|WikiProject Biology||(Rated C-class, Mid-importance)|
|To-do list for Senescence:|
|This article is substantially duplicated by a piece in an external publication. Please do not flag this article as a copyright violation of the following source:
- 1 Simple species that do not age
- 2 Senescence manifests
- 3 Link between stress and aging
- 4 The text below should be merged with the article
- 5 BEFORE YOU ADD TO THIS ARTICLE....
- 6 Proposed merge
- 7 Propose renaming to biology of ageing
- 8 Merging Aging DNA into this article and/or mentioning it
- 9 PNC1 is a Nicotinamidase, PBEF is NOT a Nicotinamidase
- 10 Re: Evolutionary theories
- 11 de Grey and SENS
- 12 Just to blow the telomerase dreamers' bubble, ...
- 13 Sources
- 14 Red Links (Wikipedians don't know bout this article's useless links)
- 15 higher organisms
- 16 Cures for Cellular Senescence
- 17 Why seemingly subtle punctuation matters
- 18 Gene regulation
- 19 Evolutionary Theories
- 20 Turtles
- 21 Gotta die of somethin!
- 22 Cellular senescence
- 23 drug eliminates senescent cells, old mice show retained health
- 24 Adding a picture to the lead section
- 25 Giving a different definition
- 26 Why do we have 2 sections bearing the same title (“Cellular senescence”)?
- 27 Borrowing from the Ukrainian and Russian versions, if needed
- 28 To-do list: “Add a proper lead section”
- 29 Expansion, structure reform
- 30 Senescence / Senesce
Simple species that do not age
I have read somewhere that some worms (like tapeworm) never get old and all of their cells keep dividing without limit. Where can I find scientific references about it?
Althought It might seem stupid to ask it's not, what is characteristic of senescence? I mean, anyone knows senescent people have wrinkles... But... Ia that all? I mean, are there any other indications of old age? Most people see the wrinkles and make the decision, if they do not see wrinkles then there is no old age... But this... It's not accurate... There are more... Mmmm... To say so "symptoms" of old age... Aren't they? _____________
Theories of aging taken from http://jap.physiology.org/cgi/content/full/95/4/1706
Biological Level/Theory -- Description
- Mutation accumulation -- Mutations that affect health at older ages are not selected against.
- Disposable soma -- Somatic cells are maintained only to ensure continued reproductive success; after reproduction, soma becomes disposable.
- Antagonistic pleiotropy -- Genes beneficial at younger age become deleterious at older ages.
- Gene regulation -- Aging is caused by changes in the expression of genes regulating both development and aging.
- Codon restriction -- Fidelity/accuracy of mRNA translation is impaired due to inability to decode codons in mRNA.
- Error catastrophe -- Decline in fidelity of gene expression with aging results in increased fraction of abnormal proteins.
- Somatic mutation -- Molecular damage accumulates, primarily to DNA/genetic material.
- Dysdifferentiation -- Gradual accumulation of random molecular damage impairs regulation of gene expression.
- Cellular senescence-Telomere theory -- Phenotypes of aging are caused by an increase in frequency of senescent cells. Senescence may result from telomere loss (replicative senescence) or cell stress (cellular senescence).
- Free radical -- Oxidative metabolism produces highly reactive free radicals that subsequently damage lipids, protein and DNA.
- Wear-and-tear -- Accumulation of normal injury.
- Apoptosis -- Programmed cell death from genetic events or genome crisis.
- Neuroendocrine -- Alterations in neuroendocrine control of homeostasis results in aging-related physiological changes.
- Immunologic -- Decline of immune function with aging results in decreased incidence of infectious diseases but increased incidence of autoimmunity.
- Rate-of-living -- Assumes a fixed amount of metabolic potential for every living organism (live fast, die young).
- Ageing is spelled aging in the US. Let's keep it senescence. Speciate 07:31, 13 January 2007 (UTC)
I watched a show on the Science Channel on TV. It mentioned that scientists had observed that ageing stops after age 95. Theoretically if they can find out how it is switched off at age 95, then they can find a way to switch it off at an earlier age, such as at a man's prime. Is this claim true? Can someone research it deeper and add the findings in the article. Kowloonese 10:54, 12 Nov 2004 (UTC)
Link between stress and aging
The text below should be merged with the article
- Careful studies of health statistics support a systems approach to aging. When enough systems are damaged, a catastrophic failure occurs.
