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#18938 - 11/05/11 03:21 PM Shades of Ponce de Leon
ryck Offline


Registered: 08/04/09
Loc: Okanagan Valley
In another thread Tacit mentioned radical longevity and, while this may/may not be part of that idea, the Mayo Clinic has done some interesting genetic engineering with senescent cells.

They haven't concluded that flushing these cells actually extends a lifetime but it sure seems it would make aging a lot more comfortable.

I have to admit feeling a bit sorry for the mice. Apparently they have specially designed mice who age rapidly, to allow for testing that represents a lifetime, and it doesn't matter how well a mouse tales care of himself - he's going to drop from a heart attack.


Edited by ryck (11/05/11 03:26 PM)
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#18942 - 11/05/11 06:38 PM Re: Shades of Ponce de Leon [Re: ryck]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
That's an interesting finding, though it's not clear to me how one would be able to destroy senescent cells without damaging cells that are still functioning normally.

Cellular senescence has long been thought to be a central factor of aging and death. There's a field of longevity research called SENS (Scientifically Engineered Negligible Senescence) which seeks ways to allow cells to continue to function normally indefinitely. Cellular senescence seems to be closely related to the fact that cells can only reproduce a certain number of times before the DNA in them is damaged to the point where the cell can't reproduce; the end caps on the genes, called "telomeres," shorten each time the cell divides, and when the telomeres become short enough, the cell can no longer divide.

Imortal cells, like single-celled organisms, produce an enzyme called telomerase which repairs the telomeres. Human and mammal cells don't generally produce telomerase, though cancer cells do. (Cancer cells usually have DNA that is radically different from the host organism; a cell that has gone cancerous typically has DNA that has been so badly damaged that a cancer tumor in a person might not even have the same number of chromosomes as the person does.) The fact that our cells have this limit on the number of times they can divide appears to be a defense against cancer, though the cost of that defense is a finite lifespan.
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#18948 - 11/06/11 01:29 AM Re: Shades of Ponce de Leon [Re: tacit]
grelber Offline


Registered: 08/05/09
Loc: North of 49th ||
Originally Posted By: tacit
... the cost of that defense is a finite lifespan.

Sounds a lot like the expulsion from the Garden of Eden, nicht wahr? smirk

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#18955 - 11/06/11 03:36 PM Re: Shades of Ponce de Leon [Re: grelber]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
If so, that expulsion came long before humanity arrived on the scene, since all vertebrates and virtually every complex multicellular organism has adopted it.

The cost of a finite lifespan isn't actually a cost for most organisms, which wouldn't live forever even if they didn't age; disease, predation, and accident will kill nearly all animals in the natural environment, including pre-agrarian humans, long before they reach the aging-imposed limits of their lifespans. There simply isn't any selective pressure in favor of an organism not aging.

The expulsion from the Garden of Eden is, I suspect, a better allegory for our abandonment of a hunter-gatherer lifestyle in favor of an agrarian lifestyle than it is for organisms not aging.
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#18958 - 11/06/11 11:26 PM Re: Shades of Ponce de Leon [Re: tacit]
grelber Offline


Registered: 08/05/09
Loc: North of 49th ||
Without belaboring the point (the quip) too much ...
The biblical story of the expulsion was to explain mortality, as a punishment for defying the creator. A talking serpent with an apple (ironic, that) which stymies telomerase ...
And "abandonment of a hunter-gatherer lifestyle in favor of an agrarian lifestyle" occurred at least 4,000 years before writing appeared (leaving aside the few subcultures which still practice hunting and gathering).
Moving right along ....

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#18959 - 11/07/11 12:38 AM Re: Shades of Ponce de Leon [Re: tacit]
ryck Offline


Registered: 08/04/09
Loc: Okanagan Valley
Originally Posted By: tacit
That's an interesting finding, though it's not clear to me how one would be able to destroy senescent cells without damaging cells that are still functioning normally.

But, if they could figure it out, it could certainly make aging a lot more comfortable and, I assume, have significant impacts on other things....like economics. If the cost of dealing with age-related illnesses was gone (or even mostly gone) there would be a lot of money available for important things at the other end of life...like improving the educational system.

Originally Posted By: tacit
Immortal cells, like single-celled organisms, produce an enzyme called telomerase which repairs the telomeres. Human and mammal cells don't generally produce telomerase, though cancer cells do.

Are there actually single-celled organisms (other than cancers) that would live forever if it was not for external effects like predation, accident? I assume disease wouldn't have an effect on something that generates telomerase.


