Re: [DIYbio] Re: DIY longevity biology

On 02/15/2014 04:21 PM, Mega [Andreas Stuermer] wrote:
> Ok. But this sounds too good ;)
>
> Transfect some cells that produce a mitochondrial protein. The protein is released into the bloodstream. The protein then enters the cells and due to its mitochondrial localization signal enters the mitos and does its job. Forever young :D of course not, as there still are other mitochondrial genes you'd have to replace this way.
>
In the original protofection methodology TFAM is only a vector, a way to
deliver an attached chunk of mitochondrial genome, and thus provide
replacements for damaged mitochondrial genes that have overtaken cell
mitochondrial populations because they are selected for in mitochondrial
cellular dynamics, despite being harmful to the organism. You can
replace the whole genome at once this way, which is why it is
interesting. The gene-by-gene allotopic expression approach of SENS is
more work, but has the upside that it absolutely fixes the problem
forever going forward. There is the nagging suspicion that delivering
new mitochondrial genes will have only a short term benefit unless you
get rid of the old damaged ones completely (whole separate topic of how
to clear and replace mitochondria safely), because if you don't then the
same mechanisms that caused clonal expansion of the damaged
mitochondrial genomes will still be operating.

I'm told other teams have had trouble replicating protofection in the
years since then, but there are other mechanisms that work or might work
or are in some stage of being made to work to deliver new mitochondrial
genomes to mitochondria. Or even deliver whole mitochondria, since
apparently there are proteins you can attach to a mitochondrion that
encourage a cell to engulf and adopt it.

The principal protofection researchers have found that TFAM in and of
itself has enough of an effect on mitochondria / metabolism / whatever
that it makes more economic sense under the present regulatory situation
to pursue that as the basis for a marginal therapy for LHON /
Parkinson's disease / whatever rather than the thing that you can't get
regulatory approval for, which is treating the "normal" mitochondrial
dysfunction that contributes to aging.

Even if you repair mitochondria and gain benefit, you're not forever
young. You still need to repair the other causes of degenerative aging.
Senile systemic amyloidosis in particular will kill you somewhere past
the age of 100 regardless of your mitochondrial status. All (seven-ish)
of the processes causing aging need to be addressed/repaired in order to
unlock radical life extension. Probably. Though I'd be surprised to find
that any of them can be ignored, given the clear links between these
processes and specific fatal age-related conditions.

Reason

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