- Dr. Leonard Hayflick discovered that mammalian cells divide only a fixed number of times. This "Hayflick limit" was later proven to be caused by telomeres on the ends of chromosomes that shorten with each cell-division. When the telomeres are gone, the DNA can no longer be copied, and cell division ceases. In 2001, experimenters at Geron Corp. lengthened the telomeres of senescent mammalian cells by introducing telomerase to them. They then became youthful cells. Sex and some stem cells regenerate the telomeres by two mechanisms: Telomerase, and alternative lengthening of telomeres (ALT). At least one form of progeria (atypical accelerated aging) is caused by premature telomeric shortening. Also in 2001, research showed that naturally occurring stem cells must sometimes extend their telomeres, because some stem cells in middle-aged humans had anomalously long telomeres.
- Experimenters discovered that mice whose pituitary glands were removed lived half again as long as unmodified mice, though with terrible side-effects. Therefore, mammals are believed to have a hormonal system that triggers some age-related disease. However, humans with their pituitary glands removed do not live longer.
- In 2002, genetic modification of a small worm (Caenorhabditis elegans) increased its lifespan sixfold. Related experiments have increased maximum life-span in mice and fruit flies. These experiments prove that there is a genetically-coded death clock that triggers some part of aging. This may be related to the hormonal death clock.
- A number of research programs have proven that mutations in body cells occur and accumulate as an organism ages, and degrade its function. In 1999, researchers discovered that naturally occurring stem cells recolonize organ systems, countering this effect by reintroducing cells from a reduced number of cellular lineages. The number of cellular lineages is further decreased because the older half of the reproduced DNA is far more likely to remain in a stem cell. The mechanism of old-strand conservation is still being researched.
- Latest researches and theories consider senescence as a programmed mechanism rather than a result of some error or accumulation of cross linkages and hence believes in the telomere theory of aging. - himanshu grover
- A number of clinicians noted that the cumulative damage in diabetic patients strongly resembled accelerated aging. This was generalized into a theory that some aging is caused when sugar chemically combines with proteins and other bodily chemicals. It is known that feeding adolescent mice a fully-nutritive diet with minimal food energy can extend their maximum life-spans by half. It is also known that feeding mice small amounts of chromium picolinate can extend their maximum life span about 15%. Chromium is an integral part of active insulin, and insulin is cleaved, to excrete chromium in normal metabolism. Most adult nonvegetarians have large amounts of inactive insulin, which may indicate a chronic deficiency of dietary chromium. Veterinarians routinely treat middle-aged animals for diabetes with chromium supplementation.
- Studies of patients with Alzheimer's disease patients and age-spotting discovered that the body builds deposits of waste within and without cells. The deposits inside cells are called lipofuscin (Latin for "fat dirt"). These deposits may decrease metabolic efficiencies, causing some age-related symptoms. Mammalian cells have enzymes to cleave and digest proteins. The most common such clean-up enzyme is triggered by a three-element chain of Ubiquinone (CoQ10) attached to the elderly protein.
- Dr. Denham Harman theorized that some aging damage might be caused by oxidative damage to the body. Experiments discovered that the body has substantial amounts of enzymes and chemicals to reverse oxidative changes. Studies also showed that longer-lived animals have larger amounts, per weight of animal of these mechanisms, in a linear relation to life-span. The experiments also found an internal mechanism, respiration in mitochondria, that creates free radicals that would cause oxidative damage. Feeding of antioxidants to mice increased average life-spans, but not maximum life spans. It is now believed that oxidative damage depletes self-repair mechanisms, whose limits are controlled by other systems.
- The failures of natural stem cells are now an active area of research. In many cases of damaged organ systems, stem cells do not migrate to the damaged area.
- Experimenters discovered that mice fed extra melatonin lived 20 percent longer than control mice.
BEFORE YOU ADD TO THIS ARTICLE....
...read WP:AWW. This article presents a myriad of scientific theories and hardly cites any of them. Most theories are preceded by "some gerontologists blieve" or "research has shown" .....you get the idea. These forms of claims are unreputable and require citations. There is a ton of good information in this article, but it needs to be appropriately cited.
If you have the information to add, it shouldn't be that much trouble to cite it. And remember, citing it does not just (or even necessarily) mean putting the title of a book at the bottom of the page. In-line citations are great, and describing the history of a development of a theory adds legitimacy as well.
