Amazing! And also remember the article about positive thinking making people younger?
I wonder how much the brain can control aging processes.
Since statistically, senescence is kind of super-exponential, one wonders if it's a mix of several factors that compound together. If you achieve improvements in just some of these factors, perhaps the human life span can be extended to hundreds of years!!
A few years back, researchers found that manipulating levels of NF-κB in the hypothalamus influenced the pace of aging in mice [1]. That work was several steps removed from any idea as to what exactly was going on under the hood; changing the amount of a specific protein in circulation can have any number of effects, both direct and subtle. NF-κB is already an area of interest in the study of aging and metabolism, and so there are many mechanisms to speculate on in this context. There was indeed speculation at the time. Other indirect evidence suggests that the quality of cellular function in the hypothalamus is connected to the pace of aging, such as results arising from investigations of autophagy and its relevance in this part of the brain. Other researchers have made some inroads into mapping possible ways in which the hypothalamus might influence the operation of metabolism throughout the body in order to modestly speed or slow aging. It is well known that the hypothalamus regulates all sorts of aspects of metabolism, but the open question is which of these relationships are relevant to the matter at hand.
The team that investigated NF-κB in the hypothalamus has since been hard at work, seeking a better understanding as to why this part of the brain is important in the way in which metabolic processes determine individual variations in aging and longevity. In a recently published paper [2], the team now points to one particular small population of stem cells in the hypothalamus that diminishes with age; losing these cells more rapidly appears to speed processes of aging throughout the body. The researchers believe that signals generated by these cells are the mechanism of action, and a closer investigation of these signals is the next step in this line of research. It has to be said that this sounds quite similar to the situation for Parkinson's disease, at least at the high level, in which one small but critical population of cells in the brain is diminished at a different pace in different individuals, and where autophagy - and disruption of autophagy in aging - might be important in determining the rate of loss. It also clearly parallels what is known of the age-related decline of stem cell populations in all tissues. We become damaged, and stem cell loss and inactivity is a downstream consequence of that damage.
Either way, this might make an interesting target for cell therapy: certainly, replacement of stem cell populations is on the rejuvenation research checklist. Whether it is a priority in this case rather depends on the size of the effect, however, which in this study looks like a ~10% gain in life expectancy resulting from a single cell therapy treatment carried out in middle-aged mice. Unfortunately, significant changes in longevity in mice on the basis of altered metabolism so far do not translate to significant changes in longevity in humans, at least in the few areas where the data exists for comparison. The life spans of short-lived mammals are far more plastic in response to circumstances and interventions than those of long-lived mammals. In the case of stem cell replacement as a way to reverse declines, however, it is hard to say how the comparisons will turn out - the data just isn't there yet. It is the fond hope of many in our community that approaches based on repairing loss and damage, very different from approaches based on altering metabolism to modestly slow damage accumulation or resist the consequences of damage, will turn out to have similarly scaled effects on life span in mice and humans. Maybe so, maybe not. As I said, the data isn't there. In order to find out, rejuvenation therapies based on repair must be rigorously tested in humans, and that hasn't yet happened in any useful way, even in the stem cell field.
It seems like evolution would have had to stumble on several different pathways for slowing aging in order to produce long-lived species to begin with.
Perhaps the smaller mammal research doesn't seem to apply to humans because our aging pathways have already been somewhat optimized?
There is no evolutionary pressure to increase the life-span of individual organisms, past a certain point.
To the contrary, there might be an evolutionary benefit in having your parents die off shortly after they've done all they can to increase your, and your siblings, chance of reproducing. The reason a timely death might increase the chance of the gene-line's survival is because the parent might otherwise consume scarce resources that are better invested in the offspring.
You are not considering the value that very old individuals might contribute (and in fact do so) in many sophisticated societies with language: teaching of younger individuals and also acquiring deep complex knowledge about life, which can be simply impossible to do if they had short lives (they would just not have time to learn any of it).
