Modern anti-aging treatments are based on a common knowledge that I will review soon. Biochemistry and molecular biology tell us that many types of chemical reactions take place in the human body. We know that the genetic information programmed in our cellular DNA defines the response that occurs. Genetic information expressed in a regulated manner constructs proteins and enzymes in the human body and controls how the enzyme performs biochemical reactions of the cells.
This information is contained in the DNA of our genome and consists of thousands of long, usually repeating, base pair sequences consisting of four basic nucleotides. The human genome map shows more than 3 billion base pairs in our DNA. It is estimated that they contain about 20,000 protein-coding genes. All body functions are controlled by the expression of genes in our genome. The mechanism that controls the aging process is thought to be programmed into our DNA, but only a small fraction of the biochemical reactions associated with the aging process have been studied in detail. Cell aging is a very complex process and many of its low level of operational details have not been discovered.
The anti-aging theory has consolidated itself along two lines: the theory of programmed cell death and the theory of cell damage. Programmed death theory focuses on the root causes of aging. The theory of cell damage focuses on the visible aspects of aging; the symptoms of aging. Both theories are correct and often overlap. Both theories are rapidly evolving as anti-aging research reveals more details. As the work progresses, these theories may take years to complete. This broad characterization also applies to the types of anti-aging treatments currently available.
The programmed theory of aging death suggests that biological aging is a programmed process controlled by many life-regulating mechanisms. They are expressed through gene expression. Gene expression also controls physical processes such as our body maintenance [hormone, steady-state signaling, etc.] and repair mechanisms. As we age, the efficiency of all such regulations will decline. Programmed cell death researchers want to understand which regulatory mechanisms are directly related to aging and how they are affected or improved. Many ideas are being sought, but one of the key areas of concern is to slow or prevent telomere shortening. This is considered to be the main cause of aging.
Except for germ cells that produce eggs and sperm, most split human cell types can only split about 50 to 80 times [also known as the Hayflick limit or the biological death clock]. This is a direct result of all cell types with fixed length telomere strands at the ends of the chromosome. This is true for all animal [eukaryotic] cells. Telomeres play a crucial role in cell division. In very young adults, the telomere chain is about 8,000 base pairs long. Each time the cell divides, its telomere strand loses about 50 to 100 base pairs. Usually this shortening process distort the shape of the telomere chain and becomes dysfunctional. Then cell division is no longer possible.
Telomerase is an enzyme that constructs a fixed length telomere chain and is usually only active in young, undifferentiated embryonic cells. Through the process of differentiation, these cells eventually form specialized cells from which all our organs and tissues are made. After cell specificization, telomerase activity ceases. Normal adult human tissue has little or no detectable telomerase activity. why? A finite length telomere chain contains chromosomal integrity. This is more able to protect species than individuals.
In the first few months of development, embryonic cells are organized into about 100 different specialized cell lines. Each cell line [and the organs they make] has different Hayflick limits. Some cell lines are more susceptible to aging than others. In the heart and brain parts, cell loss is not supplemented. As the age grew, this organization began to fail. In other tissues, damaged cells die and are replaced by new cells with shorter telomere chains. Cell division itself only results in the loss of about 20 telomere base pairs. The remainder of telomere shortening is thought to be due to free radical damage.
This limitation of cell division is the reason why effective cell repair cannot be performed indefinitely. When we are 20 to 35 years old, our cells can almost completely renew themselves. One study found that at 20 years of age, the average length of telomere chains in leukocytes was approximately 7,500 base pairs. In humans, skeletal muscle telomere lengths remain more or less in the mid-1920s to mid-seventies. By the age of 80, the average telomere length was reduced to approximately 6,000 base pairs. Different studies have different estimates of how telomere length varies with age, but it is consistently believed that between 20 and 80 years old, the length of the telomere chain is 1000 to 1500 base pairs. Later, as the length of telomeres shortened, signs of severe aging begin to appear.
Human telomerase has genetic variation. It is said that the long-lived German Jews have a more active form of telomerase, which is longer than the normal telomere chain. Many other genetic differences [eg, DNA repair efficiency, antioxidant enzymes, and free radical production rates] affect the rate of aging. Statistics show that shorter telomeres increase the chance of death. People with telomeres are 10% shorter than average, and people with telomeres 10% longer than the average die at different rates. The person who sent the telomere died at a rate 1.4 greater than the longer port of the telomere.
Many advances in telomerase-based anti-aging treatments have been documented. I only have space to mention some.
- Telomerase has been successfully used to extend the lifespan of some mice by up to 24%.
- In humans, gene therapy using telomerase has been used to treat myocardial infarction and other diseases.
- telomerase-associated mTERT treatment has successfully revived many different cell lines.
In a particularly important example, the researchers used a synthetic telomerase encoding telomere extension protein to extend the telomere length of cultured human skin and muscle cells to 1000 base pairs. This is 10% of the length of the telomere chain + extension. The treated cells then showed signs of being younger than the untreated cells. After treatment, these cells behaved normally, losing part of the telomere chain after each division.
The significance of successfully applying these technologies in humans is staggering. If telomere length is the main cause of normal aging, then using the aforementioned telomere length number, it is possible to double the healthy time period of constant telomere length; from 23 to 74 years to 23 to 120 years or Longer extensions. Of course, this is too optimistic, because it is well known that cells cultured in vitro can divide more times than human cells, but it is reasonable to expect some improvement [not 50 years, but 25 years].
We know that telomerase-based therapies are not the ultimate answer to anti-aging, but there is no doubt that by increasing the Hayflick limit, they can prolong or even immortalize the lifespan of many cell types. It remains to be seen if this can be done safely in humans.
Orignal From: Programmed cell death method for anti-aging treatment
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