Propose renaming to biology of ageing
While I acknowledge that senescence is a term typically applied to a wider range of taxa than "ageing" (e.g. plants typically "senesce" rather than "age"), I think the article would become more approachable (yes, because the links would be labelled with something intelligible for the average Joe) by renaming it to "biology of ageing". - Samsara (talk • contribs) 14:45, 13 June 2006 (UTC)
- There is always #redirect for the average Joe. Encyclopedia should use more formal terminologies instead of everyday English. Kowloonese 17:12, 13 June 2006 (UTC)
- Well, that's exactly my point. "Biology of ageing" in my experience is more commonly used to refer to the study of senescence in humans, which presumably is of interest to most people coming to read this kind of article; secondly, it would much simplify what's being done here. Just because it's latinised doesn't mean it's right. The best books in science were written in prose that a layperson could follow. - Samsara (talk • contribs) 17:22, 13 June 2006 (UTC)
Ageing is spelled aging in the US. Let's keep it senescence Speciate 07:28, 13 January 2007 (UTC)
- The article for Aging states the following: “This article is about all aspects of ageing. For the biological aspect of ageing specifically, see Senescence.” Also, this article begins with the words “Senescence or biological aging,” implying that both have the same meaning. This may or may not be a sufficient measure for clarification. Everything Is Numbers (talk) 10:59, 26 September 2012 (UTC)
The article on Aging DNA seems to be a bit orphaned, but it merits some mention, if not inclusion, in both this article and the one on DNA repair. IMHO, it should remain its own article, and we could have this article make a mention of it in one or two paragraphs. However, I am not a professional geneticist, so I would like the input of some experts on where this should be mentioned/merged. The ikiroid (talk·desk·Advise me) 15:56, 4 August 2006 (UTC)
PNC1 is a Nicotinamidase, PBEF is NOT a Nicotinamidase
The protein PNC1 has been shown to play a key role in yeast aging. Mammals do not have a PNC1 homolog. Instead, we use a Nicotinamide phosphoribosyltransferase (Nampt or PBEF or visfatin, same protein, different names) enzyme to recycle NAD from nicotinamide. Even though they both play functional similar roles, they are, in fact, different enzymes, and it is therefore improper to call Nampt/PBEF/visfatin a nicotinamidase.
Re: Evolutionary theories
Why do not man live longer than women since they can reproduce up to a very old age and women cannot leading to a higher selection. —The preceding unsigned comment was added by 220.127.116.11 (talk) 22:10, 25 January 2007 (UTC).
Evolutionary theory is a bit more complicated than that; specifically, when determining whether a particular trait would have been subject to evolutionary selection, it is important to keep in mind the historical context of that trait. For the vast majority of human history, an individual's lifespan was on the order of 30 years. Disease, predators, and harsh living conditions prevented most individuals from reaching their maximum reproductive age, thus there was little evolutionary pressure for selecting individuals that could reproduce for the longest time. This is a specific case of the general maxim "the force of natural selection declines with age".
de Grey and SENS
I recently read the book "Ending Aging" by Aubrey de Grey about his Engineered negligible senescence. There is a lot of historic (and thus outdated) information in this article and the structure of it also conforms to older theories. While I am not sure how objective de Grey's book is, I am quite sure that a complete overhaul of the article would be a good thing to point out the currently leading theories. --18.104.22.168 13:34, 13 October 2007 (UTC)
Just to blow the telomerase dreamers' bubble, ...
... I added a long-overdue mention of the fact that cancers are immortals. Yes, (parts of) humans can become immortal!. In fact, there are probably a few cells in your body that are acquiring this ghastly property right now. You and I hope they will remain few.
All available science points to the fact that, if some crazy scientist can reactivate your telomerases at age 60, you will not have enough time to see your new youth before your body fills with tumors. Your life will thus be shortened, not lengthened, and you will die with the excruciating pain of bone metastases.
- The majority of cancers, but not all, express telomerase. On the other hand, all embryonic stem cells express telomerase, and some other cells in the human body do, as well, e.g., some keratinocytes. Just as "inhibiting telomerase = curing cancer" is too simplistic, "activating telomerase = causing cancer" is, as well. --SierraSciSPA (talk) 18:08, 23 January 2008 (UTC)
If I've read the links correctly on my personal discussion page, things have to be sourced and neutral.
