15 replies to this topic

[ihatesnow]

http://www.scienceal...o-fight-disease

[Antonio2014]

Very interesting. I wonder how this will affect the mitochondrial theories of aging.

[niner]

Wow, cool!  The link above is to a report of mitochondrial DNA being spontaneously transferred from a normal cell to a cell that had it's mitochondria removed.  It appears to pass through a thin tube that runs from the donor cell to the acceptor cell.  The various signalling processes are not described, and may not be known.  This is yet another one of those things that nobody saw coming.  The authors think that it may be a general biological process, and say that preliminary evidence suggests it happens in the brain.

[Turnbuckle]

There are various types of these cytoplasmic extensions--filopodia, cytonemes and tunneling nanotubes--which have been known for some years, along with the ability of the larger ones to transfer mitochondria. For instance, this paper, and this one.

[corb]

Very interesting. I wonder how this will affect the mitochondrial theories of aging.

 

I hope the mechanism can be used to lay down to rest that theory.
It's high time for researchers to start eliminating theories by experiment, this accumulation of conflicting ideas only hampers research.

[pone11]

That finding suggests a possible mechanism for cancer spreading in the first place.   It could be mitochondria develop a cancerous mutation, take over a cell, and then use this mechanism to spread the mitochondria to other healthy cells.

 

I'm not sure I'm so excited about this finding, since cancer knows how to use this mechanism much better than we do.  It's just more cancer-cure science fiction that we are somehow going to cure the disease any time soon by using that mechanism ourselves.

[Avatar of Horus]

There are various types of these cytoplasmic extensions--filopodia, cytonemes and tunneling nanotubes--which have been known for some years, along with the ability of the larger ones to transfer mitochondria. For instance, this paper, and this one.

Yes this is around already for several years or so.
It was touched upon also in this topic:
Proposing Synthetic Mitochondria as a Treatment for Aging
Started by reason , Sep 05 2014 11:22 AM
http://www.longecity...ment-for-aging/
 

Very interesting. I wonder how this will affect the mitochondrial theories of aging.

 
I hope the mechanism can be used to lay down to rest that theory.
It's high time for researchers to start eliminating theories by experiment, this accumulation of conflicting ideas only hampers research.

Yes, I agree, experimentation would be good and important (and urgent too). Perhaps it would be a good idea, if there is interest, that the Longecity community had come up with something: like planning, designing and conducting an experiment on this subject.

BTW another BioscienceNews topic on this discovery, by reason:
Another Complication in Mitochondrial Dynamics is that Cells Can Transfer Mitochondria
http://www.longecity...r-mitochondria/

[Antonio2014]

BTW another BioscienceNews topic on this discovery, by reason:

Another Complication in Mitochondrial Dynamics is that Cells Can Transfer Mitochondria
http://www.longecity...r-mitochondria/

 

It's the same.

 

I don't think this will defeate the mitochondrial teories of aging, but probably it will affect them in some way.

[corb]

Yes, I agree, experimentation would be good and important (and urgent too). Perhaps it would be a good idea, if there is interest, that the Longecity community had come up with something: like planning, designing and conducting an experiment on this subject.

 

I don't think this will defeate the mitochondrial teories of aging, but probably it will affect them in some way.

 

It should be easy enough to test - if it works in humans it should work in yeast and worms (I still don't consider other life forms a good representation of humans but in this case the mechanism seems to be quite inclusive).

Hardest part would be to get some healthy matched mitochondria for "supplementation" I think. Then it's just a matter of "injecting it" for a period of time and collecting the data.

I'm sure there are people on the forums with experience and contacts, I don't see why this can't be done on the cheap.

Edited by corb, 11 January 2015 - 05:06 PM.

[Turnbuckle]

Transfusion of young blood into older animals is rejuvenating, and the mechanism could very well be mitochondrial transfer--and not just through nanotubes. It's known, for instance, that platelets release both free mitochondria and mitochondria contained in microparticles (exosomes), and the latter might conceivably fuse with somatic cells of the recipient. This might be a way the body seeds its cells with fresh mitochondria--which would be of no benefit to most cells, but a life saver for cells with a totally defective mitochondrial population. And in the case where the microparticles come from a young donor with superior mitochondria, it could benefit all cells.

 

Exosomes also derive from stem cells--

 

Mesenchymal stem cells (MSCs) offer great promise in thetreatment of vascular diseases. They are present in various organs, including bone marrow, adipose tissue [1], liver [2], dental pulp [3], amniotic fluid [4] and umbilical cord blood...MSCs can cause tissue regeneration and repair through several processes: a) transdifferentiation of MSCs into the specific cell type,b) fusion of stem cells with the resident cells, c) through the release of microvesicles or exosomes and most importantly, d) through the release of paracrine factors...

 

Another recently reported mechanism of cell repair is through exosomes or microvesicles, which are small, spherical membrane fragments shed from the cell surface or secreted from the endosomal compartment.MSCs release a significant amount of microvesicles  [the contents of which] can be transferred via microvesicles to recipient cells...

 

http://webcache.goog...n&ct=clnk&gl=us

 

 

Edited by Turnbuckle, 11 January 2015 - 07:52 PM.

[pone11]

 

I don't think this will defeate the mitochondrial teories of aging, but probably it will affect them in some way.

 

It should be easy enough to test - if it works in humans it should work in yeast and worms (I still don't consider other life forms a good representation of humans but in this case the mechanism seems to be quite inclusive).

