
Neural Stem Cells in the Hypothalamus Shown to Control Rate of Aging in Mice - meri_dian
https://www.sciencedaily.com/releases/2017/07/170726132107.htm
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EGreg
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!!

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reasonattlm
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.

[1]:
[http://dx.doi.org/10.1038/nature12143](http://dx.doi.org/10.1038/nature12143)

[2]:
[https://doi.org/10.1038/nature23282](https://doi.org/10.1038/nature23282)

~~~
xenadu02
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?

~~~
Expez
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.

~~~
RobertoG
I don't know why you are down-voted.

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.

~~~
philbarr
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.

~~~
RobertoG
Really? I was not aware of that. Then, I suppose is me who is not following
the rules.

It doesn't look like a rule that makes the conversation more interesting,
though.