If the statement is included, it looks like it would need multiple reliable citations. Otherwise, it is opinion, stated as fact. I looked for a reference, but could not find one. If you reinsert it, can you add the sources? WordMachine (talk) 13:10, 23 January 2008 (UTC)
- I'll look for a source. In the meantime, you might want to reconsider trying to link the two paragraphs together with a simple "conversely," since its meaning is not very clear at all. Information does have to be sourced on Wikipedia, but I notice that the programmed and stochastic theories of aging are presented without any source whatsoever to indicate that they have scientific merit, or even that they were considered to have had scientific merit in the past. I'll try to get an expert opinion on this. --SierraSciSPA (talk) 18:18, 23 January 2008 (UTC)
If a link goes nowhere (commonly called by us trolls as "that red word"), please delink it. Or unlink it. Or non-link-ify it. Or some other of your high-learning vocab that means "Clean up this article." SgtHydra 22.214.171.124 (talk) 03:03, 26 January 2008 (UTC)
- Red links are often considered useful reminders that an article on the subject should exist, and somebody needs to write it. I agree, though, that this article needs cleanup - certainly, no phrase needs to be red-linked more than once. --SierraSciSPA (talk) 00:07, 28 January 2008 (UTC)
This page frequently uses the expression "higher organisms" without explanation of what this might refer to. The term is ambiguous, obsolete and makes it impossible to understand which organisms are beig described. It would be great if an expert in this area could clarify by refering to specific evolutionary clades, rather than to outdated and nebulous concepts such as higher and lower organisms.Spamburgler (talk) 05:40, 7 August 2008 (UTC)
Cures for Cellular Senescence
Following the theory of the Hayflick Limit, replicative senescence may be cured by the  cyclic application of telomerase activators such as those found in astragalus extracts prepared with ethanol and water. For instance, see TA Sciences TA-65. The first work on telomerase activators that people can readily obtain was done by Geron Corporation (2005) and Hong Kong University in their twin patents "Compositions and Methods for Increasing Telomerase Activity" and "Formulations Containing Astragalus Extracts and Uses Thereof". TA Sciences announced TA-65 in 2007. In October of 2010 Intertek/AAC Labs, an ISO 17025 internationally recognized lab, found the largest component of TA-65 to be Cycloastragenol. One may alternate the application of telomerase activators with the application of telomerase inhibitors, making sure not to take both at the same time, since they interfere with each other. Lenthening telomeres cures cellular senescence by causing telomere t-loops to close, silencing the DNA damage signal that causes cellular senescence, modifying gene expression from that of the immortal phenotype. Lengthening telomeres provides more genomic stability, restores the immortal phenotype of mitotically dividing cells, and provides protection against forms of cancer originating in telomeric fusions in old senescent cells. However, telomere remodeling is time-consuming, so that today we typically achieve rejuvenation rates of about 0.667 to 0.75 years per month, or 8 to 9 years per year based on telomerase activation, as reported by TA Sciences based on their measurements of telomere length. In addition to lengthening telomeres to restore youthful patterns of gene expression to cells, a program of modern treatment includes DNA and lipid membrane protective antioxidants such as cocoa powder in water, treatment for mitochondrial senescence with alpha lipoic acid and acetyl L-carnitine, 2000-3000 mg/day vitamin C for collagen synthesis, homocystiene blockers featuring vitamins B6, B12, and folic acid with trimethylglycine to prevent artherosclerosis leading to heart attack and stroke, 3 grams per day arginine with exercise to produce nitric oxide for endothelial cell rejuvenation and restoration of thymic hormone levels, and other options, such as Cat's Claw extract for improved DNA repair. For additional details and options for advanced treatment, see  Greenwood Research on Anti-Aging Medicine and Longevity. JamesAGreen (talk) 16:34, 2 October 2008 (UTC) —(talk • contribs) 15:21, 2 October 2008 (UTC)
Why seemingly subtle punctuation matters
Consider this difference:
- Senescence encompasses all of the biological processes of a living organism approaching an advanced age
- Senescence encompasses all of the biological processes of a living organism's approaching an advanced age
Does senescence include all of the processes of an organism that happens to be approaching an advanced age? No: some of the processes in such an organism may happen the same was as when it was young, and may not be part of the aging process.
Does senescence include all of the processes of an organism's approach toward an advanced age? Sure—why not?
Seriously, this section is way ahead of me...I can't understand a bit of it, could anyone try to make it easier on the mind for those of us without a PhD? 126.96.36.199 (talk) 21:00, 19 March 2009 (UTC)
"The explanation for the long lifespans of primates (such as humans, monkeys and apes) relative to body size is that their rage intelligence and often sociality helps them avoid becoming prey."
