Ageing and Genes

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Introduction

Aging is a syndrome of alterations that are harmful, progressive, common and permanent. Aging damage molecules (DNA, proteins, lipids), cells and organs. Diseases of old age (disease, which enhance the frequency with age, such as different types of arthritis, osteoporosis, cardiac problems, leukemia's, diabetes mellitus, Alzheimer's disease, etc.) frequently differs from aging itself. (Battino, M. et al 2004)

But in spite of that the aging progression is dissimilar from the diseases of aging, it is however right that the damage related with aging increases the probability that diseases of old age will occur. (Barja, G., 2004)


Different gerontologists prefer to employ the word aging, as the "aging" means that over time, certainly leads to a deterioration of (biological entropy) - which is indeed not right in the early years of development, life (age 10 or 12 in people) . I will maintain the word "aging", because I believe that the relationship between aging & deterioration is a general progress and as adults, as the difference between aging & development very strongly established in ordinary language. (Ford, A.B.2006)

Effect of Ageing on Brain

It is very difficult to quantify the impact ageing has on the brain yet studies of late realization which were made on split brain subjects illustrate that the brain has the capability for one part of the brain to take over another parts tasks (plasticity)

When some damage has taken place, it may also be age linked "damage". There is some data that supports the results that the part that caries some responsibilities to some extent ignores its own responsibilities, that again makes it difficult to completely understand the effect of ageing on the brain.

The genetic material that living beings are given at birth also decides what come about to us, as we grow up. A build up error in the genetic material influences many people. The cause for these errors can be extensive and include situations like a knock on the head, a "difficult" lifestyle in common, falls and tumbles, and as well very "serious" things such as a decline in blood flow to parts in the brain that again may change some of the gene relations. (Prohaska, T. et al 2006)

All these genetic errors in the genetic material build up in a long and prosperous life and might have a great effect on the ageing method on the brain. M. Guttman (2001) in her paper argues that "genetic evolution might have still privileged those who, one time they cross the age of 35, kept the capability to instruct and give emotional support relatively than those whose brains' partial resources were devoted to new learning". Suppose we go behind her line of consideration, there is no way for the brain to work at its optimum till the age of 60 and above. This might clarify why the brain decrease in its mental ability and activity. (Barja, G., 2004)

A variety of genetic and environmental effects determine the quantity, speed, timing, and place of these brain modifications and their eventual impacts on intellectual capacities. In most cases, the changes engage complex and still weakly understood connections among multiple genes, and also the possible impacts of cerebrovascular compromise, food, diseases, brain injury, tension, pollutants, and other unknown environmental aspects. We just have to struggle to decrease the deteriorating of the brain last longer and hope, as there is very less we can do with our genetic material. (Battino, M. et al 2004)

Discussion

Genetic disorders and ageing caused by mutations in a gene or a set of genes. Mutations are changes in the DNA sequence of a gene. DNA is the chemical in side the nucleus of a cell that carries the generic instructions for making living organisms. They can happen at any time in our lives including when we are first form from a single cell right up until our deaths. Now not all mutations cause disorders because the mutations are repaired. Our cells have mechanisms for repairing DNA if mistakes are made in the sequence or if the DNA is damaged. (2003, Audesirk, Byers)

Mutations of the genes can happen in different ways but primarily they happen naturally or by environmental intervention. Multi factorial disorders result from mutations in multiple genes, often coupled with environmental causes. Heart disorder, diabetes and cancer are examples of this type of genetic disorder. (Prohaska, T. et al 2006)

The complicated bases of these diseases make them difficult to study and to treat. In some disorders, entire chromosomes, or large segments of them, are missing, duplicated, or otherwise altered in the replication process. . The results of these chromosome abnormalities are diseases in human such as Down syndrome and Turners Syndrome.

