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The Investigation of Aging on a Molecular Level

Introduction

A means of information has been collected by bio gerontologists pertaining to changes that occur during aging at various points of biological organization and development. As these aging matters extend to spread and are viewed normally, pathological modifications are being noticed among species. The table below consists of some of the essential classifications of damage to the molecular level as observed and discussed by researchers across the world.

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Macromolecule Damages
DNA Here we have a number of base modifications present in an organism and different types of mutations.
RNA Base modifications, aggregation and miscoding.
Protein Presence of the amino acids, aggregation and amino acid modifications.
Carbohydrates, lipids, and other molecular conjugates Glycation end products and aggrosomes.

Their biological consequences of the molecular damage are not the same and they vary greatly. Even though the action of damage is really strong, the chemical sequence to determine the damaged molecule and the causes damage. In this process, there are cells that may survive without damage. Significantly, it is very important to notice that it is not a direct and a simple issue to compare any given type of damage and its level in a number of cells to a particular biological outcome. However, one is required to know that the fundamental results of aging come from increased molecular damage and other associated pathogens (Rubin, 2010). This paper gives a review of the chances and mechanisms of molecular damage when one undergoes the aging process, it also elaborates the consequences of the accumulation of molecular damage during the aging period by giving out the strategies pertaining to its intervention and prevention of other diseases related to old age.

Molecular Damage during Aging

Aging begins with the damage of cells in the body caused by various factors. The three common factors are the reaction of cells to oxygen species, free radicals, and reaction to ultraviolet rays from the sun. Oxygen and metals form the other internal factors that bring about aging through damage of cells. The aging process is well captured in the radical theory of aging that was put forward many years ago to explain the process. It came from the aging phenomenon which states that a single common biochemical process may be responsible for aging and even the death of all organisms that live. In fact, a lot of death rate is being caused these molecular level substances. The biochemistry of free radicals is in fact the best theory. Free radical theory of aging (FRTA) is in fact not all that reliable as it lacks incorporation of the main and the beneficial role of the FR (Becker et al., 2009).

As individuals age, the Telomeres become shorter due to various reasons. To begin with, they become shorter following increased inflammation, increased exposure of telomeres to infectious agents in the environment and oxidative stress in the environment of person. These factors lead to the damage of telomeres, a process that affects their functioning in the body (Rubin, 2010). It is important to note that infectious diseases bring about attrition of telomere. Although tests prove that such infections bring about short telomere, further tests are needed to fulfill the hypothesis that attrition of telomere is brought about by infectious diseases.

During aging, mutations too occur. The mutation of DNA is captured in the DNA damage theory, which postulates that during aging, there is the damage of DNA at the nuclear level. The process contributes to aging either directly or indirectly based on other factors. In most cases of aging, it is the damages of the DNA that occurs and it should always be differentiated from the changes of the base sequence of the DNA, which many scholars call mutation. Damage occurs whenever there is the physical alteration of the DNA and may include the single and double strands of the DNA of the aging individual. The damages that are caused to the DNA of the aged population can increase with their age and may lead to loss of cells. However, if it happens in the cells that still exist, it may cause the gene not to express itself. The level of damaged DNA can be detected in the brain, the liver and kidney among other body parts (Frick, 2012).

Despite the scholars putting forward the effect of the damage of DNA on aging, other scholars have argued that aging is a primary outcome of mutation. In the Mitochondrial DNA, mutations are presumed to the major causes of aging as indicated by many studies. The replication of the mitochondrial DNA is done by the polymerase gama, which is an enzyme generated in the cells for the function (Rubin & Babbie, 2010).

Previous studies have postulated that aging can be accelerated by some factors including low economic status of an individual as it is the predisposing factors to diseases. The attrition of telomere is through other factors too such as lifestyle factors, social economic as well as traditional factors. For instance, a low income, poor diet and the tenure of housing affects attrition that is age related in the elderly. Concerning lifestyle, high levels of cholesterol increases the length of telomere attrition.

