Caloric restriction slows brain aging

Mike Reilly m-reilly-without-the-spam at
Mon Jul 10 17:05:04 EST 2000

If I'm reading you correctly, you are saying that while removing cells,
engineering them, and re-implanting them is being done, we are not yet at
the stage where we can manipulate the vast majority of cells that are in the
body.  We have not yet developed the techniques required to safely access
these cells (especially those in regions with minimal circulation).

I agree that this is an area that is in _real_ need of addressing.  I have
heard of some interesting work in terms of delivery of proteins to cells in
vivo, which may prove a boon both to ageing research as well as the
pharmaceutical industry.

One point I haven't seen much research on is the effect of lipofuschin on
cellular metabolism and function.  The correlation between it's buildup and
cellular age is unmistakable.  Any idea of the actual percentage of cellular
volume that is being consumed by liposomes?
Aubrey de Grey wrote in message <8kcg73$8e$1 at>...
>Mike Reilly wrote:
>> Perhaps I'm wrong, but I was under the impression that the work in
>> Edmonton was both somatic gene and cell therapy - the beta cells were
>> removed from a patient, insulin production was re-instated, the cells
>> cultured and then re-introduced.
>You're absolutely right.  My mistake was not in mis-remembering what
>was done, but in the terminology -- I always forget that introducing
>engineered DNA into cells in vitro (which are then put back into the
>body) still counts as gene therapy.  So, to restate my point: there
>are aspects of aging that might be addressed by in situ gene therapy,
>but which cannot easily be addressed by ex vivo gene therapy, because
>the number of cells that need to be altered in order to affect the
>phenotype is too large and the cells in question are postmitotic (so
>their number can't be increased after reimplantation).
>Aubrey de Grey

More information about the Ageing mailing list