Edited by ryck (11/07/11 01:49 AM)
Edit Reason: Grammar
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#18960 - 11/07/11 04:24 AM Re: Shades of Ponce de Leon [Re: ryck]
grelber Offline


Registered: 08/05/09
Loc: North of 49th ||
You might check out the process of apoptosis.
Here's a start:
Apoptosis from the Reproductive and Cardiovascular Disease Research Group in the Division of Basic Medical Sciences at St George's, University of London.

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#18969 - 11/07/11 11:12 AM Re: Shades of Ponce de Leon [Re: grelber]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
Originally Posted By: grelber
And "abandonment of a hunter-gatherer lifestyle in favor of an agrarian lifestyle" occurred at least 4,000 years before writing appeared (leaving aside the few subcultures which still practice hunting and gathering).
Moving right along ....


True, but the ancient Israelites, from whom the oldest bits of the Bible spring, came a bit late to the table. They were, for example, still in the Bronze Age when all the surrounding civilizations were Iron Age. (It's a testament to their ferocious appetite for guerrilla warfare and the quality of their tacticians that they were able to kick the collective asses of a number of societies far more technologically advanced than they were.)

Interesting timing on this conversation; I just went to a lecture by an anthropologist who talked about the story of the Fall as a kind of lament of the loss of the hunter/gatherer lifestyle.

Originally Posted By: ryck
Are there actually single-celled organisms (other than cancers) that would live forever if it was not for external effects like predation, accident? I assume disease wouldn't have an effect on something that generates telomerase.


Yep. Almost all single-celled organisms, and some simple multicellular organisms (including jellyfish) are biologically immortal. There's a brief introduction to a few of them at the Wikipedia entry on biological immortality.

The most famous line of immortal cancer cells are HeLa cells, cultivated from the ovarian cancer tumors that killed Henrietta Lacks and now used to test cancer treatment drugs (among other things). HeLa cells are a great example of how cancer cells can differ so much from the healthy cells in the host that they are, for all intents and purposes, a completely different species. Human beings have 23 chromosomes; the cancer cells that killed Mrs. Lacks have 82. Some of the extra chromosomes are duplicate copies of normal human chromosomes; some are made up of mutated human chromosomes; and some contain HPV DNA. (HPV, or human papilloma virus, is the virus responsible for almost all cases of cervical cancer. It copies bits of the viral DNA into the host DNA, in a process called "lateral transfer.")

There are some cells in human beings that produce telomerase, such as the cells in bone marrow that create blood cells. Since every human cell has a complete copy of all the human genes, it's possible for any human cell to start producing telomerase. Normally, in most cells, the gene for telomerase is switched off, but if it is accidentally switched on, by cellular damage or exposure to environmental toxins or through an error in cellular reproduction, the cell may start dividing out of control. This uncontained rapid dividing can introduce other errors in gene transcription or replication, and the result may be a cancer cell that differs genetically from the original cell.

Genes can also be switched on accidentally if a cell has shortened telomeres but fails to become senescent. If that happens, when the cell divides, the telomeres may break, exposing the raw ends of the chromosomes. We have repair mechanisms in our cells designed to repair damaged DNA, but it doesn't always deal with that situation well. If the telomeres are completely removed from a set of genes, the repair mechanisms can sometimes end up fusing those genes together end-to-end, which can have all sorts of consequences for the cell. The genes may not be read correctly, resulting in transcription of bits that should be switched off, or failure to transcribe bits that should be switched on.

The result, again, is a cancer cell that differs genetically from its host.

This is a quick and dirty overview, of course, but it gets the idea across.

We have a number of cellular defense mechanisms designed to destroy damaged cells. One of those is apoptosis, or "programmed cell death." If a cell begins to malfunction badly, the mitochondria in the cell release a protein that triggers cellular self-destruction...at least in theory.

In cancer cells, this mechanism doesn't work. There is currently a line of research aimed at figuring out why it doesn't work, and causing apoptosis in cancer cells. In lab cultures, it works really well against some cancer cells but not at all against others, and in a few types of cancer it can actually make the tumors grow more rapidly. The strains of HPV that can cause cancer carry a gene for a protein that binds to and inactivates the protein that triggers apoptosis. Since the cancer treatments that work by triggering apoptosis generally do it by prodding the mitochondria into greater activity, HPV-related cancers, which are essentially immune to apoptosis, can actually flourish in the presence of these experimental drugs.
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#18971 - 11/07/11 12:26 PM Re: Shades of Ponce de Leon [Re: tacit]
grelber Offline


Registered: 08/05/09
Loc: North of 49th ||
Originally Posted By: tacit
... Since every human cell has a complete copy of all the human genes, ....