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Methylation is the process through which there is addition of methyl group to an atom in the genes via the catalysis help of enzymes. The methylation [attern of DNA is affected by replicative senescence. However, some scholars report that upon long term culture, methylation levels decrease. Repeated cell cycles reduces the methylation of DNA, which is also an outcome of the maintenance of the methylation process of DNA through DNA methyltransferase 1. As one ages, the level of methylation increases and this could also be responsible to increased aging among individuals.

Virology and Molecular Aging

Aging sometimes is determined by the immune system of the body. If an individual or a particular organism has a strong immune system which is virus free, it will survive for long before it ages. Viruses weaken the immune system of organisms this happens when cells of the body responsible for growth and development are interfered with or permanently damaged. Once the immune system has become weak the organism will also age faster. Viruses cause damage on the cells of organisms and as a result weaken their immune thereby continuously growing weaker and weaker.

The virus causes increase in molecular level thereby enhancing aging among organisms. HIV virus can also make an individual to become old early. The virus interferes with the mitochondrion. Mitochondrion toxicity is immensely caused by the use of drugs like the HIV patients do take. Since mitochondria are known to be the energy stations of the human body, if they are damaged then it means we will not survive for long.

Homeostasis and survival

The living organisms across the world have a fundamental ability to respond and get used to the environmental conditions which can both internal and external.

Traditional concept describes this property by the use of homeostasis which has generally outweighed other disciplines like biology. However, lots of advancements have been made and thereby limiting the accuracy of homeostasis. Nevertheless, it does not also explain to the point of convincing somebody the facts about it (Kenyon, 2012).

Consequences of increased Molecular Level

The well known biological consequences is increased levels of molecular damage are just but so many, for example, alteration of gene expression, mutations and many other forms of disturbances (Kenyon, 2012). The common source for all these consequences is increased molecular level within the body cells of organisms. Since there are low chances that any two molecules will be damaged just in a similar way and extent, an increase in molecular level is inevitable (Kenyon, 2012). For example, if there are thousands of protein molecules translated from a newly formed mRNA, all the molecular heterogeneities will automatically emerge within that given molecular population. This at the end will result in inactive molecules (Kenyon, 2012).

Genetics, post-genetics and epigenetics of Aging

Having known the fact that all molecular levels in all organisms are absolutely based in and regulated by genes, an important research has been at the forefront to discover the number of genes which are responsible for aging and they are called gerontogenes (Petefrs, et al. 2012). On the contrary, the evolving explanation for the beginning of aging and shortened lifespan discussed above have openly ruled out the idea of any specific genetic program involving particular studies related to genes. However, lack of sole purpose of aging and terminating the lifespan of an individual do not really means that specific genes do not occur or on the same note, they cannot influence survival, longevity and even the rate at which organisms age (Petefrs, et al. 2012).

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To further these explanations, there is simple evidence from the studies performed on yeast among other organisms including human beings that mutation in various genes can increase or make short the lifespan of living organisms (Peters, et al. 2012). Some of these have been identified as the main sources of premature aging symptoms in human beings appear within the age range of (56-58). In addition, genetic linkage studies of an organism like mouse to stay long have identified the main histo-compatability complex regions. In a wider analysis, it has been discovered that distinct genes which have links to early aging and longevity might show up in a number of biological ranges which are specific to biological pathways like cell metabolism, kinase among others. It is clear that the identification of these genes influencing aging and longevity is that whichever their known function and mechanism of action may be, the gerontogenes do not always cause an accumulation of molecular damage which at the end causes disorders thereby terminating the lifespan of an organism (Peters, et al. 2012).

Most genes if not all have well defined role in the metabolism of various organisms both in inter and intra-cellular cells. These genes do take part in maintenance and repair of the body cells which also include stress reactions. The truth that lies behind all these involves the damages introduced by changes in terms of body regulation within the structures of an organism. These types of genes are called virtual gerontogenes (Peters, et al. 2012).

Implications for aging intervention

Studies that have been previously conducted on aging make it a little different from normal treatment of other diseases (Stachoń, et al., 2010). Even though sometimes the worn out tissues might be replaced with the artificial ones which when viewed look more durable, it cannot regulate the underlying tissues by controlling things like hormones, temperature, shock, irradiation, alcohols and food restriction among others. Death is commonly caused by potential damage of the body cells.

