106 posts · 56,764 views

Fight Aging!
106 posts

Sort by Latest Post, Most Popular

View by Condensed, Full

September 15, 2010
11:03 PM
449 views

Paths to the Development of Mitochondrially Targeted Antioxidants

by Reason in Fight Aging!

Antioxidant compounds can extend life in mice provided they are localized to the mitochondria - which doesn't happen for anything you can presently buy in a bottle. Near all antioxidants that can be ingested, injected, or otherwise introduced into the body do nothing of any great significance to healthy life span, and may even be detrimental by interfering in the processes of hormesis that help to maintain and improve health. As I'm sure you know by now, mitochondria are the cell's powerplants, converting food into the chemicals used by cells to store and transport energy. They also generate damaging free radicals - such as reactive oxygen species - as a consequence of their operation. These free radicals in turn tend to damage mitochondria in ways that eventually snowball towards larger and larger consequences in the body: this mitochondrial damage is in fact one of the important root causes of aging. In the field of targeted antioxidants, researchers have gene engineered mice to generate more natural antioxidants in their mitochondria. A group in Russia has been quite active in working on SkQ1, an ingested compound that targets mitochondria, and Australian researchers have a similar chemical under development. Out of these lines...... Read more »

Galley HF. (2010) Bench-to-bedside review: Targeting antioxidants to mitochondria in sepsis. Critical care (London, England), 14(4), 230. PMID: 20804578

Demianenko IA, Vasilieva TV, Domnina LV, Dugina VB, Egorov MV, Ivanova OY, Ilinskaya OP, Pletjushkina OY, Popova EN, Sakharov IY.... (2010) Novel mitochondria-targeted antioxidants, "Skulachev-ion" derivatives, accelerate dermal wound healing in animals. Biochemistry. Biokhimiia, 75(3), 274-80. PMID: 20370605

September 11, 2010
01:48 AM
497 views

A Representative Example of a Genetic Study of Longevity

by Reason in Fight Aging!

As the tools of genetic analysis improve by leaps and bounds, the cost falling with each advance, more and more research is taking place into genetic influences on human longevity. This is an enormously complex area of study, and has little to no relevance to any repair-based methodology for lengthening human life. Outside the field of regenerative medicine, most aging researchers do not work on repair strategies such as SENS, however. Meanwhile there is plenty of funding for genetic studies of all sorts - compared with comparatively little available for initiatives to repair the biochemical damage of aging. This is a sad state of affairs, but it is what it is: one of the numerous things we must help to change in the years ahead if we are to see significant progress towards engineered longevity in our lifetimes. In any case, here is a good (and open access) example of the sort of genetic longevity studies presently taking place: detailed associations and commonalities are being uncovered in the genomes of long-lived people, and there is a lively debate over just how important any individual longevity-associated genetic variants are likely to be. Centenarians often reach old age with delayed onset or...... Read more »

Boyden, S., & Kunkel, L. (2010) High-Density Genomewide Linkage Analysis of Exceptional Human Longevity Identifies Multiple Novel Loci. PLoS ONE, 5(8). DOI: 10.1371/journal.pone.0012432

September 7, 2010
11:37 PM
449 views

Why Are There No 400 Year Old Humans?

by Reason in Fight Aging!

Science is as much about investigating what we do not see as it is about investigating what we do see. For example, from a recent open access paper: Small rodents in captivity routinely reach ten times their mean life span in the wild. Why is it then that in human populations with an average life span of 40 to 80 years nobody has ever lived to 400 years old or more? This is a fine and valid question. Why do we see little variation in human life span in comparison to that of smaller and more short-lived mammals? The authors of this paper performed an analysis of mortality statistics across different species of mammal, the results of which lead into a very interesting and readable discussion on the interaction between evolutionary pressures and age-related frailty. This is all part of the larger question of why we age, and why we age in the way we do. In particular, these researchers argue that the end stages of frailty in aging - senescence - do not result from a lack of evolutionary pressure later in life. But the fact that senescence still exists despite pressure for increased evolutionary fitness is telling us...... Read more »

Turbill, C., & Ruf, T. (2010) Senescence Is More Important in the Natural Lives of Long- Than Short-Lived Mammals. PLoS ONE, 5(8). DOI: 10.1371/journal.pone.0012019

September 7, 2010
04:51 AM
435 views

Commonalities in Risk Factors for Age-Related Disease

by Reason in Fight Aging!

