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Genetic theories

2014-3-3 23:05| view publisher: amanda| views: 1002| wiki(57883.com) 0 : 0

description: Many theories suggest that ageing results from the accumulation of damage to DNA in the cell, or organ. Since DNA is the formative basis of cell structure and function, damage to the DNA molecule, or ...
Many theories suggest that ageing results from the accumulation of damage to DNA in the cell, or organ. Since DNA is the formative basis of cell structure and function, damage to the DNA molecule, or genes, can lead to its loss of integrity and early cell death.
Examples include:
Accumulative-Waste Theory: The biological theory of ageing that points to a buildup of cells of waste products that presumably interferes with metabolism.
Wear-and-Tear Theory: The very general idea that changes associated with ageing are the result of chance damage that accumulates over time.
Somatic Mutation Theory: The biological theory that ageing results from damage to the genetic integrity of the body's cells.
Error Accumulation Theory: The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code.
Some have argued that ageing is programmed: that an internal clock detects a time to end investing in the organism, leading to death. This ageing-Clock Theory suggests, as in a clock, an ageing sequence is built into the operation of the nervous or endocrine system of the body. In rapidly dividing cells, shortening of the telomeres would provide such a clock. This idea is in contradiction with the evolutionary based theory of ageing.[71][72]
Cross-Linkage Theory: The idea that ageing results from accumulation of cross-linked compounds that interfere with normal cell function.[72][73]
Free-Radical Theory: The idea that free radicals (unstable and highly reactive organic molecules), or more generally reactive oxygen species or oxidative stress create damage that gives rise to symptoms we recognize as ageing.[72][74]
Reliability theory of ageing and longevity: A general theory about systems failure. It allows researchers to predict the age-related failure kinetics for a system of given architecture (reliability structure) and given reliability of its components. Reliability theory predicts that even those systems that are entirely composed of non-ageing elements (with a constant failure rate) will nevertheless deteriorate (fail more often) with age, if these systems are redundant in irreplaceable elements. Ageing, therefore, is a direct consequence of systems redundancy. Reliability theory also predicts the late-life mortality deceleration with subsequent levelling-off, as well as the late-life mortality plateaus, as an inevitable consequence of redundancy exhaustion at extreme old ages. The theory explains why mortality rates increase exponentially with age (the Gompertz law) in many species, by taking into account the initial flaws (defects) in newly formed systems. It also explains why organisms "prefer" to die according to the Gompertz law, while technical devices usually fail according to the Weibull (power) law. Reliability theory allows to specify conditions when organisms die according to the Weibull distribution: organisms should be relatively free of initial flaws and defects. The theory makes it possible to find a general failure law applicable to all adult and extreme old ages, where the Gompertz and the Weibull laws are just special cases of this more general failure law. The theory explains why relative differences in mortality rates of compared populations (within a given species) vanish with age (compensation law of mortality), and mortality convergence is observed due to the exhaustion of initial differences in redundancy levels.
Mitohormesis: It has been known since the 1930s that restricting calories while maintaining adequate amounts of other nutrients can extend lifespan in laboratory animals. Recently, Michael Ristow's group has provided evidence for the theory that this effect is due to increased formation of free radicals within the mitochondria causing a secondary induction of increased antioxidant defence capacity.[75]

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