From: Aubrey de Grey (ag24@gen.cam.ac.uk)
Date: Mon Apr 21 2003 - 05:38:29 MDT
Robert Bradbury wrote:
> The working hypothesis that others (and I) have had is that if
> you increase protein recycling one gets a greater ratio of
> "new" proteins vs. "old" proteins. The new proteins are less
> damaged than the old proteins (from say oxidative or deamidation
> damage) and thus function more reliably/efficiently. An increase
> in the protein turnover rate may also cause proteins to be broken
> down before they accumulate sufficient damage that the normal
> recycling mechanisms will not work and they end up accumulating
> as lipofuscin.
Yes. However, as with all aspects of aging, the best solution is
not to slow down the progression of the problem (by methods such as
stimulating protein recycling), but to *reverse* that progression.
In this case, our best bet is to find bacterial or fungal enzymes
that can break down lipofuscin and introduce them transgenically
with modifications to target them to lysosomes. The same approach
can be used to treat atherosclerosis, neurodegenerative diseases,
and macular degeneration -- all of these are caused by aggregates
of stuff that the lysosome lacks the enzymatic machinery to degrade.
See Trends Biotechnol 20:452 for details. I will also be speaking
about such things at the Foresight Institute meeting in early May
and at the World Transhumanist Association meeting in late June.
Aubrey de Grey
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