Knowing that mutation can occur we immediately raise the question. How can I prevent it or how can I treat it? With the turn into the millennium the idea that genetic research cannot be helpful has been changed. The understanding of the effects of the genetic makeup of the human being and to what degree this will be taken is advancing ways to combat genetic disorders. Through the bioengineering that is taking place today the scientists can study how changes in the genetic order may affect how a genetic disorder is transmitted, but more importantly in how it may be stopped or better, eradicated.

The first and most used valuable tool has been the research of DNA. This alone has it made it significantly easier to try to negotiate through the genetic order and how earlier detection could help stymie some genetic disorders by mutating cells to counter various disorders. Few years later, scientists found a mutated form of the gene Lamin. It caused Progeria, but they did not understand how it worked. A typical cell would divide a certain quantity of period so that a new set can change damaged cells. When person grow older, cells drop the capability to multiply. (Barja, G., 2004)

Because of this accelerated aging, a child of ten years will have similar respiratory, cardiovascular, and arthritic conditions that a 70-year-old would have. The child is normal at birth. Intelligence is usually normal. (Battino, M. et al 2004)

The average age of death is 16 years, but survival until 26 years has been recorded. This occurs in children of both sexes and the effects of arteriosclerosis usually cause death.

Etiology and mode of genetic transmission

Etiology and mode of genetic transmission is unknown. (2001, Enersen) Progeria affects between 1 in 4 million (estimated actual) and 1 in 8 million (reported) children, with a total reported incidence of just over 100 in the century since it's been identified. (2001, Enersen) There are less than 100 known cases in history and less than 20 known cases are alive today of this extremely rare syndrome. (Prohaska, T. et al 2006)

Genetics and its impact on Ageing still has a long way to go and a number of barricades to break through. It lacks because of government funding and Laws that do not favor cell research. We have to change how society looks at these disorders. There are many disorders that, because they are not well known like Progeria, get even less funding. The lack of public knowledge for many of these disorders also detracts from the monetary funding required to carry out the research that is required to positively stop or at least slow down the development of these disorders. Stem cell research wasn't an option until Christopher Reeve began a public advocacy campaign to make people aware of the advantages. (Battino, M. et al 2004)

All research should be so lucky because they guide the science about the mutations produce with Ageing. Science is catapulting us into a biological age. The impact on our society, our values, and ourselves is forcing us to face questions that until recently were inconceivable. Every day we read of new genetic discoveries. For example, three scientific teams have now verified the link between the gene BRCA1 and breast or ovarian cancer, or both, in some families. (Prohaska, T. et al 2006)

But there are so many mutations in the gene that, in the short run, the results dash the hope of devising a simple blood test to identify people who have inherited a mutant BRCA1. So the prospects, for now, of wide scale screening look dim. (1996, Weiner)

Clearly, recent stunning breakthroughs in identifying disease genes were heralded with great enthusiasm. But knowing is not yet curing. New tests are coming in the market that looks for mutated genes that enormously increase a person's risk for a disorder. Today our DNA was designed by nature. In the future, our descendants may come across our remnants and find DNA that we designed ourselves, it is because of effects of ageing on genetic material which become spontaneous in progeny. (Barja, G., 2004)

Ageing and telomerase theory of Ageing

The study of aging has received much attention in past decades. One theory embraced by many scientists is the telomere theory. Every chromosome ends in a telomere which shortens each time the cell divides; after repeated divisions and considerable telomere loss, the cell undergoes senescence (Steel, 1995). Progeria is a genetic disorder that results in accelerated ageing, Allsopp et al (1992) found that progeria patients had shortened telomeres, strengthening the argument that telomere shortening results in aging. But there is hope of a remedy. (Lahnert, P. 2005)

Studies show that telomerase, an enzyme high in egg and sperm cells, can mediate telomere synthesis thus counteracting losses from cell division (Hodes, 1998). However, there may be weaknesses associated with these results. Lahnert (2005) attempted to improve the method used to measure telomere length because various data from other studies are conflicting with some scientists even claiming that telomere shortening was barely a myth. Lahnert established that telomere shortening can be measured but admits that the method could be improved.