A great deal of medical research into aging is built upon a foundation of correlation studies: what can we identify as more often occurring for patients who suffer from a particular age-related condition? Are there environmental factors, lifestyle choices, or genetic differences that are statistically linked to the occurrence of this condition? The next step that follows from the identification of such correlations is to pick them apart looking for commonalities. Why do these many correlations exist, and do they exist because of one underlying mechanism? For example, see this open access paper that proposes chronic inflammation as the causative process for a range of correlations: Tobacco smoking, physical inactivity and resulting obesity are established risk factors for many chronic diseases. Yet, the aetiology of age-related diseases is complex and varies between individuals. This often makes it difficult to identify causal risk factors, especially if their relative effects are weak. For example, the associations of both obesity and air pollution with several age-related diseases remain poorly understood with regard to causality and biological mechanisms. Exposure to both, excess body fat and particulate matter, is accompanied by systemic low-grade inflammation as well as alterations in insulin/insulin-like growth factor signalling and cell...... Read more »

Nicole M. Probst-Hensch. (2010) Chronic age-related diseases share risk factors: do they share pathophysiological mechanisms and why does that matter?. Swiss Medical Weekly. DOI: 10.4414/smw.2010.13072

September 3, 2010
11:28 PM
463 views

Investigating Metformin's Mechanisms

by Reason in Fight Aging!

Metformin is one of the known calorie restriction mimetics amongst drugs presently in use by the medical establishment. A calorie restriction mimetic is a drug that can reproduce some of the beneficial changes to metabolism exhibited during the practice of calorie restriction, which hopefully in turn leads to improved health and extended healthy life span. Metformin has been shown to modestly increase maximum life span in mice, though by much less than is possible through calorie restriction: chronic treatment of female outbred SHR mice with metformin (100 mg/kg in drinking water) slightly modified the food consumption but decreased the body weight after the age of 20 months, slowed down the age-related switch-off of estrous function, increased mean life span by 37.8%, mean life span of last 10% survivors by 20.8%, and maximum life span by 2.8 months (+10.3%) in comparison with control mice. In human medicine, metformin is primarily used as an anti-diabetic treatment, which has led to speculation as to just how much of the calorie restriction effect on health and longevity is due to changes in insulin metabolism - such changes made directly in genetically engineered laboratory animals have been shown to significantly affect longevity as well. Here,...... Read more »

Kane DA, Anderson EJ, Price JW 3rd, Woodlief TL, Lin CT, Bikman BT, Cortright RN, & Neufer PD. (2010) Metformin selectively attenuates mitochondrial H2O2 emission without affecting respiratory capacity in skeletal muscle of obese rats. Free radical biology , 49(6), 1082-7. PMID: 20600832

August 30, 2010
11:07 PM
366 views

Thyroid Function and Inherited Human Longevity

by Reason in Fight Aging!

There is good reason to believe that levels of thyroid hormones, and the changes in thyroid function they represent, influence human longevity. These are amongst a number of hormones in the human body that touch on almost everything you would expect to influence life span over time: metabolic rate, cell growth, use and processing of food, and so forth. You might recall studies on the thyroid hormone triiodothyronine, or T3, for example: The hypothalamo-pituitary-thyroid axis has been widely implicated in modulating the aging process. Life extension effects associated with low thyroid hormone levels have been reported in multiple animal models. In human populations, an association was observed between low thyroid function and longevity at old age ... These findings suggest that the favorable role of low thyroid hormone metabolism on health and longevity in model organism is applicable to humans as well. Here is another, more recent study of a human population that pulls in more confirming data: The objective of the study was to test whether low thyroid activity associated with extreme longevity constitutes a heritable phenotype, which could contribute to the familial longevity observed in the Leiden Longevity Study. ... Eight hundred fifty-nine nonagenarian siblings (median age 92.9...... Read more »

Rozing MP, Houwing-Duistermaat JJ, Slagboom PE, Beekman M, Frölich M, de Craen AJ, Westendorp RG, & van Heemst D. (2010) Familial Longevity Is Associated with Decreased Thyroid Function. The Journal of clinical endocrinology and metabolism. PMID: 20739380

August 19, 2010
10:17 PM
420 views

Anoxia Tolerance and Species Longevity

by Reason in Fight Aging!

