Let us discuss the remaining theories on aging......continue from theories of aging part-1 http://www.pharmainfo.net/pvabhigna/theories-aging-part-1

Genetic Theories

It includes error and mutation theory. According to these theories, sometimes error or mistake occurs in the designing of amino acid sequence in DNA which governs some important functions of cell like cell structure, its integrity etc. Such type of error occurs over a lifetime and this causes aging. As the genetic model based on the sequencing/ coding of different amino acids it is possible that some error may occurs which causes mutation¹. Error might occur because of editing the amino acid sequences or by some enzymes which are responsible for addition or cutting the amino acid sequence (like ligases and different types of restriction enzymes).

Mutation in single gene and longer life span was related and it is shown by animal studies like Drosophila fly² (shows approximately 35% longer life span on an average). But, in case of human, still there is a question related to the gene which is responsible for life span. If we consider an example of baboons and humans, they have 97% similar gene, but, life span of baboons is nearly 20 years while of human it is nearly 80 years³.

From this relation one can roughly draw two conclusions,

One, if such gene which is responsible for aging is present in human, it may be in remaining 3% gene which is not match with Baboon's gene.

Second, there is no such gene in human which is responsible for aging/ life span.

Wear and tear theory¹

According to this theory, in spite of excretion process in cell, some waste products are still accumulated in the cell as age spots until they interferes cellular activity and this interference causes aging.

Free Radical theory^4-6

The process of production of energy in mitochondria is associated with the production of unstable reactive oxygen species (ROS) such superoxide or hydroxyl radicals. These species combine with different cell components and ultimately leads to damage DNA and protein. Superoxide dismutase is an enzyme which helps to inactivate these ROS produced in the species with longer life span. The most important mechanism of ROS to damage the cell is cross linking of proteins and that to longer life proteins such as collagen and elastin. The degree of cross linking increases with age and damage will be more serious.

E.g. stiffening of arteries, age related cataract formation, premature atherosclerosis and aging in case of diabetic patients.

Senescence theory

A stage comes when cell stop dividing is termed as senescence. Question may arise why cell division stops? One major reason behind this stage is SHORTENING OF TELOMERES⁷. After every cell division telomere which is present on gene will shorten in length and this short size telomere at a particular length produces DNA damage signal. This finally, leads to senescence. But, some cells are immortal like stem cells due to presence of active telomerase enzyme which is responsible to counteract the mechanism of shortening of telomere by adding lost part of telomere in every cell division. In cell culture, it is shown to produce immortal cells by introducing telomerase in non-stem cells of human body⁸.

Actually, cell senescence turned to be a helpful mechanism to avoid cancer development by accepting aging⁹.

Neuroendocrine and Immune theory¹

The theory based upon the belief that some master BIOLOGICAL CLOCK present in hypothalamus region which controls the aging process under the influence of hormonal level. As a common observation, there is a decline in hormonal level (most often reproductive hormones), growth factor, response level for different conditions (immune function), and cell counts especially in brain with age.

Theories based on psychological behavior¹

These theories suggest how someone get detach with social network during different ages and how to adapt oneself in constantly changing environment of society and state of body (structural and functional) with due course of time so that one should not feel old mentally.

Still lots of things are not clear with these two blogs. After our next mechanism blogs the things become clearer. So, please wait for our next blogs.

Note: This blog does not contain any plagiarized content.

References

1. Theories of Aging. http://www.angelfire.com/ns/southeasternnurse/TheoriesofAgingC3.html accessed on 21 Feb' 2010.
2. Lin YJ, Seroude L, Benzer S. Extended life-span and stress resistance in the Drosophila mutant Methuselah. Science 1998; 282: 943-946
3. Miller RA. Genetic approaches to the study of aging. J Am Geriatr Soc 2005; 53: S284-S286.
4. Finkel T, Holbrook NJ. Oxidants, oxidative stress and the biology of ageing. Nature 2000; 408: 239-247.
5. Peppa M., Vlassara H. Advanced glycation end products and diabetic complications: a general overview. Hormones 2005; 4 (1): 28-37.
6. Kumar PA, Kumar MS, Reddy GB. Effect of glycation on alpha-crystalline structure and chaperone-like function. Biochem. J. 2007; 408 (2): 251-258.
7. Wright WE, Shay JW. Telomere biology in aging and cancer. J Am Geriatr Soc 2005; 53: S292-S294.
8. Bodnar AG, Ouellete M, Frolkis M. Extension of life-span by introduction of telomerase into normal human cells. Science 1998; 279: 349-352.
9. Campisi J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell 2005; 120: 513-522.