Telomeres shorten with each cellular replication; telomere length is inversely proportional to age. While telomere extension does tend to make cells "young again", telomere extension is problematic for a treatment for age because many kinds of cancer replicate indefinitely due in part to the fact they have overactive telomerase, a protein that extends the telomeres. Until the link between cancer and telomeres is understood, telomere extension therapy will not be feasible.
Telomeres
One of the long-term arguments about aging is between a person's calendar age and biological age. Calendar age being your chronological time period by measurement of days and Biological meaning your fixed age.
APEX - Perceptions of aging change with culture.
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1771 by Ludwig Galvani
It is speculated that shortening of telomeres could be the cause of aging, or could be speeding the aging process up. It is known that telomeres preserve the life of the cell and may even extend the life of the cell. To understand how aging of the cell happens, we have to look back at the life of the chromosome. The cell divides and the telomeres continue to get shorter and shorter until it reaches such a critical length that the cell loses its ability to divide. Some cells might die or as mentioned earlier, they will lose their reproductive capability, or cellular senescence. Cellular senescence will have an overall affect on the organism, contributing to decline of tissue function that is the main trait of aging. Therefore, it is right to assume that telomere dysfunction which leads to senescence, has an effect on the aging process.
The telomere is the protective cap of DNA on the tip of chromosomes. You lose a small amount of these telomeres each time the cell divides. Eventually the telomeres be lost as you age. Short chromosomes because of lack telomeres are one reason aging occurs.
When telomeres shorten, the cell's ability to divide and replicate gradually diminishes. This can lead to cellular senescence or programmed cell death (apoptosis), ultimately impacting tissue regeneration and overall aging. Shortened telomeres are also associated with an increased risk of age-related diseases like cancer and cardiovascular conditions.
Maintaining telomere length has been associates with aging. The enzyme telomerase adds nucleotides to the ends of telomeres thereby maintaining their length. This enzyme is able to function only until a certain limit, called the Heyflick limit (named after the person who first reported this phenomenon). When the heyflick limit is reached, telomeres cannot be enzymatically lengthened and are programmed for death
Telomeres, located at the ends of chromosomes, play a role in aging and cancer. They protect the chromosome from degradation and help regulate cell division. Loss of telomere function has been associated with both aging and cancer development.
Telomeres are the special DNA sequences located at the ends of chromosomes that protect them from deterioration and contribute to aging and cell death when they become too short. Telomeres gradually shorten with each cell division, eventually reaching a critical length that triggers cellular senescence or death.
Aging is the most common form of degenerative disease. It infects everyone and is 100% fatal. Although long looked at as a natural process, there has been significant progress in combating it's effects. It is thought to be caused by a decrease in the length of telomeres in the process of cell replication.
The end replication problem refers to the gradual shortening of telomeres, which are protective caps at the end of chromosomes, with each cell division. Telomerase is an enzyme that can rebuild telomeres, but its activity is often reduced in aging cells. This leads to cell senescence, reduced tissue repair, and contributes to the aging process in humans.
It is difficult to predict when the first experiment on humans to stop all genes of aging will take place, as such a development would need thorough testing and ethical considerations. Research is ongoing in the field of aging and genetics, but more time and studies are needed before reaching a point where interventions on all aging genes would be feasible in humans.
Elizabeth Blackburn was awarded the Nobel Prize in Physiology or Medicine in 2009 for her discovery of how chromosomes are protected by telomeres and the enzyme telomerase. Her research shed light on the role of telomeres in cellular aging and cancer development.
Mitosis is a form of cell division. Cancer is a mutation in cell division, generally in such a way that cell divide too often and are unregulated and end up developing a mass. Those cells also carry the mutation and those cells divide and create new mutated cells, on and on and on.
Yes. We all begin as 1 cell and as it divides the telomeres become shorter. Larger people have more cells than smaller people and therefore have shorter telomeres.