterochronic parabiosis studies, how did they manage to deactivate the immune systems of both animals and prevented them from attacking each other? And what repercussions such deactivation had?

#42 Logic

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Posted 14 April 2013 - 04:16 AM

Am I correct in understanding that an infected in-utero cell is very similar to an old cell!?


Geez no. I said our guts are colonized still in utero. But technically gut is actually outside and thus anything in it cannot be considered 'infecting' us (well, maybe worms can, but thankfully, it's not the western world problem).

When I speak of an infected cell, I mean intracellular pathogens that actually live inside a cell, such as a liver cell, a blood cell, a neuron, an immune system cell, etc. When such a cell is persistently infected, its autophagy machinery is sabotaged and its apoptosis programs are suppressed by the invaders' metabolites. This is what allows them to persist. As a result, an infected cell soon acquires the senescent phenotype: it becomes filled with junk that further compromises its function and emits toxic and inflammatory compounds into its environment (summoning up the immune sys cells for the rescue), etc.

That's what I meant by an infected cell being very similar to an old cell. I believe that we slowly acquire various such infections throughout our lives and they contribute to the gradually growing dysfunction of old age. It starts with an infection in a cell that slowly spreads to other cells, eventually affecting the function of a given organ, and then the organism as a whole.

I am also more and more inclined to believe that sub-acute infection, especially of the gut, is a major reason for aging.


Actually, this old idea was popularized back in the 19th C by Élie Metchnikoff (1908 Nobel in immunology). He went as far as advocating colectomy (= surgical removal of colon (!) I know) but later settled on the use of yogurts, sauerkraut and other fermented foods for gut health.

I don't know enough about fasting to know what pathogens are killed by it and how long a fast it takes to accomplish this?


Again, I was not talking about the gut microbes. They technically live outside us. There is a mucouid layer covering intestinal epithelium and it is completely soaked with antimicrobial peptides (=small positively charged proteins that have high affinity for the negatively charged bacterial membranes). This layer prevents the gut microbes from getting inside us (= getting access to epithelial cells and then to our plasma and blood). But blood is very inhospitable place for most microbes. Thus those who managed to get in must quickly find a niche by infecting a cell and establishing their new home in it. No cell will take such an invasion without putting up a fight. Autophagy is the usual line of defense. If the invaders manage to sabotage it with their metabolites, they will persist until a stronger signal will overcome their jamming of the cell's machinery. Starvation is one such signal.

Capisci? :)


Thx xEva. I "Capicci" you now. :)

Are there studies saying that fasting will overcome the autophagy blocking that occurs in infected cells?

#43 Logic

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Posted 14 April 2013 - 04:36 AM

IThis study points to bad gut bacteria as the reason for the increase in chemokines.
Cryptosporidium parvum, Bacteroides fragilis, and Nocardia brasiliensis are mentioned.
http://www.ncbi.nlm....les/PMC2728352/

Again; I have not studied this study well at all and am way out of my depth here, but it seems that the eradication of bad bacteria in the gut and good intestinal health in general may reduce chemokines?
Perhaps some of the positive effects of fasting, like those mentioned by xEva, has a lot to do with decreased chemokines due to the starvation of bad bacteria in the gut?


In that paper, the chemokines aren't produced by the bacteria. (Bacteria can't do that AFAIK) Are these bacteria thought to somehow be responsible for the particular chemokine seen here? These were not normal guts, they were diseased, which is probably related to those chemokines.

I think we're getting way ahead of ourselves with the idea that gut microbes are responsible for aging. I don't think there's any evidence of that, and the fact that antibiotic treatment doesn't make people any more youthful suggests that bacteria aren't the problem.


