There are 11 syndromes that result in premature aging, or PROGERIAS (pro- towards / geria – elderly). Scientists have determined the genetic and molecular causes for them, so what can those details tell us about aging in general?
——————– THE PROGERIAS
(adapted from a chart from: “Shared Phenotypes Among Segmental Progeroid Syndromes Suggest Underlying Pathways of Aging,”
Hofer, AC et al , J Gerontol A Biol Sci Med Sci (2005) 60 (1): 10-20)
You may notice that only four of the Progerias show accelerated telomere shortening, but since 10 of 11 involve DNA maintenance problems, I believe a Telomere theory of aging still applies insofar as telomeres are made of DNA and therefore a subset of DNA maintenance. My own version of the telomere theory of aging can be found at the bottom of this page from my website: http://www.rechargebiomedical.com/aging.html
Here is a closer examination of Progerias by molecular etiology:
1) Helicases (in Blue above) are enzymes (like nanomachines) needed to unwind the double helix for all manner of DNA processing
2) DNA Transcription (in Orange) is the matching of complimentary strands for existing sequences (reading GGGTTA causes a ‘writing’ or transcription of CCCAAT on the opposing strand). Removal and repair of ‘typographic’ errors.
3) DNA Repair (in Red) fixes breaks in DNA, caps the telomeres, and permits checkpoints to hypnotize or kill off genetically-damaged cells.
4) Nuclear membrane integrity (in Yellow) is poor, making chromosome sorting and synthesis difficult
5) Telomerase dysfunction (in Green) allow for rapid shortening and uncapping of chromosome ends
Q: So what do all these cell processes have in common?
A: They all cause poor maintenance of our genetic integrity.
To quote from my older blog post:
“There are 50 billion cell divisions x 6 billion base pairs copied per cell division every day. This means there are 300 quintillion (300,000,000,000,000,000,000) chances to make a mistake every day.”
But the biggest problems are probably not from simple transcription “typos” but rather when telomeres become critically short, or uncapped. Uncapped DNA triggers repair mechanisms because the repair systems see them as DNA breaks which must then be joined together.
When the cell divides the next time, the fused chromosome is torn apart like trapeze artists that can’t let go, because the points of failure after end-to-end chromosome fusion are no longer the natural “fingertips”.
Now that you understand that premature aging, we can apply the same principles to regular aging, which simply reflects loss of data integrity made possible by telomere attrition (both from replicative senescence and oxidation) and by poor DNA repair and transcription in general.
By taking TA-65, you will recharge your telomeres and that is always a good thing. Call now before any more of your stem cell chromosomes become uncapped.
As a new feature to these blog posts, I’m offering this video ‘walk through’ of the main ideas. Click the image below to view it.
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