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Theories of Aging have been around for more than 2000 years
Galen (A.D. 129 c. 199)
-Thought that aging was due to changes in body humors that began in early life
-These changes caused a slow increase in dryness and coldness of the body Roger Bacon (c. 1220-1292) - One of the first to suggest a wear and tear theory - Aging is the result of abuses and insults to the body system - Good hygiene might slow the aging process Charles Darwin (1809-1892) - Attributed aging to the loss of irritability in the nervous and muscular tissue
Aging is, at least in part, the result of accumulating damage to molecules in our bodysuch as: Proteins
lipids, and
nucleic acids (DNA and RNA)
Cellular Aging
CELLULAR AGING
Even though, understanding cellular aging is at the heart of a great deal of research, there remain many unanswered questions about how aging happens at the cellular level
Free radicals form from environmental factors such as X-rays, strenuous exercise, sunlight, pollution
alcohol and smoking
Example of ROS
ROS or reactive oxygen species can be formed by different processes including normal cell metabolic processes.
Free radicals
Cell damage
aging
Scientists have already uncovered clear links between reactive oxygen compounds and aging Fruit flies genetically engineered to produce high levels of enzymes that destroy reactive oxygen species lived almost 50 percent longer than normal flies
The same enzymes also made the microscopic roundworm Caenorhabditis elegans live significantly longer than normal
Substances that prevent the harmful effects of oxidation are known as antioxidants. Natural antioxidants include vitamin C, vitamin E and beta carotene, the substance that our body uses to produce vitamin A. Enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase can neutralize free radicals
These antioxidant and enzymes that trap free radicals may slow or reverse the oxidation of proteins during aging
Once a cell's telomeres shrink to a critical minimum size, the cell takes notice and stops dividing.
The 46 human chromosomes are shown in blue, with the telomeres appearing as white pinpoints.
For humans, the length of the remaining telomere is usually an indicator of how many divisions a dividing cell has left The Hayflick limit (or Hayflick Phenomenon) is the number of times a normal cell population will divide before it stops, presumably because the telomere reach a critical length Germ cells, stem cells and "immortalized" cancer cells contain an enzyme called telomerase that replaces lost telomeres, thus preventing them from experiencing a Hayflick Limit Telomerase usually absent in most somatic tissues
Telomerase activity
Unless precisely repaired, nuclear DNA damage can lead to mutation and/or other deleterious cellular and organismal consequences
An example of cellular aging that occur via DNA repair defect is Werner Syndrome
Its physical characteristics may include short stature (common from childhood on) and other features usually developing during adulthood: wrinkled skin, baldness, cataracts, muscular atrophy and a tendency to diabetes mellitus, among others
Mutations in the WRN gene cause Werner syndrome. The WRN gene provides instructions for producing the Werner protein, which is thought to perform several tasks related to the maintenance and repair of DNA
The disorder is inherited and transmitted as an autosomal recessive trait. Cells from WS patients have a shorter lifespan in culture than do normal cells
Werner syndrome is estimated to affect 1 in 200,000 individuals in the United States. This syndrome occurs more often in Japan, affecting 1 in 20,000 to 1 in 40,000 people
CONCLUSION
Perhaps, the combination of the three theories (free radicals, telomeres and DNA repair defect) contribute to the process of cellular aging
Research is still going on as it has been going on for over 2000 years to understand the complex process of cellular aging