Recapitulation

Living organisms survive by their ability to defend, maintain and repair their body cells and tissues. A number of genes interacting within the body results to this type of mechanism which has been discussed above. Successful homeodynamics play a great task for the development and maturation of an organism until that defined time when it will reach its reproduction period. This happens by providing an absolute assertion to continue extending from one generation to the other generations. In short, no living organism can stay for long if its tissues are not replaced and maintained as per requirement of the body. Some defined unified theories of biological aging involving genes do explain the fact that acquiring a definite shape can be the main basis of aging intervention, prevention and the way it should be modulated (Stachoń, et al., 2010).

Research Questions

In investigating the molecular basis of aging, we consider how genes determine the lifespan of a mammalian theory on gene support the fact that people with parents who lived long are likely to live long together with their generations, the molecular and physiological changes in the body and the role of DNA in the molecular level of aging. The study will investigate how knowledge can help in prevention of related diseases in aging? (Peters, et al. 2012).

The Aim of Research

The aim of this investigation of aging at molecular level is to investigate whether the research done may also investigate gerontology, the study of the aging process in the aspect of longevity, aging and death. Therefore, research on molecular virology in brief will be examined and entail the molecular basis of viral interaction with their hosts (Zglinicki, 2003). The investigation will also center on the genetic theory telomeres, research on DNA (deoxyribonucleic acid) replication in microorganisms and repair of mammalian cells when exposed to damaging agents of DNA signals transduction and Gene regulation, which will basically focus on transcriptional responses and signaling of cells in relation to their environment and to microbial pathogens (Stachoń, et al., 2010). The focus will be on Research done by the Department on Microbiology and Molecular Genetics in the University of Pittsburgh shows that due to cellular senescence process, most cells cannot divide indefinitely (Kenyon, 2012).

Methodologies

The methods to be used in the research will include both qualitative and quantitative approaches where experiments could also be used to establish the process of aging with regards to involvement of cells (Salkind, 2009).

Expected Outcome

In conclusion, biogerontology aging is mostly concerned with genes, and studies are more focused on biology, chemistry, genetic life extension or anti aging treatments (Wisdom, Cavaleri, Onwuegbuzie & Green, 2012). Some biogerontologists argue that before we can cure aging, we must understand it fully, and due to the remedy of aging. In one of the studies conducted on projection of demographics, it was established that people who maintain a healthy lifestyle usually increase their lifespan as compared to those who do not (Fu, Csanaky & Klaassen, 2012).

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References

Becker, M., Kleinsmith, L. J., Hardin, J., & Bertoni, G. P. (2009). The World of the Cell. 7 ed. San Francisco, CA: Pearson Benjamin Cummings.

Frick, M. (2012). Building a better hormone therapy? How understanding the rapid effects of sex steroid hormones could lead to new therapeutics for age-related memory decline. Behavioral Neuroscience, 126(1), 29-53.

Fu, Z. D., Csanaky, L., & Klaassen, D. (2012). Gender-divergent profile of bile acid homeostasis during aging of mice. PloS One, 7(3), 504-512.

Gaillard, E., & Hua, F. (2009). Aging in the human lens: molecular level studies of possible mechanisms of damage. Illinois: Northern Illinois University

Kenyon, M. (2012). Healthy Aging in the 22nd Century. Futurist, 46(5), 40-43.

Peters, L. et al. (2012). Lead concentrations in relation to multiple biomarkers of cardiovascular disease: the normative aging study. Environmental Health Perspectives, 120(3), 361-366.

Rubin, A. & Babbie, E. (2010). Research methods for social work. New York, NY: Cengage Learning.

Salkind, N. (2009). Exploring research. Upper Saddle River, NJ: Prentice Hall.

Stachoń, A., Burdukiewicz, A., Pietraszewska, J., Andrzejewska, J., & Chromik, K. (2010). Biological symptoms of aging in women regarding physical activity and lifestyle. Human Movement, 11(2), 172-178.

Wisdom, P., Cavaleri, A., Onwuegbuzie, J., & Green, A. (2012). Methodological reporting in qualitative, quantitative, and mixed methods health services research articles. Health Services Research, 47(2), 721-745.

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