It seems they are Niner.
Quote:
"Immunofluorescence analysis of colonic biopsy samples from UC patients demonstrated eotaxin-1 expression by intestinal epithelial cells and CD68+ macrophages. Notably, the eotaxin-1 signal from intestinal epithelial cells was restricted to the basolateral compartment. Consistent with this, we observed the accumulation of eosinophils between and beneath the intestinal epithelium. Previous studies with human intestinal epithelial cells have demonstrated Cryptosporidium parvum- and Bacteroides fragilis-induced basolateral expression of the CXC chemokines IL-8, and GROa(60, 61). In both human and mouse studies we also demonstrated that macrophages are a primary source of eotaxin-1. Intestinal macrophage levels have been shown to be elevated in IBD and activation correlated with disease severity (62). Furthermore, previous immunohistochemistry analysis examining eotaxin-1 production in mucosal tissues derived from CD and UC identified a minor population of eotaxin-1-positive mononuclear inflammatory cells; however the cell type was not identified (26). Experimental studies using macrophage-deficient op/op mice have demonstrated a role for macrophages in Nocardia brasiliensis infection-induced eosinophil recruitment (63)."

I was hoping that some such as yourself would read this interesting study: It would take me ages to Google all the bits I don't understand and fully understand and summerise it.




#44 Avatar of Horus

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Posted 14 April 2013 - 11:01 AM

Do the beneficial properties of actovegin have anything to do with this ? ("highly purified hemodialysate extracted from vealer blood by ultrafiltration.")?
http://en.wikipedia.org/wiki/Actovegin
It's widely available, some even use it as a nootropic, or to recover from injury, or before an athletic event to boost endurance...
Just google and pubmed it...

Thanks for the suggestion.
It possibly has some relevances, like on the part of the background of the molecular mechanisms of the blood induced tissue repair, which are currently largely unknown.

This would be one of the possibilities, that can belong to that category which I referred to as nutriment deficiency before, i.e. since the various cells and tissues of an organism are interdependent on each other, and if one part of system, for example the tissues which are responsible for the development of the nutrient molecules, is impaired then their products' quantity will decrease in the main transit system, the blood, and this will impede the other otherwise healthy parts of the body too, which then causes further problems and so on. This can be a feedback mechanism which is what we can see and call as part of aging.

This Actovegin seems to be a blood extract product, that enhances the glucose and oxygen uptake of the cells, by which means it increases their energy and other production. Which would be dangerous on the long run however because the major reactive oxygen species creating process is exactly the sugar to ATP conversion in the mitochondria. However this extract is also supplied with large amounts of superoxide dismutase and magnesium, which are part of the antioxidant defense in the cells. So there is sense behind all this.

This can be a similar thing that was called in the #12 post: 'Young Blood Supplement'

Also all this puts the spotlight to another important matter on the general scope too, that is I think that we, the LE community, need to focus some also on the concrete products and interventions in our journey. This is what was touched in a recent broadcast with Dr. Marios Kyriazis, one of the longecity users, available here: http://www.longecity...arios-kyriazis/

Apart from the approach which is to look at complex systems, the other thing that came to my mind is, think about it, what is there we can do in order to live longer? Do a bit of exercise, don’t smoke, take a few supplements and what else? There is nothing else. We have to wait for new research to come through, stem cells, nanotechnology or other developments, so that we could take it in tablet or injection form and influence our aging. Apart from the ordinary things we have been talking about 20,30 years ago, even 40 years ago (don’t smoke, exercise, fresh air) what else is there in practical terms? Yes, there is a lot of research, and a lot of work done, but this is still in the laboratory. There is very little that can be applied now to the people in the street so that they can extend their lives.


Also there is a relevant citation quoted by Eric/brokenportal in one of his articles on the transhumanity.net:
“Alpha Thinkers” are the Transhuman Wave of the Future
http://transhumanity...e-of-the-future

As the social and economic theorist Richard Florida says,

“Technology and innovation are critical components in driving economic growth. To be successful, communities and organizations must have the avenues for transferring research, ideas, and innovation into marketable and sustainable products.”


Therefore I think it is good that ImmInst/Longecity is already on this track, at least on its start, I mean with the VIMMORTAL. This should be pursued further too. Possibly with some similar young blood supplement/extract product.

