Month: September 2022

NO AGING GENES. “Many confuse aging with longevity determination, which is indirectly driven by genes. There are no genes for aging. There are genes to maintain the biological functionality of an organism up to and including reproductive success. There is no mechanism that immediately causes death after reproductive maturation; it’s too costly. Longevity determination asks ‘Why do we live as long as we do?’ Aging research asks ‘Why does everything ultimately fail?’ and that is a huge difference.” https://lnkd.in/dQMB4k7 View in LinkedIn

CYCLE ARREST. “Cellular senescence is an irreversible cell cycle arrest caused by intrinsic or extrinsic stress, such as shortened telomeres, DNA damage, induced oncogenes, or chromatin perturbation.” https://lnkd.in/dKvxxVz View in LinkedIn

TELOMERASE. “A current hypothesis gaining prominence proposes that activation of the enzyme telomerase is necessary for cells to become immortal, or capable of proliferating indefinitely. The theory suggests that almost all cancer cells must attain immortality for progression to malignant states and, hence, require activation of telomerase.” http://jnci.oxfordjournals.org/content/87/12/884.short View in LinkedIn

MITOTIC CLOCK. “Hayflick first described the limited replicative capacity of normal human fibroblasts more than 30 years ago. Since then, numerous other somatic cell types, including epithelial cells, endothelial cells, myoblasts, astrocytes, and lymphocytes, have also shown evidence of a mitotic clock which limits their division capacity.” https://lnkd.in/dFjeJA3 View in LinkedIn

REPLICOMETER. “Telomeric shortening appears to be the replicometer that determines the number of times that a normal cell is able to divide. Once a threshold number of telomeric (TTAGGG) repeats is reached, downstream events presumably are triggered that signal the cessation of DNA replication. Wright and Shay have offered an alternative explanation of how telomere shortening acts as a replicometer.” https://lnkd.in/esfPTAR View in LinkedIn

TICK TOCK. “Eukaryotic chromosome termini consist of telomeres, short sequence repeats. According to the telomere hypothesis, DNA replication leads to telomere shortening, resulting in a cellular mitotic clock. Telomerase resets it by telomere synthesis.” https://lnkd.in/dm7mtBZ View in LinkedIn

SOMA VS STEM CELLS. “In mammals with a limited growth phase, telomerase activity in somatic tissues is restricted to stem cell derivatives with high proliferation potential. But other animals, like some fish, grow throughout their life with little senescence. All somatic cells require a high proliferation capacity and telomerase should be active in all cells, irrespective of fish age” http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(98)01020-5/full View in LinkedIn

TELOMERES AND AGING."Telomeres are the protective caps on the ends of chromosomes that affect how quickly cells age. They are combinations of DNA and protein that protect the ends of chromosomes and help them remain stable. As they become shorter, and as their structural integrity weakens, the cells age and die quicker." However, lifestyle may affect telomere activity.” http://www.ucsf.edu/news/2013/09/108886/lifestyle-changes-may-lengthen-telomeres-measure-cell-aging View in LinkedIn

“TELOMERASE ACTIVATION may be possible, to help reverse natural senescence in cells. Humans lack sufficient telomerase enzyme to stop telomeres from shortening and causing aging. Telomerase activation is an area of research aimed to try and slow cellular aging.” https://lnkd.in/deXSTEu View in LinkedIn

TETRAHYMENA THERMOPHILA “contains telomerase, that could replenish telomeres. Dr Blackburn established this unequivocally by mutating the telomerase gene in the tetrahymena and showing that this caused cell malfunction.” https://lnkd.in/d-EtCGX View in LinkedIn