In many times of our history the resources weren't that scarce to begin with. Primitive tribes don't need to dig for rare metals to make their Teslas, they could survive and thrive on very abundant resources.
All that evolution "care about" are genes, no individuals.
That doesn't mean that sometimes big life-span of individuals can't be a good strategy for some genes.
About the down-voting thing: it seems to me that if you disagree with somebody, instead of down voting, the best strategy is to answer.
If you don't care enough about the comment for answering maybe you shouldn't be down-voting.
In my opinion, down-voting should be use for keeping the conversation civil and on the subject at hand, or things like fighting spam, not for expressing disagreement.
I agree with that, and it makes sense, but unfortunately pg (Paul Graham) said years back that you CAN use downvotes to disagree on HN and so now it's law or something.
11 comments
[ 3.4 ms ] story [ 40.8 ms ] threadI wonder how much the brain can control aging processes.
Since statistically, senescence is kind of super-exponential, one wonders if it's a mix of several factors that compound together. If you achieve improvements in just some of these factors, perhaps the human life span can be extended to hundreds of years!!
The team that investigated NF-κB in the hypothalamus has since been hard at work, seeking a better understanding as to why this part of the brain is important in the way in which metabolic processes determine individual variations in aging and longevity. In a recently published paper [2], the team now points to one particular small population of stem cells in the hypothalamus that diminishes with age; losing these cells more rapidly appears to speed processes of aging throughout the body. The researchers believe that signals generated by these cells are the mechanism of action, and a closer investigation of these signals is the next step in this line of research. It has to be said that this sounds quite similar to the situation for Parkinson's disease, at least at the high level, in which one small but critical population of cells in the brain is diminished at a different pace in different individuals, and where autophagy - and disruption of autophagy in aging - might be important in determining the rate of loss. It also clearly parallels what is known of the age-related decline of stem cell populations in all tissues. We become damaged, and stem cell loss and inactivity is a downstream consequence of that damage.
Either way, this might make an interesting target for cell therapy: certainly, replacement of stem cell populations is on the rejuvenation research checklist. Whether it is a priority in this case rather depends on the size of the effect, however, which in this study looks like a ~10% gain in life expectancy resulting from a single cell therapy treatment carried out in middle-aged mice. Unfortunately, significant changes in longevity in mice on the basis of altered metabolism so far do not translate to significant changes in longevity in humans, at least in the few areas where the data exists for comparison. The life spans of short-lived mammals are far more plastic in response to circumstances and interventions than those of long-lived mammals. In the case of stem cell replacement as a way to reverse declines, however, it is hard to say how the comparisons will turn out - the data just isn't there yet. It is the fond hope of many in our community that approaches based on repairing loss and damage, very different from approaches based on altering metabolism to modestly slow damage accumulation or resist the consequences of damage, will turn out to have similarly scaled effects on life span in mice and humans. Maybe so, maybe not. As I said, the data isn't there. In order to find out, rejuvenation therapies based on repair must be rigorously tested in humans, and that hasn't yet happened in any useful way, even in the stem cell field.
[1]: http://dx.doi.org/10.1038/nature12143
[2]: https...
Perhaps the smaller mammal research doesn't seem to apply to humans because our aging pathways have already been somewhat optimized?
To the contrary, there might be an evolutionary benefit in having your parents die off shortly after they've done all they can to increase your, and your siblings, chance of reproducing. The reason a timely death might increase the chance of the gene-line's survival is because the parent might otherwise consume scarce resources that are better invested in the offspring.
All that evolution "care about" are genes, no individuals. That doesn't mean that sometimes big life-span of individuals can't be a good strategy for some genes.
About the down-voting thing: it seems to me that if you disagree with somebody, instead of down voting, the best strategy is to answer.
If you don't care enough about the comment for answering maybe you shouldn't be down-voting.
In my opinion, down-voting should be use for keeping the conversation civil and on the subject at hand, or things like fighting spam, not for expressing disagreement.
It doesn't look like a rule that makes the conversation more interesting, though.