This aging theory is related to a rare disease known as “Werner Syndrome” (WS). Werner Syndrome is often referred to as adult progeria and is defined by premature aging diseases such as cancer, atherosclerosis and inflammatory diseases. People suffering from WS can at the age of 30 to 40 endure old age predicaments such as wrinkled skin, cataracts, diabetes mellitus, muscular atrophy and baldness amidst “other pathologies”.
Werner Syndrome reduces the lifespan of cell culture in contrast to normal people. Cells from people suffering from WS do genetically fluctuate as they are not stable. “There is high propensity of DNA deletion as well as nonclonal translocation”. WS is “apparently caused by a mutation” of a particular gene known as WRN.
Werner Syndrome is thus a “hellicase deficiency Disease”. Hellicases are particular enzymes that are important in living organism and present in many cellular processes such as DNA replication, transcription, translation, recombination, DNA repair, and ribosome biogenesis. Typically WRN gene plays a key role in correcting abnormal DNA structures that can be developed from DNA metabolic practices such as repair, recombination and replication to ascertain that “cells are genetically accurate”.
There appears to be immediate connection between WS patient and the contemporary theory of “Telomere Shortening & Damage”. A “recent research conducted on mouse shows” that telomere dysfunction is affected by Werner Syndrome. It increases the tumorigenesis and aging process. The result of the tests showed that both deprivation of WRN gene and telomere functioning can provoke cancer as well as early aging.
The attribute of telomeres and cell senescence according to some researchers is a substantial issue related to WS. It is believed that WS function mainly through cell damage as well as telomere erosion caused by induced stress. Refer to “study 1” and “study 2”
Understanding Level
As a subsidiary theory on aging, it isn’t any clear understanding or rather a minor research has been conducted in the field of WS correlated to normal aging. Yet, hellicase enzyme and its negative mutation WS gene can be treated with intervention for instance with the activation of telomerase. Moreover, it is expected that some solutions that deal with Werner Syndrome can also contribute to deal with normal aging.
Evaluating various connections between “Hutchinson-Gilford Progeria Syndrome (HGPS)” and Werner Syndrome (WS) gives some possible hints about aging. Two aspects of HGPS and WS are:
1. Early aging phenotypes are experienced such as cardiovascular disease, wrinkled skin and baldness.
2. Genomic mechanism of the syndromes is different. The dissimilar genes and the functions of proteins are both different for HGPS and WS.
It is quite difficult to understand aging process. It is thus a mere fact that aging can be a result of different action of proteins. As for the “accumulation of progerin” a feasible treatment can be FTIs whereas with WS telomerase activation seems a better path.
There is no lifestyle or supplement recommended for this theory of aging as much research is still required to amplify the overview of Gene Mutation Leading To Hellicase Abnormalities
Further Reading
1. Road Map to Anti-Aging Theories
Reference
1. Helicase Wikipedia
2. Anti- aging firewalls the science and technology of longevity.
Anti Aging, Anti Aging Theories, Health And Aging, Longevity
Sat, Jan 2, 2010
Anti Aging, Anti Aging Theories, Health And Aging, Longevity