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Telomerase Supplements

Why isn’t it possible to supplement telomerase in cells to prevent senescence (cell aging)?

Why isn’t it possible to supplement telomerase in cells such that senescence (cell aging) does not occur?
Telomeres shorten during DNA replication but are replenished by telomerase. As cells run out of telomerase, telomeres disappear, resulting in problems in DNA replication. Why can’t cells be supplemented with telomerase to prevent this?

You’ve got the right idea but cellular and system aging is far more complex than just the length of telomeres at the end of chromosomes. While telomere length is indirectly related to the aging of the organism, other factors come into play as well such as the accumulation of mutations in the DNA, decreasing efficiency in the DNA repair mechanism over time, the deterioration of cell membrane receptors, the build up of oxidants such as free radical in the cells and tissues, disease, and much more.

However, all other factors being equal, I do believe that if it was possible to turn the genes on and off at the appropriate time and for the appropriate duration for the production of telomerase, this would have a signifcant influence upon the aging process. This would be very, very hard to accomplish in an adult, but could be possible at the early embryo stage of development. In the early embryo, say before 10 days post fertilization, if the genes for telomerase could be linked with a “marker” gene that, when activated, produces a protein that stimulates the telomerase gene to produce telomerase as long as the marker gene remains active, then stop manufacturing telomerase whenever the marker gene turns off, some control over the aging process might be had. It would be necessary for the marker gene to respond to some stimulus that is neutral to all other genes in the genome and not toxic to life. Perhaps some harmless drug could act as the stimulus for the marker gene.

The thing can get quite complex with all of the positive and negative feedback loops necessary to manage system regulation and distribution of telomerase.

Here’s what I know about telomerase: it is found in abundance in both the early embryo and in many forms of cancer cells. With early embryo, the amount of telomerase usually falls off as the embryo develops and undergoes cellular and tissue differentiation (mature expression), and by the time that a baby is born, the genes for telomerase are put much turned off. Now, in cancer cells, the reverse is true. In a typical mature differentiated somatic cell there is very little, if any, telomerase present. When a normal cell mutates and becomes cancerous, over time it loses its mature gene expression or cellular differentiation and tries to revert back to an embryonic state. The more aggressive cancer cells are almost completely embryonic, and as such they revert back to producing telomerase in abundance again.

In fact, there was this one experiment done back in the 80s by Professor Robert Gilmore McKinney at the University of Minnesota where he extracted a nuclei from a type of frog cancer, cloned that nuclei, and got a living frog from it. This suggest that telomerase plays a significant role in development.

See: Telomerase Activity in Early Bovine Embryos Derived from Parthenogenetic Activation and Nuclear Transfer

http://www.bioone.org/doi/abs/10.1095/biolreprod64.3.770?journalCode=bire

CLONING: A Biologist Reports
by Robert Gilmore McKinnell
ISBN: 0-8166-0883-0

and

CLONING: of Frogs, Mice, and Other Animals
by Robert Gilmore McKinnell
ISBN: 0-8166-1360-5

also

CLONING: Nuclear Transplantation in Amphibia
by Robert Gilmore McKinnell
ISBN: 0-8166-0831-8

The Immortal CELL
by Dr. Michael D. West
ISBN: 0-385-50928-6

telomere repair – o’connor

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