Just a minor correction (and excuse the pedantry): Only diploid cells have this characteristic; haploid cells (stereotypically germ cells, spermatozoa and ova) normally have only half that number — which, of course, is why there's a full complement in a fertilized ovum.

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#18975 - 11/07/11 01:44 PM Re: Shades of Ponce de Leon [Re: grelber]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
True. smile
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#18978 - 11/07/11 05:52 PM Re: Shades of Ponce de Leon [Re: tacit]
ryck Offline


Registered: 08/04/09
Loc: Okanagan Valley
Thanks very much for taking a complex subject and explaining it in a way that even my old brain can handle.
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#19004 - 11/08/11 10:58 PM Re: Shades of Ponce de Leon [Re: ryck]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
Except that telomere shortening is no longer a valid hypothesis; no real evidence for this has been found. In fact the ability to generate stem cells from adult cells completely negates this theory. Telomerase studies have been important and got their researchers a Nobel prize recently (only the creator of the theory was as usual not found among the laureates), but telomeres do not really shorten during life.
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#19005 - 11/08/11 11:51 PM Re: Shades of Ponce de Leon [Re: macnerd10]
grelber Offline


Registered: 08/05/09
Loc: North of 49th ||
Originally Posted By: macnerd10
Except that telomere shortening is no longer a valid hypothesis; no real evidence for this has been found. In fact the ability to generate stem cells from adult cells completely negates this theory. Telomerase studies have been important and got their researchers a Nobel prize recently (only the creator of the theory was as usual not found among the laureates), but telomeres do not really shorten during life.

Lucy, you got some 'splainin' to do. (Grâce à Desi Arnaz in persona of Ricky Ricardo, for those who don't go as far back as some of us.)
Three majorly contentious claims here, all of which require substantial peer-reviewed evidence to be considered.

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#19074 - 11/11/11 10:26 AM Re: Shades of Ponce de Leon [Re: macnerd10]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
Originally Posted By: macnerd10
Except that telomere shortening is no longer a valid hypothesis; no real evidence for this has been found. In fact the ability to generate stem cells from adult cells completely negates this theory. Telomerase studies have been important and got their researchers a Nobel prize recently (only the creator of the theory was as usual not found among the laureates), but telomeres do not really shorten during life.


Do you have a citation? That contradicts everything I can find published.
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#19131 - 11/12/11 11:36 PM Re: Shades of Ponce de Leon [Re: tacit]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
For generation of induced stem cells, hopefully, no citations are necessary because it is fairly obvious. Immortal cells are generated by inducing the expression of four genes in basically any adult cell studied. If these cells had their telomeres shortened and this were important for their lifespan, the resulting stem cells would be soon dead, which does not happen. For other stuff, here you go:
1. Trends Ecol Evol. 2006 Jan;21(1):47-53. Epub 2005 Nov 23.
Do telomere dynamics link lifestyle and lifespan?
Monaghan P, Haussmann MF. Shows that in long-lived birds there is no correlation of telomere length and aging.
2.http://learn.genetics.utah.edu/content/begin/traits/telomeres/
Cancer cells that are usually immortal have shortened telomeres.
3. http://longevity.about.com/od/whyweage/a/telomere_shortening.htm
Lay language account of findings. No direct correlation between telomere length and aging. In fact, in some people (about 30% of studied group, telomeres remain the same or even get longer!)
4. http://www.pnas.org/content/101/49/17312.long
Stress can induce telomere shortening and telomerase inhibition in premenopausal women.
5. http://www.scientificamerican.com/article.cfm?id=anti-aging-pill-targets-telomeres
Animals do not age through telomere shortening

And so on. It may be safe to say that telomere shortening may produce replicative senescence. It means that the number of divisions that a cell undergoes can be limited by this. Whether this reduces lifespan remains to be established because there are other mechanisms of senescence. It may be just a protection against cancer. Telomere shortening has been associated with some diseases that are frequent in aging population. However, it is unknown whether this is a sign/cause of real aging or an accompanying phenomenon. If telomere shortening is indeed associated with aging, this association may be indirect and other factors may be more important.


Edited by macnerd10 (11/13/11 12:44 AM)
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#19134 - 11/13/11 12:09 AM Re: Shades of Ponce de Leon [Re: macnerd10]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
I've been reading your links, and I don't think they say what you think they say.

For example, you made the assertion, "telomeres do not really shorten during life." Yet the link you provided at

http://learn.genetics.utah.edu/content/begin/traits/telomeres/

specifically says they do: "Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell no longer can divide and becomes inactive or "senescent" or dies." Similarly, it says that some cancers have shortened telomeres, but it odes not say that they continue to shorten each time the cancer cell divides (and in fact they do not do so; cancer cells express telomerase, which your cited article also explicitly says).

