During cell division, the complete replication of DNA has been found to be simultaneously related to aging and diseases. Elizabeth H. Blackburn, Jack W. Szostak, and Carlo W. Greider, three American scientists, did research into telomeres and discovered telomerase, and were able to explain the mechanism of DNA sequence replication and prevention of decomposition. This won them the 2009 Nobel Prize in Physiology and Medicine.
There are many different theories that try to explain the biological causes of aging, and in 2015, Michael Fossel, the author of The Telomerase Revolution: The Enzyme that Holds the Key to Human Aging and Will Lead to Longer, Healthier Lives, issued a simple “Telomere Theory,” but was often misunderstood. However, he clearly explains that the aging of cells causes the aging of the human body, and suggests that the shortening of telomeres is the main cause of cell aging.
Human beings have been searching for various methods to reverse the symptoms of chronic diseases, but not until 2016 was a high concentration of telomerase released from the U.S. Many case studies were done in the past two years, and it was proven that only a concentration of telomerase above 68% has the best chance to reverse the symptoms of diseases.
According to experiments done in a medical center in 2018, a high concentration of telomerase is able to grow 14% of nerve cells within two weeks, while simultaneously protecting cells. The actual case studies are demonstrated in both English and Chinese.
細胞分裂過程中染色體DNA的完整複製，也同時關係著老化與疾病。伊莉莎白．布萊克本（Elizabeth H. Blackburn）、傑克．索斯塔克（Jack W. Szostak）以及卡羅．格雷德（Carol. W. Greider）這三位美國科學家在端粒（telomere）與端粒酶（telomerase）的發現及研究，解答了DNA序列之所以能完整複製與預防分解的機制，而榮獲2009年的諾貝爾生理醫學獎。
解釋老化的生物學原因，有許多不同的理論，在2015年《端粒酶革命：扭轉老化的關鍵》（The Telomerase Revolution）作者麥可．佛賽爾（Michael Fossel）主張的，是一個更簡易但也常被人誤會的理論，也就是端粒理論，他用很清晰明了的方式解說為何身體的老化來自細胞的老化。作者提出，端粒隨著時間的縮短，是造成細胞老化的主因。
人類一直在尋找可逆轉慢性疾病的方法，而高濃度的端粒酶在2016年才真正由美國研發完成。我們在這二年做了許多的個案，也證明了只有超過68%濃度的端粒酶才有逆轉疾病的機會。
根據醫學中心在2018年的實驗，高濃度的端粒酶，在兩星期後可增生14%的神經細胞，並同時保護細胞。而實際的使用效果，則會在各案例以中/英文
A telomere is a region of repetitive nucleotide sequences at each end of a chromosome and it is responsible for the completeness of the chromosome. When entering mitotic phase, each time the cell divides, the telomeres become shorter, every division causes telomere shorten a bit and induces the ageing of the cell. Uncapped telomeres result in the end of the chromosome unprotected and the chromosome will gradually decline and the cells begin programmed cell self-destruction.
端粒是真核生物染色體末端的DNA重複序列，負責保持細胞中染色體的完整性。當細胞進行有絲分裂時，染色體每一次的複製和分裂會使端粒變短，每分裂一次，染色體就會縮短一點，造成染色體末端端粒逐漸縮短，進而造成身體老化。如果沒有端粒的保護，染色體會遭到破壞，細胞則會進入凋亡程序。
Telomerase is a complex of RNA and protein and it is an enzyme that maintains the length of telomere. When the damage of the telomere occurs, telomerase will use its own RNA as a template to produce the new sequence and assist in the reconstruction of telomeres.
The enzyme telomerase composed of two subunits, the telomerase reverse transcriptase and the RNA component is used as a template for the de novo addition of telomeric repeats to chromosome ends.
端粒酶是一個由RNA和蛋白質組成的一種酵素，負責延長及維持端粒長度，當染色體尾端的端粒耗損時，端粒酶會合成序列並加到端粒上，來穩定染色體的結構。
端粒酶由兩個亞基端粒酶逆轉錄酶和RNA元件組成，用作染色體末端添加端粒重複序列。
Telomere length is hypothesized to be a biomarker of ageing. The enough length of telomere result in the cell processes normal function instead of ageing. There are two possible reasons caused the shorten of the telomere length: cellular replication and oxidation. Telomere length most likely reflects cellular senescence and oxidative stress after puberty.
端粒長度是衰老的生物標誌。端粒夠長可以使細胞維持正常功能，不會因為端粒縮短造成細胞老化。目前影響端粒長度的可能原因有兩個：細胞複製及氧化壓力。端粒長度最有可能反映青春期後的細胞衰老和氧化。