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Telomere |90120|

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Aging & Longevity
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“Telomeres”

Telomere
  In our body's cells, the essential genetic element Telomere, consisting of thousands of non-coding single G-rich DNA repeated TTAGGG hexanucleotide sequences, is the terminal section of each chromosome, which has a specialized structure, involved in the chromosomal replication and stability processes, bound to an array of associated proteins, and that play an essential role in chromosome capping.
  In our body's cells, Telomeres as DNA endcaps on chromosomes protect the ends from damage, and telomeric shortening, and is thought to govern the number of times a cell can divide.
The gradual shortening of telomeres through cell divisions leads to Aging at the cellular level when the telomeres reach a limit called Hayflick limit, the cell can no longer divide and becomes senescent or it dies.
  Senescence process is complex and derived from different mechanisms. Telomere shortening is a major intrinsic reason. when the telomeres reach a limit called Hayflick limit, the cell can no longer divide and becomes senescent or it dies *

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Telomeres

Telomere Shortening Mechanisms

“Telomere Shortening Mechanisms”

Telomere Shortening Mechanism
  In our body, the cells are constantly growing and dividing and eventually dying off, a process controlled by the chromosomes within each cell. These chromosomal end caps, which have been likened to the tips of shoelaces, preventing them from fraying, become shorter with each cell division, and when they are gone, the cell dies.

Aging
  In our body, the telomere shortening mechanism limits cells to a fixed number of divisions and can be regarded as a biological clock. Gradual shortening of telomeres through cell divisions leads to aging on the cellular level and may limit lifetimes. When the telomeres become critically short the cell undergoes death.

Telomere Theory of Aging
  Telomere have experimentally been shown to shorten with each successive cell division. Shortened telomeres activate a mechanism that prevents further cell multiplication.
This may be an important mechanism of aging in tissues like bone marrow and the arterial lining where active cell division is necessary. **

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References & Citations:


1. Ferrón S. et al "Telomere shortening and chromosomal instability abrogates proliferation of adult but not embryonic neural stem cells" Development. 2004 Aug;131(16):4059-70
2. Willeit P. et al "Cellular aging reflected by leukocyte telomere length predicts advanced atherosclerosis and cardiovascular disease risk" Arterioscler Thromb Vasc Biol. 2010 Aug;30(8):1649-56
3. Harley CB. et al "A natural product telomerase activator as part of a health maintenance program" Rejuvenation Res. 2011 Feb;14(1):45-56
4. Shi W. et al "BRE plays an essential role in preventing replicative and DNA damage-induced premature senescence" Sci Rep. 2016 Mar 22;6:23506
5. Rice C. et al "Structure and function of the telomeric CST complex " Comput Struct Biotechnol J 2016 Apr 14;14:161-7

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