Cells and Aging

Thomas Mahoney excelife at earthlink.net
Wed Mar 10 07:21:53 EST 1999


 
>> In article <36E41B46.958BF089 at ryley.com>, james at ryley.com says...
>> 
>> >I didn't say it wasn't diminished.  I said it was sufficient for
>> >them to lead normal lives in many cases.  The point is this:  If
>> >a person with muscular dystrophy can go through 4X (just to pick
>> >a number -- there is no basis for that number, but whether it is
>> >really 2X or 20X the argument still holds) as many satellite cell
>> >divisions throughout the course of their life, and still have
>> >some reserve potential left during old age, that means that a
>> >person without muscular dystrophy should have 4 times more
>> >replicative potential than they need.  So, how can you argue that
>> >a normal old person is anywhere near having a problem with
>> >replicative potential of their satellite cells?
>> 
>> The severe musculature loss seen in the elderly starting at around the age 
>> of
>> 70 and increasing dramatically thereafter would be suggestive that the
>> replicative capacity of the satellite cells has been somewhat impaired.
>
>No, it doesn't suggest that -- unless you are stuck on using
>telomeres to explain everything about aging.  It suggests that
>SOMETHING is going on which causes decreased muscle mass.  That
>something could just as easily be a change in various hormone
>levels (which we KNOW occurs), or a decline in mitochondrial
>function, or any one of a hundred things.  
>
>Please point out to me what makes it more likely that telomeres
>are involved.  The argument that I have already presented would
>seem to say that reduced replicative capacity is a very unlikely
>candidate answer, or people with MD could not sustain their
>muscle past even middle age.
>
>And for the record, I'm not even saying I'm right here.  The
>argument that I am presenting is somewhat indirect, and perhaps
>there is an explanation that I am overlooking.  Maybe telomeres
>are the answer in this case, and maybe they aren't.  It isn't
>your conclusion that I object to -- it's how you arrive at it. 
>You say one thing logically follows from another, when in fact it
>doesn't.  I would speculate that you're just making arguments of
>convenience because you already "know" that telomeres are the
>answer.
>
>Sincerely,
>James

The musculature loss noted could very well be related to any number of the 
factors you noted as well as loss of nerve function or denervation.  
Telomeric shortening would only apply to the satellite cells which would be 
stressed to the point of replicative in-capacity trying to restore the muscle 
cells lost for whatever reason.

This position is supported by Dr. Decarys' work previously cited and in the 
paper; J Neurobiol 1992 Jun;23(4):407-19, "Transient neonatal denervation 
alters the proliferative capacity of myosatellite cells in dystrophic 
(129ReJdy/dy) muscle.", Ontell MP, et al, (Work done at my alma matter, The 
Univ. of Pittsburgh).

The research most on point is; (Somat Cell Mol Genet 1990Nov;16(6):557-65 
"Accelerated age-related decline in replicative life-span of Duchenne
muscular dystrophy myoblasts: implications for cell and gene therapy.", 
Webster C, Blau HM), where they say "Our results suggest that the myoblasts 
(satellite cells) of even the youngest DMD patients have undergone extensive 
division in an attempt to regenerate degenerating myofibers." and "A decline 
in replicative capacity was observed with increasing donor age, which was 
markedly accelerated for DMD, (Duchenne muscular dystrophy).

To restate my position, based on the research cited, the loss of musculature 
in the elderly is, most likely, unrelated to telomeric loss or replicative 
senescence, but the satellite cells ability to restore lost muscle cells is 
compromised by telomeric loss leading to replicative senescence.


Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
http://home.earthlink.net/~excelife/index.html  










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