I noticed a paper on longevity in turtles today that speculates on a link between species life span and tolerance of low-oxygen environments. It seems to be as interesting a line of research as any opened up by the comparison of differences in biochemistry and longevity between species. Why are long-lived species long-lived, and can we expect the answers to translate, as for calorie restriction research, into potential benefits for human health? Forever young: mechanisms of natural anoxia tolerance and potential links to longevity While mammals cannot survive oxygen deprivation for more than a few minutes without sustaining severe organ damage, some animals have mastered anaerobic life. Freshwater turtles belonging to the Trachemys and Chrysemys genera are the champion facultative anaerobes of the vertebrate world, often surviving without oxygen for many weeks at a time. The physiological and biochemical mechanisms that underlie anoxia tolerance in turtles include profound metabolic rate depression, post-translational modification of proteins, strong antioxidant defenses, activation of specific stress-responsive transcription factors, and enhanced expression of cytoprotective proteins. Turtles are also known for their incredible longevity and display characteristics of "negligible senescence". We propose that the robust stress-tolerance mechanisms that permit long term anaerobiosis by turtles may also...... Read more »

Krivoruchko A, & Storey KB. (2010) Forever young: mechanisms of natural anoxia tolerance and potential links to longevity. Oxidative medicine and cellular longevity, 3(3), 186-98. PMID: 20716943

August 11, 2010
12:32 AM
484 views

Impairment of Blood Vessels in the Brain Isn't a Good Thing

by Reason in Fight Aging!

Exercise correlates with a reduced risk of suffering dementia in later life, just as excess visceral fat is correlated with an increased risk of later developing dementia. The underlying mechanisms are somewhat different, but they both boil down to the quality of the blood vessels in your brain. Impaired blood vessels mean a lower blood flow or the breakages and lesions of vascular dementia - neither of which is good for you in the long term. Another issue to consider in this context is the ongoing impact of atherosclerosis, the build-up of fatty material on blood vessel walls. This can result in sudden death due to blockage and rupture of larger deposits, but the condition harms your brain across the years leading up to that point: Atherosclerosis, dementia, and Alzheimer disease in the Baltimore Longitudinal Study of aging cohort We examined the relationship between systemic atherosclerosis, Alzheimer type pathology, and dementia in autopsies from 200 participants in the Baltimore Longitudinal Study of Aging, a prospective study of the effect of aging on cognition, 175 of whom had complete body autopsies. ... we found that the presence of intracranial but not coronary or aortic atherosclerosis significantly increased the odds of dementia....... Read more »

Dolan H, Crain B, Troncoso J, Resnick SM, Zonderman AB, & Obrien RJ. (2010) Atherosclerosis, dementia, and Alzheimer disease in the Baltimore Longitudinal Study of aging cohort. Annals of neurology, 68(2), 231-40. PMID: 20695015

August 10, 2010
12:27 AM
538 views

An Addendum on Solar Radiation, Reliability Theory, and Longevity

by Reason in Fight Aging!

A few years ago, I pointed out some speculative work on environmental radiation during embryonic development and its possible effects on later longevity: Speculation on Solar Radiation and Longevity More on Solar Radiation and Life Expectancy The amount of [solar] radiation varies according to where you are in the world, what time of year it is and cyclic changes in the sun’s behaviour. The Equator generally gets the most radiation, and in the northern hemisphere, the usual radiation peaks will be in June and July, but there will be variations from year to year according to "solar cycles." Every 11 years the Sun goes through a cycle when the magnetic field changes and the number of sunspots grows and dwindles. This affects the amounts of radiation produced. The Maine researchers suggest that high radiation levels either stress the immune system of embryos and foetuses or cause small mutations in their DNA, which can either predispose or protect from disease, mould brain characteristics and influence length of life. The reliability theory of aging and longevity models complex organisms such as humans as an array of systems composed of many redundant component parts. It suggests that we are all born with a...... Read more »

Shamir L. (2010) Does cosmic weather affect infant mortality rate?. Journal of environmental health, 73(1), 20-3. PMID: 20687328

July 13, 2010
09:40 PM
401 views

Analysis of Gene Expression and Longevity is Forging Ahead

by Reason in Fight Aging!