Ditto for your citation at

http://longevity.about.com/od/whyweage/a/telomere_shortening.htm

The very first paragraph in that article explicitly contradicts your "telomeres do not really shorten during life" claim. And the notion that some people have longer telomeres as they age is based on a study which looks only at blood cells. Blood cells are produced from stem cells in bone marrow which express telomerase, so looking at the telomeres in blood cells does not *necessarily* mean that the person's telomere length in other cells is similarly lengthening (further study, such as examining different types of cells in the same subject, is warranted).

That citation ends with a conclusion very different to you "telomere length is not involved in aging" conclusion; the cited article ends with "What does this mean? Nobody knows. It could be that those people have an amazing cellular anti-aging mechanism or it could be that they have an early sign of cancer (researchers tried to rule this out) or it could be fairly meaningless." and then says "What we do know for sure is that aging is a lot more complicated than simply looking at the shortening of telomeres"--which I think everyone involved in longevity research would agree with.

Telomere length may be one significant factor in aging as it relates to cellular senescence, but it certainly isn't the only factor. If it were, a simple shot of telomerase would be the Fountain of Youth.
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#19136 - 11/13/11 12:39 AM Re: Shades of Ponce de Leon [Re: tacit]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
You probably should read the whole article(s) rather than some sentences. There is no significant contradiction. The role of telomeres in aging is not established, period. What you say about blood cells that originate from bone marrow stem cells is correct. However, your logic does not explain why in 70% people these same cells have telomeres shortened in the course of a long study, while in 30% others there is no such thing, and some people even show increase in their length. My first post was provocative and the verdict was maybe too strong, I admit. The one with references should tell you that telomere shortening is not an aging factor, especially, one cannot say, like you did, that people age because their telomeres shorten during life. And experiments with birds suggest that the whole thing about telomeres may not be as some researchers tend to present it, with a lot of oversimplification and pizzazz, possibly, as part of grantsmanship. And please don't forget the whole cancer story (one can induce it by both removing telomerase or activating it) and the induced stem cells story.
By the way, all cells express telomerase but the activity decreases with age. Concerning the Fountain of Youth, Geron and another company (see one of the links) are trying to prove just that. We'll see... The problem with telomerase activity is also with oxidative stress influence, but the latter is not really correlated with aging.
Bottom line: we still do not know what are the mechanisms of aging and how can they be manipulated. This rhymes well with your last sentence, except that telomerase story is only one of several senescence mechanisms.


Edited by macnerd10 (11/13/11 12:44 AM)
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#19138 - 11/13/11 04:51 AM Re: Shades of Ponce de Leon [Re: macnerd10]
ryck Offline


Registered: 08/04/09
Loc: Okanagan Valley
Originally Posted By: macnerd10
For generation of induced stem cells, hopefully, no citations are necessary because it is fairly obvious. Immortal cells are generated by inducing the expression of four genes in basically any adult cell studied. If these cells had their telomeres shortened and this were important for their lifespan, the resulting stem cells would be soon dead, which does not happen. For other stuff, here you go.....

And so on.

Thanks for the interesting links (although I will admit my speed getting through is likely a bit slower than yours). However, without being too simplistic, there is one thing that seems to pop up often in associated links which I find quite interesting.

It seems that, in the end (and dreadful diseases aside), aging better and possibly longer seems very connected to all the stuff family Doctors have been saying for decades...don't smoke, get exercise, reduce stress, et cetera.

Maybe there's more than humour in Rompin' Ronnie's statement: "If I had known I was going to live this long I would have taken better care of myself."


Edited by ryck (11/13/11 04:52 AM)
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#19142 - 11/13/11 09:09 AM Re: Shades of Ponce de Leon [Re: ryck]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
This is so true!
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#19147 - 11/13/11 01:00 PM Re: Shades of Ponce de Leon [Re: macnerd10]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
Originally Posted By: macnerd10
My first post was provocative and the verdict was maybe too strong, I admit. The one with references should tell you that telomere shortening is not an aging factor, especially, one cannot say, like you did, that people age because their telomeres shorten during life. And experiments with birds suggest that the whole thing about telomeres may not be as some researchers tend to present it, with a lot of oversimplification and pizzazz, possibly, as part of grantsmanship. And please don't forget the whole cancer story (one can induce it by both removing telomerase or activating it) and the induced stem cells story.


