Aging Theories

This report outlines the main theories of how the process of aging works. Since researchers have not discovered a universally-accepted theory of aging, the theories discussed are potential explanations of how we age. The likelihood of each hypothesis is considered roughly equal. The different theories discussed focus on the workings of different parts of the body, from the molecular level of DNA mutations and replication, to the organism level of becoming worn out. Aging is a very complex and gradual process, and its ongoing operation is present to some degree in all individuals.

It is a journey to the maturity, s well as to the degeneration of the body. Because aging affects every part of the body, many different steps are involved and various types of reactions occur. Changes in DNA take place, which can and often do affect the way the body functions; harmful genes are sometimes activated, and necessary ones deactivated. A decrease in important body proteins like hormones and certain types of body cells is almost inevitable. These, among many, are characteristic changes that take place in our bodies as time moves on and aging continues.

At present, a universal explanation for how we age or why we age does not exist, ut there are many theories to explain this puzzle, and they are supported by continuous research. In this report, some of the how theories of aging will be examined. Among them are theories concerning spontaneous mutations, damage from free radicals, the clock gene, cellular aging, a weakened immune system, wear and tear, and hormonal and neuroendocrinous changes. Spontaneous Mutations The spontaneous mutations theory, also known as the somatic mutation hypothesis, states that the crucial events that cause aging are mutations.

These are changes in a cell=s DNA, which are passed on to daughter cells during mitosis. Since genes on DNA code for specific proteins, mutated genes may produce defective proteins, which do not work properly. Many proteins can be affected, such as enzymes, proteins comprising muscle tissue, and a recently discovered type of protein called transcription factors, which bind to DNA and regulate the individual activities of genes themselves. Physical mutagens are substances that increase the chance of mutation and include such physical phenomena as x-rays and radioactivity from radium.

The atomic bombs dropped on Hiroshima and Nagasaki in Japan are examples of physical mutagens that caused an increase in he number of cases of leukemia. Certain chemicals and radiation cause mutations to occur in DNA by giving off high energy particles. These particles collide with the DNA and knock off atoms of the DNA randomly, damaging it. DNA consists of sequences of four possible nitrogenous bases: adenine, guanine, cytosine, and thymine, paired so that adenine always pairs with thymine, and guanine always pairs with cytosine.

As cells repair the damaged DNA, a different DNA base is often substituted. This base-substitution is known as a point mutation and can cause the production of a defective or damaged protein. Apart from being caused y radiation or chemicals, mutations also occur spontaneously but at lower rates. Physicist Leo Szilard and biochemist Denham Harmon proposed that because most mutations are harmful, the more spontaneous mutations that arise, the more abnormalities that arise as defective proteins are produced.

These could ultimately kill an individual (Ricklefs and Finch, 1995, 20). Although it has been proven that many proteins undergo alterations during aging, the spontaneous mutations theory is not the cause (Ricklefs and Finch, 1995, 21). It has, however, been proven that DNA is chemically altered during aging. Modifications n DNA bases, called I-spots, have been found to increase in number during aging. Besides I-spots, another modified base known as 8-hydroxyguanine, the DNA base guanine with an added OH group, has also been found to increase during aging.

It is unclear how changes such as these arise, but similar changes seem to be caused be exposure to mutation-causing chemicals, some of which are found in tobacco smoke (Ricklefs and Finch, 1995, 21). Another factor supporting the spontaneous mutations theory may lie in the temporal occurrence of genetic mutations. Certain cancers and abnormal growths seem to appear more frequently s the process of aging continues. Two tumour suppressor genes called p16 and p53 are responsible for slowing cell proliferation, and therefore keep certain cells from becoming cancerous.

However, if they become mutated, they do not carry out their function properly so cells with these mutations begin to grow and divide quickly, causing cancer and other growths (Ricklefs and Finch, 1995, 22). Werners syndrome is a disorder that significantly accelerates the aging process starting at around 20 years of age. Molecular geneticist Gerard Schellenburg has suggested that the function of the enzyme helicase, which ormally unzips the DNA double helix before replication and removes randomly occurring mutations like base substitutions, does not function properly in people afflicted with Werners.

Therefore, the unzipping of the DNA double helix is disrupted and mutations are overlooked (Lafferty et al. , 1996, 60). Moreover, DNA occasionally loses one or more bases through the process of spontaneous deletion. This type of mutation seriously affects the mitochondria of the cell, a main source of energy within the cell. Mitochondria have their own DNA, mtDNA, which allows them to self-replicate. The mtDNA encodes for nzymes found within the mitochondria which help produce ATP, energy-storing molecules. During aging, the amount of mtDNA that possess lost segments of DNA increases.

