Update On Recent Werner's Syndrome Research

Werner's syndrome is one variety of apparently accelerated aging. It is less aggressive than Progeria, the other most common varient of this class of rare conditions, but still horrible enough. Scientists have already shown that Progeria is accelerated aging (rather than just appearing to be accelerated aging), a fact that makes this condition even more compelling for aging researchers. Curing Progeria should pave the way for advances in our understanding of the aging process in healthy adults.

But back to Werner's Syndrome. An article from the ever-reliable Betterhumans brings us up to date on the latest:

A new discovery about a protein's role in a premature aging disease has given researchers a better understanding of the illness and provided insight into normal aging.

The disease, Werner's syndrome, causes young people who would be otherwise healthy to suffer from such aging-related conditions as osteoporosis, heart disease, cataracts, wrinkled skin and grey hair.

Sufferers are known to lack a protein called RecQ helicase WRN. However, until now scientists were unsure why the absence of this protein affected so many different cells.

...

Telomeres are like ticking clocks, normally shortening when cells divide and initiating cell death when they get too short. But without RecQ helicase WRN, Karlseder and colleagues found, telomeres can often be lost instead of just shortening.

The researchers believe that the lost telomeres can lead to chromosomal instability which can result in cancer. This could explain why many Werner's sufferers die of cancer by middle age.

"The finding that the loss of individual chromosome ends (telomeres) can induce cellular aging is significant for aging in general, since it contradicts the hypothesis that all telomeres in a cell gradually erode, and at a certain critical length induce an aging program," says Karlseder.

...

"The biggest implication of our studies lies in the understanding of age-related cancer development," says Karlseder. "One could hypothesize that avoiding individual telomere loss (by that I mean loss of a telomere from a single chromosome) would avoid genome instability and therefore cancer."

So it comes back to telomeres, just like many other threads of modern research into aging and cancer. Developing therapies for Werner's may bolster our understanding of telomere science, and thus aid the fight to cure aging and cancer.

Comments

You might be interested to know that we think ACE is the aging gene. We've applied for patent-protection on the idea, for what it's worth. Here are some relevant publications for your website, in reverse order of publication:

1. Moskowitz DW, Johnson FE. The central role of angiotensin I-converting enzyme in vertebrate pathophysiology. Curr Top Med Chem. 2004;4(13):1433-54. PMID: 15379656 [PubMed - indexed for MEDLINE]

2: Moskowitz DW. Pathophysiologic implications of angiotensin I-converting enzyme as a mechanosensor: diabetes. Diabetes Technol Ther. 2003;5(2):189-99. PMID: 12871609 [PubMed - indexed for MEDLINE]

3: Moskowitz DW. Is "somatic" angiotensin I-converting enzyme a mechanosensor? Diabetes Technol Ther. 2002;4(6):841-58. PMID: 12685804 [PubMed - indexed for MEDLINE]

4: Moskowitz DW. Is angiotensin I-converting enzyme a "master" disease gene? Diabetes Technol Ther. 2002;4(5):683-711. PMID: 12458570 [PubMed - indexed for MEDLINE]

5: Moskowitz DW. From pharmacogenomics to improved patient outcomes: angiotensin I-converting enzyme as an example. Diabetes Technol Ther. 2002;4(4):519-32. PMID: 12396747 [PubMed - indexed for MEDLINE]

Best regards,
Dave
--

David W. Moskowitz MD, MA (Oxon.), FACP
Chairman, CEO, and Chief Medical Officer
GenoMed, Inc. (OTC Pink Sheets: GMED)
http://www.genomed.com

9666 Olive Blvd., Suite 310
St. Louis, MO 63132
Tel. 314-983-9938
FAX 314-983-9939
dwmoskowitz@genomed.com

Posted by: David Moskowitz MD MA(Oxon.) FACP at April 8th, 2005 7:08 AM

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