I don't think that anyone will claim that people age because their telomeres shorten; that's an oversimplification of the argument. The actual argument is that aging may related to cellular senescence, and that telomere length may be a factor in senescence. (Other factors, such as accumulated cellular debris inside and between cells, changes in mitochondrial function over time, and accumulation of genetic damage have also been presented as factors in cellular senescence.)

It makes sense that suppressing telomerase functioning can trigger cancer, as one of the factors that may trigger cells to go cancerous involves genetic damage caused by destruction of telomeres and subsequent incorrect fusing of the chromosomes. However, once that happens, the cell then does begin to express telomerase; otherwise, it can't continue to divide indefinitely. (I doubt you'll see cancer cells that don't, though you may see cancer cells with abnormally short telomeres when compared with non-cancerous cells from the same organism.) Almost any kind of genetic damage can, in the right circumstances, turn a cell cancerous.

I'm supposed to have dinner with a local researcher here in Oregon soon; he has a Ph.D. in neurobiology and runs a lab that's looking for ways to halt or reverse aging-related cumulative damage to brains. He doesn't subscribe to personhood theory, so the two of us are on for a celebrity nerdcore dinner cage philosophical deathmatch on the topic, with a lovely young lady who's a friend of mine in attendance. I plan to bring up your claims about telomere shortening not being a factor in cellular aging and see what he says on the subject. smile
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#19148 - 11/13/11 01:09 PM Re: Shades of Ponce de Leon [Re: tacit]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
I re-read your post and found that you really did not make a causative link between telomere length and aging. It can only be inferred from your context. Anyway, tell us what he thinks from the neurobiology perspective. In neurons, BTW, this shortening process may not go on at all because they usually do not divide. I still think that giving a Nobel prize for telomerase was a premature thing...
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#19170 - 11/14/11 11:37 AM Re: Shades of Ponce de Leon [Re: macnerd10]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
Originally Posted By: macnerd10
In neurons, BTW, this shortening process may not go on at all because they usually do not divide.


That's true, but a lot of the focus that goes on in helping prevent or reverse aging-related damage in the brain looks at glial cells rather than neurons.

Back when I was in college, the world was a simple place. People assumed trickle-down economics would actually work, Apple had not switched processors away from the Motorola 68K line, and neurobiologists knew that glial cells were just support systems for neurons and weren't involved in the process of cognition or memory.

Nowadays, of course, all that is in disarray. And as it turns out, in mammalian brains the actions of glial cells like astrocytes appear to be central to the formation of new neural pathways...and astrocytes are critical in brain aging, playing key roles in neurogenesis, response to injury, and formation of glial scar tissues. Neurons don't divide, but (sone) glial cells do, and the brain's structure changes as we age in part (possibly) because of cellular senescence in some glial cells.

And it turns out that even microglia, which generally used to be thought nothing more than the brain's immune and scavenging system, can play a role in cognition and behavior. How's THAT for weird?
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#19173 - 11/14/11 02:08 PM Re: Shades of Ponce de Leon [Re: tacit]
macnerd10 Offline


Registered: 08/04/09
Loc: Los Angeles, CA
Actually, this microglia has been the most fascinating thing for me in the last two years. To make things more complicated, there are two kinds of it. The one that sits in the tissue as a watchdog against pathogens and injury is generally deleterious; the only thing it can do is starting inflammation as a "whistleblower" and scavenger of sorts. The second one that actually does repair comes from the bone marrow, possible recruited by this inflammation. Amazing stuff. Also, mice without immunity seem to be significantly more stupid than wild type!
Franklin, I am impressed about your knowledge of biology!
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#19174 - 11/14/11 02:39 PM Re: Shades of Ponce de Leon [Re: macnerd10]
tacit Offline


Registered: 08/03/09
Loc: Portland, Oregon, USA
Originally Posted By: macnerd10
Actually, this microglia has been the most fascinating thing for me in the last two years. To make things more complicated, there are two kinds of it. The one that sits in the tissue as a watchdog against pathogens and injury is generally deleterious; the only thing it can do is starting inflammation as a "whistleblower" and scavenger of sorts. The second one that actually does repair comes from the bone marrow, possible recruited by this inflammation. Amazing stuff. Also, mice without immunity seem to be significantly more stupid than wild type!


And it gets weirder. There are genetic mutations to hox genes, which normally only affect body layout, that can affect the behavior of microglia as well...and those mutations can lead to really complex high-level behaviors. I actually blogged about it recently, in fact.

Originally Posted By: macnerd10
Franklin, I am impressed about your knowledge of biology!


Thanks! I actually majored in neurobiology, back in my misspent college days. Didn't end up in a field even remotely related, though.
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