Is "rage intelligence" a biological concept? If this is supposed to be "rage, intelligence" then is rage really a technical term whose relation to "being a predator" is analogous to the relationship between intelligence and "being smart," as the subsequent sentence in the article suggests? --anon 188.8.131.52 (talk) 19:48, 9 August 2009 (UTC)
- the main article on the phenomenon specifies the types of animals, so I don't see any need for doing the same in this article. Everything Is Numbers (talk) 14:25, 25 September 2012 (UTC) Indeed, some genera of the order are negligibly senescent. It is already mentioned in this article that negligible senescence is present in some groups of animal organisms, and
Gotta die of somethin!
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|The following discussion has been closed. Please do not modify it.|
Look, everything we know of other than God dies of some cause - even whole planets, stars and galaxies. (Perhaps even God could die of loneliness at the end of the universe). Immortality is a theory at best and more likely a fantasy. Let's separate wishful thinking from reality. --184.108.40.206 (talk) 03:37, 2 October 2010 (UTC)
Greetings, The section "Cellular senescence" could be significantly improved. Here are some relevant excerpts from a scientific book, which may help to those who will do such improvement: http://longevity-science.org/pdf/Biology-of-Lifespan-5.6.pdf Good luck! Gavrilov (talk) 02:49, 21 August 2011 (UTC)
- splitting the section into an article in its own right, as the topic probably deserves. I suppose that it's not the best time for me to immerse into all of this, but if no-else will, I intend to take up the task eventually. And thank you for the link! Everything Is Numbers (talk) 14:07, 25 September 2012 (UTC) Good idea. I know there's enough room for expansion. In fact, I've been thinking about
drug eliminates senescent cells, old mice show retained health
http://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html — Preceding unsigned comment added by 220.127.116.11 (talk) 00:11, 3 November 2011 (UTC)
- It's been all over the news last year. I suppose we can cite the study in this article. I heard they had decided to halt funding for the research, on undue grounds. How very regrettable! Everything Is Numbers (talk) 14:14, 25 September 2012 (UTC)
Adding a picture to the lead section
It's typical for an article as important as this to have a picture placed in its lead section—which, at least to me, often makes the impression of a credential—and I imagine it to be desirable. Now, the next step, as I see it, is to reach a consensus on whether it should be done and, if the result will be affirmative, proceed to choose a picture optimally fitting the requirements. Everything Is Numbers (talk) 21:56, 26 September 2012 (UTC)
- Everything Is Numbers (talk) 07:37, 28 September 2012 (UTC) I have reconsidered this proposal and concluded that no additional pictures are needed.
Giving a different definition
The current definition has three flaws: (1) first, it doesn't sit well with the existence of negligibly senescent organisms, which experience changes in metabolism after maturity despite their lack of senescence; (2) then also, it ignores the fact that some aging processes may be at work even before maturity; (3) finally, it fails to acknowledge that not all changes in an organism's biology occurring after maturity are necessarily senescent in nature. This is unsatisfactory. For nomination of a more precise definition, I suggest the following candidates:
- accumulated damage to macromolecules, cells, tissues and organs with the passage of time;
- collection of cumulative changes to the molecular and cellular structure of an adult organism, which result in essential metabolic processes but which also, once they progress far enough, increasingly disrupt metabolism, resulting in pathology and death;
- gradual deterioration in function that, over time, leads to increased mortality risk, and declining fertility;
- gradual build-up of genetic and cellular error, resulting in deterioration of basic biological functions;
- a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability;
- condition resulting from the transitions and accumulations of the deleterious aging processes.
Why do we have 2 sections bearing the same title (“Cellular senescence”)?
Borrowing from the Ukrainian and Russian versions, if needed
||This article may be expanded with text translated from the corresponding article in the Russian Wikipedia. (September 2012)|
There's plenty of extensive information there. If we wish to keep expanding this topic, they could undoubtedly be of aid. I am in a position to translate the material. Everything Is Numbers (talk) 07:51, 28 September 2012 (UTC)
To-do list: “Add a proper lead section”
Expansion, structure reform
I'm considering adopting the following as the base arrangement:
- 1. Cellular senescence
- 2. Organismal senescence
- 3. Effects
- 4. Hypotheses
- 5. Treatment
- 6. Differences between taxa
- 7. Evolution
- 8. Accelerated aging-disorders
- 9. Cloning
Senescence / Senesce
Can anyone explain the difference between Senescence & Senesce. Is senesce an actual word. It is mentioned once in the article and can be found else where on the net. Are they used interchangeably? Ctbolt (talk) 04:49, 9 August 2013 (UTC)
- American Analytical Chemistry Laboratories Analysis Document #100710-236 of TA-65