The theories of aging do provide the best possible answer to the enigma that is cell senesce. However there is much dispute among theorists and no single factor has been deemed the cause. This suggests all the pieces to the puzzle have not been uncovered. Future studies can only confirm or refute claims. In the meantime, until the phenomenon is unravelled and the underlying causes of aging are identified, it is more important to focus on a good quality of life than a longer one.

Analysis

As a cause of death the relative incidence of cancer increases exponentially to age 65 and decreases thereafter. At age 65, 30% of North American deaths are due to cancer, whereas at age 80 only 12% of deaths are due to cancer - mostly because the relative increase of cardiovascular and Alzheimer's disease is faster than the increase in cancer with age. Nonetheless aging is a major risk factor for cancer, and aging is associated with cancer. (Prohaska, T. et al 2006)

Two thirds of mouse cancers are lymphomas, with the remainder being one-sixth sarcomas and one-sixth carcinomas. In Werner's syndrome sarcomas (connective tissue malignancies, usually) are more common than carcinomas. As with the mouse, this may be due to cellular immortalization by ALT rather than telomerase. These patterns do not indicate a simple relationship between aging and cancer. (Barja, G., 2004)

That there is a distinction between aging and cancer is suggested by the fact that ionizing radiation increases cancer rate, but has less (if any) effect on the rate of aging. (Lahnert, P. 2005) Atomic bomb survivorsand populations living near a nuclear test site showed increased non cancer mortality from aging-associated diseases (stroke, heart disease, respiratory disease), but there is no proof that this constituted accelerated aging. During experiments animals exposed to chronic sub fatal ionizing rays (alpha-, beta-, gamma- & X-rays that cause atoms & molecules to form ions) have produce generalize atrophy ("premature aging") and shortened lifespan, but single X-ray & ionizing radiation exposures have more noticeably increased kidney degeneration and cancer (especially leukemia).

Other mutagen causing agents enhance the threat of tumor-production without decreasing utmost lifespan. These outcomes show that permanent mutations & chromosome breakage are not normal contributors to aging. Cancer is a disease of dividing cells - especially the rapidly dividing cells of the epithelium & blood-forming tissues. Non-dividing cells like neurons or muscle cells don't become cancerous, but aging affects all tissues. (Battino, M. et al 2004)

DNA must eventually be dependable for the great distinction of maximum lifespan between species. But in this respect DNA (the genome) partly is responsible for the production of reactive oxygen species as well as for the capacity of tissues to withstand oxidative stress & glycation as well as other chemical challenges. defective cell cycle control & defective recombination (respectively) leading to high rates of skin cancer, leukemia & sarcomas (respectively). The cancer symptoms are more prominent with XP & AT, whereas the progeria is more prominent with Werner's Syndrome.

Down's Syndrome & Hutchinson - Gilford syndrome are not mainly related with high cancer threat. Defective DNA disparity repair leads to a form of colon cancer (HNPCC) without symptoms of accelerated aging. What is the relative contribution of reduced vulnerability to cancer due to reduced Insulin-like Growth Factor-1 (IGF-1) to the extended lifespan of dwarf mice and to what extent or by what mechanism is the rate of aging slowed? (Barja, G., 2004)

Dietary factors, smoking and environmental chemicals can play a significant role in the incidence of cancer, as indicated by the fact that breast cancer in North American women is ten times more common than for women in Japan. And dietary antioxidants - if not supplemental - appear to reduce the risk of cancer. Better DNA repair allows the deer mouse to live much longer than the house mouse. It may be that mutagens damage both DNA as well as cellular defenses against DNA damage, but that when DNA repair is defective cells can respond by inducing cellular senescence or apoptosis - preventing cancer, but accelerating aging. (Battino, M. et al 2004)

