[extropy-chat] AGING: research progress

[jpnitya at sapo.pt]

Hi!

Sorry for the late reply but only now did I have a chance to read the paper. It
certainly is an interesting experiment but, like Robert mentions, it doesn't
necessarily translate into life extension. In fact, George Martin has an
editorial in the same issue that I totally agree with. He mentions that despite
being a nice work, the real breakthrough will occur when scientists engineer
mice to have a "better" mitochondrial polymerase and thus, hopefully, live
longer. You can find his editorial:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15164048

All the best,

Joao

Citando "Robert J. Bradbury" <bradbury at aeiveos.com>:

>
> Well, it looks like the mitochondrial theory of aging
> is getting some support.  Scientists created mice
> with a defective mitochondrial DNA polymerase and it
> significantly shortened their lifespans.
>
> URL:
> http://www.sciencedaily.com/releases/2004/05/040527234844.htm
>
> Abstract from PubMed:
> Point mutations and deletions of mitochondrial DNA (mtDNA)
> accumulate in a variety of tissues during ageing in humans, monkeys and
> rodents. These mutations are unevenly distributed and can accumulate
> clonally in certain cells, causing a mosaic pattern of respiratory chain
> deficiency in tissues such as heart, skeletal muscle and brain. In terms
> of the ageing process, their possible causative effects have been
> intensely debated because of their low abundance and purely correlative
> connection with ageing. We have now addressed this question experimentally
> by creating homozygous knock-in mice that express a
> proof-reading-deficient version of PolgA, the nucleus-encoded catalytic
> subunit of mtDNA polymerase. Here we show that the knock-in mice develop
> an mtDNA mutator phenotype with a threefold to fivefold increase in the
> levels of point mutations, as well as increased amounts of deleted mtDNA.
> This increase in somatic mtDNA mutations is associated with reduced
> lifespan and premature onset of ageing-related phenotypes such as weight
> loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature
> of the spine), osteoporosis, anaemia, reduced fertility and heart
> enlargement. Our results thus provide a causative link between mtDNA
> mutations and ageing phenotypes in mammals.
>
> URL for Nature article:
>
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v429/n6990/abs/nature02517_fs.html
>
> Now it looks like the problem is due to an accumulation of mutations in
> the mitochondrial DNA.  But whether that problem causes decreased
> production of ATP (meaning the cells may have reduced protein production
> capacity) or in more production of free radicals and is thus linked to the
> free radical theory of aging (which IMO is linked in complex ways to the
> somatic mutation theory of aging) doesn't seem to be clear.
>
> However it should be considered that there are probably
> many ways to shorten lifespan -- but that doesn't immediately
> translate to methods that may be used to extend lifespan.
>
> Robert
>
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