Edited by Avatar of Horus, 14 April 2013 - 11:06 AM.


#45 Avatar of Horus

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Posted 14 April 2013 - 01:56 PM

As best as I can tell from researching the subject of plasma for dollars, in the U.S., it is not now, nor has it been for a long time, permissible to pay for blood or plasma (a personal pet peeve of mine for a long time). For plasma donation, this rule is side stepped slightly by reimbursing people for the time it takes for them to donate the plasma (I have not donated plasma personally, but understand it takes a few hours for the filtering).


90 minutes on average, and up to $300/mth from this company:

http://www.cslplasma...ma-donation-FAQ

Blood and plasma buying and selling directly are illegal, because it would qualify as organ trading.
So in my opinion the only possible solution that comes to mind is the autologous bio-artificial blood, which I already mentioned in that project idea article above.
This is a relatively new direction, but it is being pursued by for example the US Army/Pentagon too, as can be seen e.g. here: wikipedia.org/Artificial_blood#Potential_techniques.
However their approach is general on the blood cells of O type with some blood substitute, which is, of course, fully good for their goal, while my method is based on the ex vivo fully autologous blood cells and also blood plasma creation, so it would be literally one's very own young blood/plasma, and such it is more appropriate for the regeneration/rejuvenation goal.

...
It seems that perhaps old blood differs from young blood in that its adapted to prevent inflammation etc. from a lifetime of collected low level infections?
Infections that can be eradicated...

thank you for the good links.
Yes, this is an important reflection I think, this is why I mentioned in that CCL11 post the possible necessity of the blood purifier. However IMHO not only and not specifically the gut bacteria are the main cause, but all of the pathogens together. First because of their own harmful behavior, and also for the immune system cells' reactions, because this can be tissue destructive too, like e.g. what I mentioned: the reactive oxygen species produced by the eosinophils. Because what is toxic to one organism, like to its DNA molecule, that can be toxic to the host own molecules, too; due to the biological similarity of all the living things on this planet Earth.
Like as it was written here in the first and second articles you listed:
1) "Eosinophils also secrete many potentially toxic products that may further impair lung function",
and
2) "Eosinophils are multifunctional leukocytes involved in the initiation and propagation of inflammatory reactions and the modulation of innate and adaptive immunity and can serve as a major effector cell, inducing tissue damage and dysfunction."

So overally it would be probably good for the organism if the pathogens could be removed as much as possible from the body.

So I partially agree too, with the view of niner and Mind:

...
I think we're getting way ahead of ourselves with the idea that gut microbes are responsible for aging. I don't think there's any evidence of that, and the fact that antibiotic treatment doesn't make people any more youthful suggests that bacteria aren't the problem.

I am with Niner here. Gut bacteria are a small factor in health, but are not a major cause of aging, IMO.

Other threads on this topic:

HUMAN MICROBIOME.

Hacking your body's Bacteria.

Pathogenic Microbes and Aging.

Thanks here too for the good links.

So the truth can be somewhere in the middle.

One more thing:
The discussed CCL11/eotaxin1's receptor is the CCR3. And I found that not only this chemokine is elevated in the aging process, but also its receptor, at least in certain cell types, e.g. here:
Upregulation of CCR3 by age-related stresses promotes choroidal endothelial cell migration via VEGF-dependent and -independent signaling, 2011. pubmed link: http://www.ncbi.nlm....pubmed/21917937
Its Figure 1C:
Posted Image

So this CCL11/CCR3 thing may be one of the underlying mechanism of ageing.

This receptor is also one of the cell surface molecules that is used by the HIV virus to enter the cells. And speaking of AIDS, it is a good example to what happens when the balance between the immune cells and the pathogens becomes upset, and the latter ones gain the upper hand.

Edited by Avatar of Horus, 14 April 2013 - 02:17 PM.


#46 Avatar of Horus

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Posted 14 April 2013 - 02:19 PM

About these heterochronic parabiosis studies, how did they manage to deactivate the immune systems of both animals and prevented them from attacking each other? And what repercussions such deactivation had?

