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I read that the drug deprenyl concentrates at a part of the brain called the substania nigra, and that it makes 3 species of mammals live 25% longer. I think some researchers think it is from preserving the substania nigra area.
What if you use aptamers (the glomming part of antibodies) to concentrate
the deprenyl just at the brain? Might the localization cause greater longevity without alertness (jitteriness) side effects? Another approach is to link the deprenyl molecule to a photoactivatable molecule (like a porphyrin) so that it was only active where lasers illuminate the body?
Either of these strategies could also be used with rapamycin, another longevity drug with crummy side effects. So the technology here is photoactivated, area localized, longevity drugs with fewer side effects.
A website of potential anti-ageing compounds
http://agefactdb.jenage.de
[MaxwellBuchanan, Nov 02 2016]
phenformin longevity stidies on mammals, at the jenage.de database databse phenformin does about as well as metformin
http://lifespandb.s...search?q=Phenformin
[beanangel, Nov 03 2016]
[link]
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For those of you who, like me, were confused by
the sudden appearance of Deprenyl, it turns out
that it's a drug used to treat Parkinson's and which
also appears to significantly increase lifespan in
rats. |
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Rapamycin is an immune suppressor used to
control transplant rejection, and which has also
been convincingly shown to increase lifespan in
rats. |
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As to using aptamers (which are not, in general,
parts of antibody molecules; but which do bind to
specific targets) to target either of these drugs to
particular regions - I dunno, [beany]. For one
thing, just bolting a whopping great aptamer onto
a small molecule is likely to mess with its
activities. For another, the aptamer would
probably stop the drug crossing the blood/brain
barrier. And for yet another, I don't think there's
any evidence that the longevity actions of these
drugs are related particularly to the brain. |
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I bet the rapamycin mechanism for increasing longevity is the same as the reduced calorie mechanism. |
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Yes, that's the current theory. If you came up with
that idea independently, then huge kudos to you,
[bung]. |
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//rapamycin mechanism for increasing longevity// |
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Well, yes, the mTOR (mammalian target of rapamycin)
pathway is influenced by caloric restriction. There is, of
course other things going on. |
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//deprenyl concentrates at a part of the brain called the
substania nigra, and it makes 3 species of mammals live
25% longer// |
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bah, now, that's a monoamine oxidase inhibitor, which
interestingly is metabolized into methamphetamine...
Anyhow, all the life extension stuff is done in animals
which don't live very long. That's like making a bus go
round a race track faster, it's pretty easy to make
dramatic improvements on the baseline, but in the end
you will end up needing the strategies that existing racing
cars use. Mice, for example, aren't very metabolically
adaptable in the same way we are, they get pretty
stressed after a few hours without food, we're better at
reversibly breaking down and re building tissue over long
periods. In addition, we have a whole extra system for
redox metabolism, the uric acid system. It's not so well
studied (bias toward the systems that exist in model
organisms) but it's likely our chief circulating antioxidant. |
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Mice have to be nearly 50 fold better just to get to where
we already are. |
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Same thing we do everyday Pinky... |
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[mb] I read at science news there is an antibody drug that gloms onto beta amyloid (unless it is tau) at the brain, so i think apatamers could localize to various brain regions, so getting an antibody drug past the blood brain barrier is a demonstrated technology. |
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I mentioned the substania nigra concentration effects of deprenyl to suggest that longevity effects have been (speculatively, by a scientist) to specific area of the brain. |
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actually though I am fascinated with something you previously wrote, that you have a list of perhaps dozens of longevity chemicals (or possibly factors). If you like describe them at an annotation. even if i did a recombinant effort (titanium resveratrol!) There might be something fresh to think of. |
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[Bungston]'s comment makes me think that if they could do brain localization of insulin, or a CR mimetic drug perhaps brain aging could be reduced. I once read the brain runs off lactic acid (!) rather than glucose though. |
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//a list of perhaps dozens of longevity chemicals (or
possibly factors)// |
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The list is about 50 items long, and ranges from
simple chemicals to things like caloric restriction.
However, you can also browse a website devoted to
life-extending drugs <link> |
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// so that it was only active where lasers illuminate the body? |
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We're shooting lasers inside brains now? |
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Yes, but miniature sharks guide them to the correct
site. |
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[mb] thanks for the reference, many of the chemicals were completely new to me, yet there are many published at peer reviewed literature that were missing, so I wrote them a note with some of the missing ones. "Deprenyl (selegiline) 3 mammal species (mice, rats, dogs), about 20-25% greater longevity
the peptide epithalon, mammals
Reishii fungus, mammals
charcoal enterosobent, mammals
royal jelly, mammals
C60 Buckminster fullerene at olive oil, mammals" |
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What's the deal with mitochondria or whatever where
it loses a chunk every time a cell splits? Isn't that the
main time bomb all life forms have at the cellular
level? |
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Don't know where I read that. Don't know if it's a
theory or fact or even if I'm quoting the concept
correctly, but I seem to remember there's more than
just getting the chemistry right to get past 150 years. |
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//What's the deal with mitochondria or whatever
where it loses a chunk every time a cell splits?// |
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That's not mitochondria - that's telomeres.
Telomeres are short stretches of repetitive DNA at
the ends of chromosomes. Every time a
chromosome replicates (which happens in cell
division), the telomeres get shorter, because the
replicating machinery can't copy all the way to the
very end of the chromosome. After enough cell
divisions, the telomeres are down to zero length,
and then further divisions result in loss of
important stuff. |
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Mitochondria are little internal structures with
their own DNA - they're basically intracellular
bacteria, but stripped down. They divide as
needed to make more mitochondria. However,
their DNA replication/repair machinery isn't
perfect, so they tend to accumulate mutations and
become dysfunctional with age. |
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[drremulac] the mouse genetically engineered to live twice as long as controls was engineered to make more telomerase as well as a cancer preventing thing called p53. A human, Elizabeth Parish, has sought out telomere lengthening with gene therapy to improve her longevity. So if you have some extra money, there is a human protocol. |
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Also if you are willing to order deprenyl and phenformin [link] (or metformin) online you might live much longer for less than $365/year. |
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