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Of Nobels and Telomeres: The Disease Management Care Blog Explains

Posted Oct 05 2009 10:01pm
The 2009 Nobel Prize in Medicine has been awarded to Drs. Blackburn, Greider and Szostak for their work in ‘telomeres and the enzyme telomerase.’ According to the cluttered news web sites CNN and MSNBC, telomeres guard chromosomes and telomerase protects telomeres which is important in diseases like cancer. Unfortunately for the main stream media, this news is competing with the swine flu scare, Kate minus Jon Plus Eight, Mr. Letterman’s foibles and the death of Gourmet Magazine.

The Disease Management Care Blog to your rescue with a brief analysis.

Chromosomes contain DNA, which is literally the computer used by cells to run the machinery of life. ‘ Telomeres ’ are pieces of inert or inactive DNA that are present at the ends of all chromosomes. They protect the rest of the interior and important functional genetic material from being degraded by other normal cellular enzymes that clean up unneeded or leftover molecules, including DNA. If there are no telomeres to protect the DNA, valuable genes on the inside are damaged, leading to cell malfunction and an inability to replicate.

Telomerases are proteins that build telomeres. No telomer ase means no telo meres means early cell death. Lots of telomerase means lots of telomeres means cells can theoretically live forever.

Many types of cancer cells seem to have an abnormal ability to increase telomerase, which may explain how those cells continue to live, divide and invade normal tissues. If that can be turned off, it may offer a tool to fight cancer. In addition, there are some diseases of premature aging like Werner’s Syndrome which seem to be caused by accelerated telomere shortening. While rare, they speak to the role of telomeres in normal aging.

It has been observed that as humans age, their telomeres seem to progressively shorten. This ‘exhaustion’ has been known about for decades. With each cell division (called ‘mitosis’) in our bone marrow, gastrointestinal tract, skin and other tissues, our telomeres appear to grow shorter. As a result of this 'mitotic clock,' over the course of aging, we are left with DNA that is increasingly vulnerable, fractured, malfunctioning and unable to maintain normal health. In other words, our life span may be a function of our telomerase.

If we can determine how to 'up-regulate' telomerases in our normal tissues, we may not only be able to battle diseases like arteriosclerosis but to lengthen time of fertility, engineer tissues for transplantation and possibly significantly increase our human life span beyond the accepted maximum of approximately 120 years.

According to this 2006 article in the New England Journal of Medicine, our newest Nobel Prize Laureates' research 30 years ago on how telomerase inactivation led to telomere shortening and eventual senescence in yeast laid the foundation for our current understanding about telemeres.

The DMCB adds its hearty congratulations to Drs. Elizabeth Blackburn, Carol Greider, and Jack Szostak.

Coda: While thinking about the content of today's blog, the DMCB went for a walk with the DMCB spouse. Unable to restrain it's telomeric excitment, it opened a conversation by asking if she knew what the latest Nobel Prize had been awarded for. Feigning lachrymose disappointment, she exclaimed 'What!? Did they skip you again?'
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