It's a good question, I wondered on this same thing when I first read about the parabiosis studies.

#47 xEva

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Posted 15 April 2013 - 12:44 AM

Avatar of Horus, that is a very pertinent question, considering the central role of the immune system in health and => longevity.

Anyone knows how they did it?



Are there studies saying that fasting will overcome the autophagy blocking that occurs in infected cells?


Not directly. But:

1. There are plenty of in vitro studies that show how intracellular pathogens, both viruses and bacteria, establish persistent infections in cells. A handful of bugs exploit authopagy machinery for their own replication. But most simply block it on one of its various stages, such as, for example, autophagosome maturation or its merging with a lysosome, etc. The studies show that in many cases when autophagy is impeded, a stronger, or an entirely different signal, can overcome the block, allowing the process to complete, which ends with death of the bugs. (this is a simplified version)

2. It is well known and widely acknowledged that starvation is the strongest inducer of autophagy known.

1 + 2 implies that fasting should be effective in many infections and there is plenty of empirical evidence for this. The old proverb 'starve the fever feed the cold' also reflects what people observed long ago, and that is that some ills resolve quicker on a fast and that a fast is contraindicated in others.

Edited by xEva, 15 April 2013 - 12:48 AM.


#48 Gerald W. Gaston

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Posted 15 April 2013 - 05:01 AM

Hmm... completely off the cuff, but this reminds me of something I have wondered about for a few years but never checked into to see if it has been done/thought about until now:

hemodialysis/hemofiltration in middle aged, otherwise healthy mice? Not at the typically three days a week frequency with dialysis for renal failure, but much less frequent. I guess we would have to know what we want to filter out and just how to go about filtering them. A quick look on SD finds this article from 2008 dealing with a proposed 'hemopurifier' that use 'thin fibers to capture and remove viruses from the blood it filters'. :

http://www.scienceda...ected_blood.htm

Will this type of thing be part of our anti-aging future?



More to help possible perfect a "hemopurifier":

Nanosponges Soak Up Toxins Released by Bacterial Infections and Venom
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#49 Avatar of Horus

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Posted 16 April 2013 - 09:38 PM

... the one mentioned by Mind in his post above, titled:
The ageing systemic milieu negatively regulates neurogenesis and cognitive function
Nature. 2011 Aug 31;477(7362):90-4. doi: 10.1038/nature10357.
by Dr. Villeda and others.
Available on Pubmed too: http://www.ncbi.nlm....ubmed/21886162


This study is the topic of two articles:
a post from the fightaging.org blog, where a summary article about it was discussed, here:
Old Blood Versus Young Blood From a Programmed Aging Perspective
http://www.longecity...ng-perspective/

and a mainstream media coverage from the Guardian:
Young blood can reverse some effects of ageing, study finds
17 October 2012
http://www.guardian....-effects-ageing
some quotes from this:

Saul Villeda of Stanford University, who led the work, found that blood from young mice reversed some of the effects of ageing in the older mice, improving learning and memory to a level comparable with much younger animals. He said that the technique could one day help people stave off the worst effects of ageing, including conditions such as Alzheimer's.

"Do I think that giving young blood could have an effect on a human? I'm thinking more and more that it might," said Villeda. "I did not, for sure, three years ago."

He presented his results at the annual meeting of the Society for Neuroscience in New Orleans on Wednesday.
Villeda connected the circulatory systems of an old and young mouse so that their blood could mingle. This is a well-established technique used by scientists to study the immune system called heterochronic parabiosis. When he examined the old mouse after several days, he found several clear signs that the ageing process had slowed down.

