Why_Do_We_Age

WHY DO WE AGE' A TALE OF TWO THEORIES As we learned as to who ages and how we age, now we will find out why we age. We will examine how individual molecules in our tissues work together to bring us the aging process. This means we are going to examine not the world of the organ, but the world of the cell. We will find that survival of some cells depends on their ability to stop the activation of a pre-programmed self-destruct mechanism. We will start by describing two theories of aging that incorporate the selective activation and deactivation of genes in the cells. Then we will review some basic molecular biology, talking about how genes and proteins normally work in a healthy cell. A description of how genes know when to turn on or off. The two dominant theories about aging are error accumulation and genetic program activation. The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code is known as error accumulation. This theory hypothesizes that the aging of aging of organisms occurs because of a genetic conspiracy, that a much deliberate breakdown occurs, with banks of suicide genes, turning on at specific times, making cells debilitate and tissues deteriorate. These two hypotheses are mutually exclusive. The world of molecular biology is a complex, fascinating interaction between many tiny players. The Lilliputians genes, permanently chained to their nuclear dungeon, must somehow communicate their protein-making information to cytoplasm. They do this by employing a molecular Xerox machine, the now familiar RNA polymerase, to copy the instructions. This copy, this mRNA, can leave the nucleus and communicate with the rest of the world. Growing old ultimately comes down to asking why cells decide to quit working. This chapter has given to us the background necessary to discuss these ideas in terms of genes turning on and off. ERROR ACCUMULATION In the following chapter of error accumulation we discovered the observation that supports this idea of inadvertent degeneration. We learned about reactive set molecules termed free radicals. Free radicals are form of waste associated with the aging process. Then discussed about genes deeply involved in cellular reactions to stress, the so-called heat shock genes. When a cell is “shocked” there is a dramatic response change in the expression of certain genes. They encode a family of proteins that provide the stress-induced, or as it is commonly termed heat-shock response. As we age, the heat shock responses are greatly diminished. The elevation of helpful gene products is not nearly as dramatic in older organisms when compared to younger ones. The role of other molecules in the aging process, ranging from sugars to proteins to DNA, in terms of error accumulation theory and ended by describing role of this theory in current biological research. Our bodies normally add sugar molecules to certain biochemical’s. There are proteins which supervise the addition of glucose to other kinds of proteins this process is called glycosylation. In later adulthood sugars bind to proteins and to DNA molecules in such a way that very complex, unwanted structures are created. These structures are called advanced glycosylation end products. The accumulation of odd, potentially hazardous biochemical’s to normal cells is a hallmark of the error accumulation theory of aging. What we observe in the error accumulation theory is self-killing through neglect. In some way, an important mechanism like repair or glycosylation or waste disposal begins to malfunction. This failure occurs because a gene product, a protein, is no longer able to perform its normal duties. This absence may occur because the gene itself is no longer active. In aging research, the next frontier is to understand why these processes fail in critical areas like shock response and replication. The boundaries also begin to blur between the Error Accumulation theory and the hypothesis of programmed death. PROGRAMMED DEATH The programmed death theory states that aging may occur through a form of pre-planned, obsolescence; that certain genetic programs are activated in our cells, which after a time cause them to age and die. This is in a stark contrast to error accumulation theory, in which death is a lot like one might think of natural land erosion in the face of “seas of time”. In this section we explored the aspects of the programmed aging hypothesis. We learned gene products that govern the cell cycle. Then we discussed the biochemical’s whose presence decides the fate of living tissue, and explained how this applies to aging of the whole creatures. Finally we talked about how the discovery of these genes affects former theories about aging in general, and specifically cell death. In this chapter we learned to discover how programmed death fits into this overall scheme. In aging research, one of the great mysteries is trying to understand why cells stop replicating and start dying. The idea of programmed death, complete with deliberate activation of suicide genes, came into fashion. It had been noted for many decades that cell death in embryonic organisms was the manner by which many vital organs were constructed. But linking process primarily concerned with beginnings of life to process primarily concerned with the endings of life still seemed a little far-fetched. It wasn’t until the genetic sequences were isolated that such hypotheses came down to earth. It was then easy to incorporate their biochemistries into solid development program theory. As more molecular data was published, it became more obvious that both mechanisms were important. Research into aging process involved asking questions like why does that gene urn off at a certain period of time' What alters the levels of proteins in that cell' How do these changes affect the life span of an organism' These are the kinds of questions we ask today. The explanation involves both theories and neither theory. Toxic waste products accumulate because genes shut off. Genes shut off because toxic waste accumulates. As we have seen over and over again, aging is the result of many genetic processes. WINDING BACK THE CLOCK In this final chapter we will go over the process of aging and its affects to human beings in brief. By taking a tour of various organ systems and tissues, we examined how exercise slows down some of the effects of later adulthood. The aging process discussed in part two affects all three layers of our skin. The turnover rate of the skin cells diminishes with age, and the skin naturally weakens. Lack of sebaceous glands and dryness is inevitable as well. Exercise can only selectively slow down parts of the aging process on our skin. Other activities such as reduction to the exposure of the environment, or direct chemical intervention, may be required to slow down these effects. Same way exercise changes the muscles of our body making our bones stronger and healthier. As the muscles are built stronger with exercise so are the bones and joints as they are interconnected to each other. Some of the aging events occur in our heart, blood vessels and lungs as they form the highways that feed us and take away our molecular trash. Their tissues are extremely resilient, and some can be strengthen even in old age. As discussed in earlier, hormonal loss is an actual fact of the aging process. Hormones that are involved in the maintaince of sexual tissues are affected. In this chapter we have sought to identify several of the factors that play a role. We have examined the power of exercise to improve our quality of life, and perhaps we have been surprised at how little relevance there is to life span. We have also looked at diet, perhaps being equally surprised to see its great relevance to animal and human longevity. There has been a great power in human genes to turn on and off in response to external and internal cues. This activation and de activation forms the basis for fusing the ideas of error accumulation with a genetic program. There are active researcher’s in the field today who think we may soon have protocols that could double or even triple normal human life spans. There are two main objectives of examining the clock of the ages. First to show how many mechanisms must come into lay in order to make an organism age. This helps us see how others have gone through the process of aging. THE CLOCK OF THE AGES CHAPTERS #12,13,14,15 SUMMARY #5 LAILA MOOSA PSYCH 218