Introduction In this assignment I am going to compare some areas of molecular revolution with genomics revolution.
As a result, sorting out these nuances is a key first step in organizing a discussion on this slippery topic. I think we need to consider six kinds of "longevity genes.
Genes that cause aging and do so for a living. This category an empty set, I thinkwould, if it existed, include genetic Genetic of aging essay that evolved to bring about the aging process--that is, genetic variants molded by selective pressures to transform healthy young adults into senescent, vulnerable old organisms.
I mention this notion only to dispose of it: There are many scientists, including some gerontologists, who are confident that genes that cause aging can be positively selected because they create old individuals whose prompt death will promote the success of their offspring.
That may be true for salmon and other semelparous species whose convenient death provides quick nutrition for needy fry; but for other kinds of organisms, an allele that promotes rapid aging and early death can only diminish the number of healthy offspring produced by its unlucky owner.
Genes that alter longevity because they increase the risk of a specific illness early in Genetic of aging essay. Genes that cause phycomelia, blindness, congenital cardiac abnormalities, or juvenile diabetes will in most environments lead to a dramatic diminution of life-span.
In my view, these genes, however much they might tell us about development, physiology, and pathology, are unlikely to provide important insights into aging. Although these mutations affect life expectancy, they do so by different means other than aging. These mutations affect life expectancy, and so does aging, but by different means.
In some situations, particularly experiments that use genetically identical rodents, it may be hard to distinguish genes of this kind from hypothetical genes that actually do alter aging per se.
Consider a population of mice, for example, in which nearly all the mice die, at about 12 months, from an autoimmune syndrome for which a specific recessive allele is a key risk factor.
In this situation, other alleles at the susceptibility locus are likely to have a major positive effect on longevity simply by preventing the autoimmune syndrome. The literature is filled with publications whose titles announce genes for "accelerated aging" or "senescence-accelerated mice," based largely on evidence that the genes shorten life-span.
I endorse David Harrison's pithy discussion of such claims 1 and believe that authors of such papers should be required to present very strong evidence that their allele of interest speeds up multiple aspects of the aging process.
These effects should be observed at the cellular, extracellular, and intracellular levels and in multiple organs and tissues before one accepts the radical claim that the shortened life-span is really the result of accelerated aging.
Genes that alter longevity because they increase the risk of a specific illness early in life whose features resemble, to some extent, some of the consequences of aging. Werner syndrome and Hutchinson-Guilford progeria are the poster children for this category, as Klotho 2 is the poster rodent.
In some cases, including Werner syndrome, the list of traits seen in both patients and in normal old people is impressive, but so is the oft-omitted list of traits that don't overlap. I think those who wish to work out the pathogenesis of these "premature aging" syndromes and want to determine whether the same pathways contribute to pathogenesis in normal aging are working on a problem of real interest.
And there is a reasonably good chance that these studies will provide important clues about aging. But the notion that these loci play a major role in timing aging per se seems to me much less likely, if only because it is so easy to tell the difference between a Werner patient and an old person.
Genes that affect what kind of old person you are. There are a lot of these: Estimates of the number of genes that "influence aging"--bruited in the famous essay by George Martin 3 on "segmental progerioid genes"--are based on the following kind of criterion: A locus where a mutation produces one or more of the changes seen in old people can be scored as "age-related.
Evolutionary theory provides useful insights into why the genome accumulates so many polymorphic variants whose late-life consequences are unfortunate:Essay about Progeria: The Rare 'Aging Disease' Therefore, progerin is a key component to how and why humans age.
Although everyone makes a small amount of progerin that accumulates over a lifetime, children with Progeria produce more amounts quicker (“Progeria /FAQ"). Biology of the aging process. The oxidative stress, mitochondrial dysfunction, telomere shortening and genetic mechanisms form the core of aging perspective from cellular and molecular biological sciences.
Genetic Mechanisms for Aging. If you are the original writer of this essay and no longer wish to have the essay published on the UK. Physiological changes do not occur uniformly for all individuals but are jointly affected by genetic and environmental factors. This fact further heightens the difficulty of finding a universal theory regarding aging.
Universal in this case means what the human race is . G enetics of Skin Aging. Joseph Banis, MD As with all of our organ systems, our skin quality, function and rate of physiologic aging is determined not only by extrinsic factors such as diet, stress, and exposure to toxic agents, but also, and even more significantly, by intrinsic genetic factors.
Physiological Changes Of Aging Biology Essay. Print Reference this. Disclaimer: This work has been submitted by a student.
This is not an example of the work written by our professional academic writers. Physiological changes do not occur uniformly for all individuals but are jointly affected by genetic and environmental factors. This fact. Physiological aging: Aging due to normal senescence of cells (senescence and genetic makeup).
Pathological aging: Aging due to pathological conditions (e.g. oxidative stress, poor nutrition, comorbidities, inflammation and environmental factors).