The number of stem cells in the brain, for example, had increased. More important, he found a 20% increase in connections between brain cells. "One of the main things that changes with ageing are these connections, there are a lot less of them as we get older," said Villeda. "That is thought to underlie memory impairment – if you have less connections, neurons aren't communicating, all of a sudden you have [problems] in learning and memory."
...
Turning the idea into a therapy for humans will take much more research, but Villeda said there was no reason not to think that, at some point in the future, people in their 40s or 50s could take therapies based on the rejuvenating chemical factors in younger people's blood, as a preventative against the degenerative effects of ageing.
...
Chris Mason, professor of regenerative medicine bioprocessing at University College London, said that real scientific breakthroughs "are often the result of an astonishing observation that if robustly examined may occasionally contain a nugget of great value. This may be one such occasion. The important questions are: what is in the blood of the younger mice that impacts the ageing process, and is it applicable to humans? Neither will be easy questions to answer."
He added: "Even if the finding leads only to a drug that prevents, rather than reverses the normal effects of ageing on the brain, the impact upon future generations will be substantial – potentially outweighing other wonder drugs such as penicillin."


Edited by Avatar of Horus, 16 April 2013 - 09:47 PM.


#50 Logic

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Posted 19 April 2013 - 07:11 AM

We are living in a bacterial world, and it's impacting us more than previously thought
http://phys.org/news...ght.html#ajTabs

"It is hard to summarize a single 'most important conclusion,' other than the admonition to biologists studying animals, from behavior to physiology and ecology to molecular biology, that no matter what process you think you are studying, you must look for and consider a major role for bacteria,"
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#51 xEva

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Posted 27 April 2013 - 06:04 AM

The question still remains about these heterochronic parabiosis studies, how did they prevent the immune systems of both animals from attacking each other. Here is an interesting read on what can go wrong: Chapter 3. Blood transfusions and the immune system
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#52 revenant

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Posted 27 April 2013 - 04:35 PM

A factor here is the blood plasma proteome. The relatively young liver's capacity to produce blood plasma proteins, compared to that of a relatively old liver's, is very different. This plasma proteome supports the endothelial cells, red/white blood cells and conveys everything we need to the extra cellular matrices. The extracellular environments affects all cells' expression of surface receptors, which in turn affect the machinery of the cells themselves. Liver function also affects the thymus. The thymus is responsible for nurturing immune cells found in the blood. The liver is likely a big player in the results of the study. The transplanting of a young liver (or a grown liver?) along with a blood transfusion would be a good experiment. The proteome of young transfused blood plasma would return to an old proteome unless perhaps there were a young liver introduced too!

#53 Logic

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Posted 28 April 2013 - 09:22 AM

The question still remains about these heterochronic parabiosis studies, how did they prevent the immune systems of both animals from attacking each other. Here is an interesting read on what can go wrong: Chapter 3. Blood transfusions and the immune system


A wild guess would be that they cloned the old mice, but wasn't Dolly the Sheep 'old' at birth due to short telomeres?

#54 Logic

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Posted 28 April 2013 - 09:53 AM

A factor here is the blood plasma proteome. The relatively young liver's capacity to produce blood plasma proteins, compared to that of a relatively old liver's, is very different. This plasma proteome supports the endothelial cells, red/white blood cells and conveys everything we need to the extra cellular matrices. The extracellular environments affects all cells' expression of surface receptors, which in turn affect the machinery of the cells themselves. Liver function also affects the thymus. The thymus is responsible for nurturing immune cells found in the blood. The liver is likely a big player in the results of the study. The transplanting of a young liver (or a grown liver?) along with a blood transfusion would be a good experiment. The proteome of young transfused blood plasma would return to an old proteome unless perhaps there were a young liver introduced too!


Hmmm...
Perhaps this ties into the effects of C60oo?
Having done intensive festive season experiments on the protective effects that C60oo has on the liver; I can say nothing protects the liver as well! :-D
Perhaps the liver of C60oo users is able to produce blood plasma proteins like that of a young liver and this has system-wide effects??

