"Reversing Human Aging" by M. Fossel

Todd A Carter tac2 at konichiwa.cc.columbia.edu
Mon Jun 10 21:27:53 EST 1996

In article <31BAF175.2B8E at biomed.med.yale.edu>,
Public Workstation <public at BIOMED.MED.YALE.EDU> wrote:

>Fossel believes that the evidence accumulated in past five years 
>suggests that aging is due to telomere shortening occuring as a result 
>of cell division. All other theories of aging are explaining secondary 
>phenomena or effects, not the causes, of aging. 
>According to Fossel, to prevent aging, it suffices to 'cap' the 
>telomere with a protein that serves a primar for initiating 
>replication (see the patent application PCT Publication No. 93/23572). 

Regardless of the validity of the telomerase-aging theory, the methods
described in "capping" the chromosomal ends and/or increasing telomerase
activity in normal cells seem way too simplistic.  As i understand it, the
major hypothesis connecting telomerase with aging supposes that genes on
the distal regions of the chromosomes  get "chewed up" as telomere length
reduces.  Any aging reversals would need ot replace these genes

Regarding the theory itself, I believe that although telomerase activity
has been correlated with the number of passes a cell culture can
withstand, it has never been proven that this is directly related to
organismal aging.  Although the fact that cell cultures from elderly
individuals can withstand fewer passes than those of infants is
suggestive, as is the same phenomenon seen with Wener's Syndrome patients
relative to normal controls without the disease.  Even so, the isue is
somewhat a controversial one.

--Todd Carter
--Dept. Genetics
--Columbia University

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