Hardest part would be to get some healthy matched mitochondria for "supplementation" I think. Then it's just a matter of "injecting it" for a period of time and collecting the data.

I'm sure there are people on the forums with experience and contacts, I don't see why this can't be done on the cheap.

 

 

So has any researcher tried to do a mitochondrial replacement experiment in vivo for any mammal?    Any eukaryote?

[pone11]

 

Transfusion of young blood into older animals is rejuvenating, and the mechanism could very well be mitochondrial transfer--and not just through nanotubes. It's known, for instance, that platelets release both free mitochondria and mitochondria contained in microparticles (exosomes), and the latter might conceivably fuse with somatic cells of the recipient. This might be a way the body seeds its cells with fresh mitochondria--which would be of no benefit to most cells, but a life saver for cells with a totally defective mitochondrial population. And in the case where the microparticles come from a young donor with superior mitochondria, it could benefit all cells.

 

Exosomes also derive from stem cells--

 

 

Do you have any studies to link on this idea?   How long are they extending life by transfusing younger blood?    It would be very interesting to see them test giving the blood once, then once each month, and perhaps once each week.   Where is the point of diminishing returns?

 

And I guess if your theory is correct, they could extract the red blood cells (since those do not contain mitochondria) and transfuse just the remaining components in blood that contain mitochondria?

[Turnbuckle]

 

 

Transfusion of young blood into older animals is rejuvenating, and the mechanism could very well be mitochondrial transfer--and not just through nanotubes. It's known, for instance, that platelets release both free mitochondria and mitochondria contained in microparticles (exosomes), and the latter might conceivably fuse with somatic cells of the recipient. This might be a way the body seeds its cells with fresh mitochondria--which would be of no benefit to most cells, but a life saver for cells with a totally defective mitochondrial population. And in the case where the microparticles come from a young donor with superior mitochondria, it could benefit all cells.

 

Exosomes also derive from stem cells--

 

 

Do you have any studies to link on this idea?   How long are they extending life by transfusing younger blood?    It would be very interesting to see them test giving the blood once, then once each month, and perhaps once each week.   Where is the point of diminishing returns?

 

And I guess if your theory is correct, they could extract the red blood cells (since those do not contain mitochondria) and transfuse just the remaining components in blood that contain mitochondria?

 

 

Here is a link--Young Blood Renews Old Mice

 

They believe it is a protein, a growth factor, that explains part of the effect. Mitochondria may explain the rest.

[pone11]

 

 

 

Transfusion of young blood into older animals is rejuvenating, and the mechanism could very well be mitochondrial transfer--and not just through nanotubes. It's known, for instance, that platelets release both free mitochondria and mitochondria contained in microparticles (exosomes), and the latter might conceivably fuse with somatic cells of the recipient. This might be a way the body seeds its cells with fresh mitochondria--which would be of no benefit to most cells, but a life saver for cells with a totally defective mitochondrial population. And in the case where the microparticles come from a young donor with superior mitochondria, it could benefit all cells.

 

Exosomes also derive from stem cells--

 

 

Do you have any studies to link on this idea?   How long are they extending life by transfusing younger blood?    It would be very interesting to see them test giving the blood once, then once each month, and perhaps once each week.   Where is the point of diminishing returns?

 

And I guess if your theory is correct, they could extract the red blood cells (since those do not contain mitochondria) and transfuse just the remaining components in blood that contain mitochondria?

 

 

Here is a link--Young Blood Renews Old Mice

 

They believe it is a protein, a growth factor, that explains part of the effect. Mitochondria may explain the rest.

 

 

Here is some random speculation that the effect was due to oxytocin:

http://phenomena.nat...blood-oxytocin/

 

I have always wanted a reason to try it.

 

Do you happen to know how much they extended life, and how often they were transfusing?

[corb]

Here is a link--Young Blood Renews Old Mice

 

They believe it is a protein, a growth factor, that explains part of the effect. Mitochondria may explain the rest.

 

This is an interesting idea, it was always unclear to me how in the parabiosis experiment the young mice aged faster - none of the groups doing the experiments delved too much into that.

In my thinking if aging was programmatic the young mice should not have aged faster, if our biology is set to promote homeostasis while we're young the shortage of some proteins would have simply been complemented by the young mice cells.

 

If the increase in aging damage was caused by something like damaged mitochondria penetrating the young organism it makes much more sense.
 

[Turnbuckle]

 

Here is a link--Young Blood Renews Old Mice

 

They believe it is a protein, a growth factor, that explains part of the effect. Mitochondria may explain the rest.

 

This is an interesting idea, it was always unclear to me how in the parabiosis experiment the young mice aged faster - none of the groups doing the experiments delved too much into that.

In my thinking if aging was programmatic the young mice should not have aged faster, if our biology is set to promote homeostasis while we're young the shortage of some proteins would have simply been complemented by the young mice cells.

 

If the increase in aging damage was caused by something like damaged mitochondria penetrating the young organism it makes much more sense.
 

 

 

And those who can afford it--like the billionaire owner of a company I once worked for--can get young blood if they want it, while everyone else gets random blood. In the US there is no upper age limit for donating, and that may be a bad idea.

 

A review is being done that may answer the question: Effect of blood donor characteristics on transfusion outcomes: a protocol for systematic review and meta-analysis. Or it might not, as it won't tell us about longevity.

Edited by Turnbuckle, 12 January 2015 - 01:17 PM.