Conclusion

Genetic disorders and ageing caused by mutations in a gene or a set of genes. Mutations are changes in the DNA sequence of a gene. DNA is the chemical in side the nucleus of a cell that carries the generic instructions for making living organisms. They can happen at any time in our lives including when we are first form from a single cell right up until our deaths. Now not all mutations cause disorders because the mutations are repaired. Our cells have mechanisms for repairing DNA if mistakes are made in the sequence or if the DNA is damaged. (Prohaska, T. et al 2006)

There is a distinction between aging and cancer is suggested by the fact that ionizing radiation increases cancer rate, but has less (if any) effect on the rate of aging. Atomic bomb survivorsand populations living near a nuclear test site showed increased non cancer mortality from aging-associated diseases (stroke, heart disease, respiratory disease), but there is no proof that this constituted accelerated aging. (Barja, G., 2004)

During experiments animals exposed to chronic sub fatal ionizing rays (alpha-, beta-, gamma- & X-rays that cause atoms & molecules to form ions) have produce generalize atrophy ("premature aging") and shortened lifespan, but single X-ray & ionizing radiation exposures have more noticeably increased kidney degeneration and cancer (especially leukemia). (Battino, M. et al 2004)

References

Barja, G., 2004, Aging in vertebrates, and the effect of caloric restriction: a mitochondrial free radical production-DNA damage mechanism?, Biological Reviews, vol. 79, no. 2, pp. 235-51

Allsopp, R., Vaziri, H., Patterson, C., Goldstein, S., Younglai, E., Futcher, A., Greider, C. and Harley, C., 1992, Telomere Length Predicts Replicative Capacity of Human Fibroblasts, Proceedings of the National Academy of Sciences, vol. 89, pp. 10114-18

Battino, M. and Ferreiro, M., 2004, Ageing and the Mediterranean diet: a review of the role of dietary fats, Public Health Nutrition, vol.7, no. 7, pp. 953-58Guarente, L., 2000, 'Sir2 links chromatin silencing, metabolism and ageing, Genes & Development, vol. 14, pp. 1021-26

Hodes, R., 1998, Telomerase research: a perspective from the National Institute on Aging, National Forum, vol. 78, no. 2, pp.19-21

Lahnert, P., 2005, An Improved Method for Determining Telomere Length and Its Use in Assessing Age in Blood and Saliva, Gerontology, vol. 51, pp. 352-56

Merry, B., 2004, Oxidative stress and mitochondrial function with aging- the effects of calorie restriction, Aging Cell, vol.3, pp.7-12

Quiles, J., Barja, G., Battino, M., Mataix, J. and Solfrizzi, V., 2006, Role of Olive Oil and Monounsaturated Fatty Acids in Mitochondrial Oxidative Stress and Aging, Nutrition Reviews, vol. 64, no.10, pp. 31-39

Rotman, D., 2006, The Fountain of Health, Technology Review, vol.109, no.1 pp.72-76

Sharma, S. and Kaur, I., 2004, Development and evaluation of sesamol as an antiaging agent, International Journal of Dermatology, vol. 45, pp. 200-08

Steel, M., 1995, Telomerase that shape our ends', Lancet, vol. 345, no. 8955, pp. 935-36Weindruch, R., 2006, 'Calorie restriction and ageing', Scientific American, vol. 16, no.4, pp. 54-61

Ford, A.B. (2006) A neglected dimension of health care The Gerontologist Vol. 46 (5) pp. 704-708

Jamshidi, R., Oppenhermer, A.J., Lee, P.S., Lepar, F.H., and Espenshade, T.J. (2004) Ageing in America: Limits to life span and elderly care options Population Research and Policy Review Vol. 11 (2) pp. 161-170

Minion, A.M., and Smith, B.L. (2001) Deaths: Preliminary data for 2000 National Vital Statistics Report Vol. 47 pp. 1-40

Prohaska, T., Belansky, E., Belza, B., and Buchner, D. (2006) Physical activity, public health and ageing: critical issues and research priorities The Journal of Gerontology: Series B: Psychological Sciences and Social Sciences Vol. 61B (3) pp. 267-269

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