The Mitochondrial Free Radical Theory of Aging - Supernova: Pliki

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84 The Mitochondrial Free Radical Theory of Aging 79. Shoubridge EA. Mitochondrial DNA diseases: Histological and cellular studies. J Bioenerg Biomembr 1994; 26:301-310. 80. Weber K, Wilson JN, Taylor L et al. A new mtDNA mutation showing accumulation with time and restriction to skeletal muscle. Am J Hum Genet 1997; 60:373-380. 81. Boulet L, Karpati G, Shoubridge EA. Distribution and threshold expression of the tRNA(Lys) mutation in skeletal muscle of patients with myoclonic epilepsy and ragged-red fibers (MERRF). Am J Hum Genet 1992; 51:1187-1200. 82. Zeviani M, Moraes CT, DiMauro S et al. Deletions of mitochondrial DNA in Kearns-Sayre syndrome. Neurology 1988; 38:1339-1346.
CHAPTER 7 The Status of Gerontological Theory in 1995 The central motivation of this chapter is a fact that may surprise, if not appall, non-biologists: that theoretical biology has a bad name. Theoretical gerontology, moreover, has a particularly bad name: it is considered to be a magnet for sloppy thinkers with half-baked ideas. As a theoretical gerontologist, I am therefore obliged to dissuade the reader from prejudging what I have to say; this I hope to do in the following sections. 7.1. What Is a “Theory of Aging”? In gerontology, as in any field of science, the development of a hypothesis involves a perpetual oscillation between creative and analytical thinking. Advances of understanding are rarely achieved by purely deductive analysis of existing data; instead, scientists formulate tentative and incomplete generalisations of that data, which allow them to identify which questions are useful to ask by further observation or experiment. (In this respect, gerontology differs from most other scientific disciplines only in how little we have so far progressed along the path to that understanding.) The further any such path is travelled, the more complete and detailed are the hypotheses under active investigation. The above is, in fact, so universally accepted as a cornerstone of the scientific method that some may wonder why I have chosen to belabour it. I have three reasons. The first is that there is a long-standing and widespread tendency, in the study of aging, to over-sell a hypothesis. Many of the physiological or molecular changes that occur in our bodies as we age can be proposed, with reasonable plausibility, to influence the rates of other changes—and, in some cases, their own rate. But there is a huge difference between proposing that a process influences the rate of aging and proposing that it is the dominant influence. This difference has too often been glossed over: the process under consideration is presented as being the dominant determinant of the rate of aging, when the supporting arguments actually only suggest that it makes a non-zero contribution. This is all the more regrettable because hypotheses which propose a non-zero contribution by a particular process are perfectly legitimate stepping-stones to more ambitious hypotheses; the only requirement is to keep the two types of hypothesis distinct. A recent review of the free radical theory 1 took care to stress the distinction between the weak statement: “oxidants contribute significantly to the process of degenerative senescence” and the strong statement: “oxidants determine maximum lifespan potential”; the field will benefit greatly if this example is widely followed. My second motivation is to dispel a view which has gained some popularity recently: 2,3 that aging is, broadly, already understood. The foundation of this view is that we have discovered most, if not all, of the major mechanisms by which our macromolecular organisation gradually breaks down, so that all that remains is to flesh out the finer details The Mitochondrial Free Radical Theory of Aging, by Aubrey D.N.J. de Grey. ©1999 R.G. Landes Company.
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COMPANY de Grey The Mitochondrial F
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ISBN: 1-57059-564-X MOLECULAR BIOLO
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7. The Status of Gerontological The
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17. Conclusion: The Role of the Ger
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I cannot overstate my profound grat
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CHAPTER 1 Introduction 1.1. What Is
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Introduction Some may feel that all
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6 The Mitochondrial Free Radical Th
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10 The Mitochondrial Free Radical T
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18 Fig. 2.7. The respiratory chain.
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24 Fig. 2.9. Types of protein impor
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26 Fig. 2.10. Why the DNA bases pai
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Frequently-Asked Questions Referenc
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Frequently-Asked Questions 45. Clay
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CHAPTER 11 A Challenge from Textboo
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A Challenge from Textbook Bioenerge
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CHAPTER 14 Ablation of Anaerobic Ce
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Ablation of Anaerobic Cells: Techni
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CHAPTER 15 Transgenic Copies of mtD
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Transgenic Copies of mtDNA: Techniq
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CHAPTER 16 Prospective Impact on th
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Prospective Impact on the Healthy H
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Prospective Impact on the Healthy H
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Index Symbols “~”, 19 A Acetald
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Index Copper 35, 107 see also trans
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Index Heart comparison to man-made
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Index genetic code 23, 115-118, 177
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Index Perhydroxyl radical 41, 122,
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Index protonation see protonation (
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MOLECULAR BIOLOGY INTELLIGENCE UNIT
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