Although still unproven, it is believed that this abnormal mtDNA may cause defects in energy production. Most mtDNA deletions occur in brain, muscle, and other tissue with little cell division. By the end of ones lifespan, certain parts of the brain consist of as much as 3% abnormal mtDNA (Ricklefs and Finch, 1995, 22). Many characteristics of aging have been proven to develop as a result of spontaneous mutations. However, many other changes associated with ging cannot be adequately explained by this theory.

Damage from Free Radicals A free radical is a fragment of a molecule or atom that contains at least one unpaired electron. Because unpaired electrons are unstable, an uneven electrical charge is created and the electrons attract those of other atoms or molecules to become stable and rectify the electrical imbalance. As they gain electrons from other molecules, they modify the other molecules. In this way, free radicals can damage DNA, and it is known that damaged DNA is involved in the aging process.

Free radicals can be formed when atoms collide with one another, as in the mpact of x-rays or UV radiation from sunlight on living cells. They can start a chain reaction in which atoms or molecules snatch electrons from one another. This process of losing electrons is known as oxidation. Though oxidative damage can be slowed through the help of enzymes and the absorption of free radicals by antioxidants like vitamins E and C, free radicals continue to cause damage, however little, to DNA (Kronhausen et al. , 1989, 78).

Cross-linking, or large-scale fusion of large cell molecules, is involved in a process responsible for the wrinkling of skin, the loss of flexibility, and rigor mortis. It occurs when little or no antioxidant activity is present to alleviate the rapid stiffening of body tissues (Kronhausen et al. , 1989, 74). In older individuals, oxidized proteins in tissues have been found, and when proteins become oxidized, they usually become inactive. Lipids, which constitute a large part of the cell membrane, may also become oxidized, thereby reducing the fluidity of the cell membrane.

Also, it is possible that vascular diseases are caused by oxidative damage since oxidized lipids in the blood cause arteries to thicken abnormally (Ricklefs and Finch, 1995, 24). In addition, some scientists believe that difficulty in, or slowness of movement (when we age), as well as tremors associated with the aging disease called Parkinson=s disease are caused by oxidative damage (Ricklefs and Finch, 1995, 26). The neurotransmitter dopamine, found in the brain is damaged by free radicals produced by enzymes during the removal of dopamine from the synapses of the brain.

During aging, damaged mtDNA is thought to collect in parts of the brain with high dopamine concentrations and is thought to be caused indirectly by the presence of these free radicals (Ricklefs and Finch, 1995, 25). Some regions of the brain high in dopamine and damaged mtDNA happen to be the basal ganglia, the parts that aids in movement control (Ricklefs and Finch, 1995, 25). A Free Radical Reaction with Glucose As the body continues its normal survival processes, insulin becomes less effective in encouraging the uptake of glucose from the blood.

In this way, the body develops insulin resistance. This condition is similar to the more serious type of diabetes called maturity-onset diabetes, or type II diabetes. If diabetes was left untreated, the excess glucose in the bloodstream would not be taken into cells because of insulin esistance. Instead, the excess glucose in the blood would react with hemoglobin in a free radical reaction through a process called non-enzymatic glycation. Other proteins such as collagen and elastin, which make up the connective tissues between our brain and skull, and in our joints, can also become glycated.

Once this occurs, they stop functioning properly. The result of this is that diverse compounds called advanced glycosylation end products (AGEs) become attached to proteins. The combination of AGEs with proteins forms a sticky substance that could dramatically reduce joint movement, clog arteries, and loud tissues like the lens of the eye, leading to cataracts (Lafferty et al. , 1996, 56). Once glycated proteins are formed, they can cause further damage by interacting with free radicals from other sources (Ricklefs and Finch, 1995, 26).

The Lethal Clock A gene called clock-1, which was believed to determine an organism=s lifespan was found in small organisms and a very similar gene has also recently been found in humans (Lafferty et al. , 1996, 58). Although it is uncertain whether the clock genes affect how susceptible cells are to infections, or if they control the actual aging process, it is generally agreed pon that these genes have something to do, either directly or indirectly, with aging (Allis et al. 1996, 64).

It has been proposed in the clock theory that the demise of brain cells, of which we lose thousands each day, is due to regular, programmed cellular destruction, and not to random *accidents= (Keeton, 1992, 50). As cells divide, the number of divisions that they undergo is monitored and kept track of. After a certain number of divisions, the clock genes are triggered and may produce proteins responsible for cell destruction (Keeton, 1992, 50).

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