#55 revenant

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Posted 28 April 2013 - 06:48 PM

Here is an old-ish study demonstrating that young liver derived plasma proteins can have a rejuvenative affect on older stem cells : http://be115.blogspo...itor-cells.html

#56 revenant

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Posted 28 April 2013 - 08:39 PM

Here is an old-ish study demonstrating that young liver derived plasma proteins can have a rejuvenative affect on older stem cells : http://be115.blogspo...itor-cells.html

I should be more specific: the study points to "serum components" (not "liver derived proteins"). It could be that the serum components responsible are liver derived IGF binding proteins.

These in vivo and in vitro studies show that serum components alone are capable of increasing muscle satellite stem cell restorative capacity in mice.


Edited by revenant, 28 April 2013 - 09:23 PM.


#57 Elus

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Posted 09 May 2013 - 10:34 PM

http://hereandnow.wb...n-heart-disease

Scientists Discover Protein That Reverses Heart Disease In Older Mice

Scientists at Harvard University think they have found a way to possibly reverse the aging process in human organs.

Dr. Richard Lee, director of regenerative medicine at Brigham and Women’s Hospital, and Amy Wagers, of the Department of Regenerative Biology at Harvard, made the discovery when they were working with younger and older mice.

They took an older mouse with the most common form of human heart failure and merged the mouse’s blood stream with that of a healthy young mouse using a Siamese twin technique known as parabiosis. They found that the older mouse’s diseased heart was able to reverse to a younger healthier condition.

They later identified a protein in the blood of young mice called GDF-11, which diminishes with age. They injected this protein directly into the older mice and had the same positive results. They are using this protein to restore other aging/diseased tissues and organs. Their results are published online today in the science journal Cell.

Edited by Elus, 09 May 2013 - 10:36 PM.

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#58 niner

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Posted 10 May 2013 - 01:14 AM

Here's the abstract and figures. The protein GDF11, a cytokine that I think is the same thing as BMP11 was shown to shrink a hypertrophic heart. Myostatin is in the same family. I'm not sure this is the fountain of youth- there might be a bunch of other factors in young blood that improve other aspects of the aging organism. Cardiac hypertrophy is only one thing, although if you happen to suffer from it, it's awesome that shots of GDF11 will fix it. You can already buy it. Better hope you don't need a lot, since with shipping it's $313 for 20 ug. I didn't shop around though. Prices ought to come down with more demand, but life-saving therapies command insane prices.

If nothing else, this is proof of the principle that young vs old blood can be analyzed via proteomics to find the components that do good things. There may also be non-protein substances that are important, too.

The media is going to screw this one up and over-hype it.
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#59 Avatar of Horus

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Posted 10 May 2013 - 06:38 AM

The protein GDF11, ...
If nothing else, this is proof of the principle that young vs old blood can be analyzed via proteomics to find the components that do good things. ...

This same method was used in the previously discussed Villeda study too:

...also they tried to identify the factors with proteomic screening, and they've found some things...


Also this GDF11 finding is an example to what was discussed in that above (#49) Guardian article, in these parts:
"...therapies based on the rejuvenating chemical factors in younger people's blood, as a preventative against the degenerative effects of ageing."
and
"...there may be significant benefit in working out what the 'good stuff' is in the high octane young blood, so that we can provide just those key components to the elderly."

BTW here is a figure from the Villeda article about a number of plasma proteins, and their age related change:
Posted Image
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#60 Logic

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Posted 10 May 2013 - 01:18 PM

That's a nice graphic Avatar of Horus, but its a bit difficult to read as the ages don't progress from young to old.
One would have to take the averages for each age and make a graphic with just 4 columns for age to get a better idea of what it shows.
Not an easy task as the difference in colours is small.

ie: For CCL11:
6 months: (-2-2-2-1.5-1)/5= -1.7
12 months: (-1.5-1-2-2-2)/5= -1.7
18 months: (-1.5-1.5-1-2-0.5)/5= -1.3
24 months: (-0.5+2.5+2+2.5+3)/5= +1.7
But I probably got the colour-value wrong for some of the above #s

Then there is the small matter of increasing or decreasing these proteins in the blood..?!

Edited by Logic, 10 May 2013 - 01:31 PM.





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