The process of gene expression, in which a gene is used as a blueprint to construct a protein, is anything but static. Levels of gene expression for individual genes rise and fall with environmental circumstances, health, injury, and over the course of aging. It's a tremendously complex system, with a lot of feedback loops and switches, but fortunately the cost of analyzing gene expression profiles over a whole genome is falling rapidly. It is now feasible to run hundreds of such profiles over the course of a study. At the same time the tools of analysis are starting to catch up with the amount of data being generated: researchers are able to more rapidly and effectively draw conclusions from the mountainous databases they construct. So, for example, see this study on flies, which compares groups of flies selected for their longevity versus a control group of average length lives. It demonstrates that systematically sweeping the whole genome for changes in gene expression with age is a viable way to evaluate the importance of other lines of research and find new avenues for future study: We evaluated the gene expression profile in young, middle-aged, and old male flies, finding that 530...... Read more »

Sarup P, Sørensen P, & Loeschcke V. (2010) Flies selected for longevity retain a young gene expression profile. Age (Dordrecht, Netherlands). PMID: 20607427

July 8, 2010
11:24 PM
502 views

Immunosenescence and What Can Be Done About It

by Reason in Fight Aging!

Immunosenescence is the steady degeneration of the immune system that occurs with age. For the adaptive immune system at least, researchers have a good picture as to why and how this happens - which means that they also have starting points to develop ways to reverse immunosenescence. Here is an open access review paper on the topic: The elderly frequently suffer from severe infections. Vaccination could protect them against several infectious diseases, but it can be effective only if cells that are capable of responding are still present in the repertoire. Recent vaccination strategies in the elderly might achieve low effectiveness due to age-related immune impairment. ... Ageing dampens the ability of B cells to produce antibodies against novel antigens. Exhausted memory B lymphocyte subsets replace naive cells. Decline of cell-mediated immunity is the consequence of multiple changes, including thymic atrophy, reduced output of new T lymphocytes, accumulation of anergic memory cells, and deficiencies in cytokines production. Persistent viral and parasitic infections contribute to the loss of immunosurveillance and premature exhaustion of T cells. In essence, the immune system fails because the thymus, source of immune cells, ceases production and withers away. At the same time, the population of immune...... Read more »

Ongrádi, J., & Kövesdi, V. (2010) Factors that may impact on immunosenescence: an appraisal. Immunity , 7(1), 7. DOI: 10.1186/1742-4933-7-7

July 1, 2010
12:42 AM
476 views

An Update on Progeria Research

by Reason in Fight Aging!

Hutchinson-Gilford Progeria Syndrome (HGPS, or just "progeria") is perhaps the best known of the accelerated aging conditions. Considerable progress has been made over the past decade in uncovering the biochemical mechanisms of this disease, and in the process it has come to seem plausible that a viable therapy for progeria may have some modest use in tackling normal aging as well. The same follows for other accelerated aging conditions, meaning that it's worth keeping an eye on this field of medical research. With this in mind, here is an open access paper that outlines some of the latest advances in progeria research. Matters look a lot closer to a viable therapy than they did a few years back, and studies continue to show that the changing biology of normal aging shares - to a lesser degree - some of the unwanted biochemical signatures of progeria: Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare premature aging disorder caused by a [mutation within the] LMNA gene encoding A-type nuclear lamins. [Nuclear lamins are fibrous proteins providing structural function and transcriptional regulation in the cell nucleus.] ... We analyzed global gene expression changes in fibroblasts from human subjects with HGPS and found that a...... Read more »

Marji J, O'Donoghue SI, McClintock D, Satagopam VP, Schneider R, Ratner D, J Worman H, Gordon LB, & Djabali K. (2010) Defective lamin A-Rb signaling in Hutchinson-Gilford Progeria Syndrome and reversal by farnesyltransferase inhibition. PloS one, 5(6). PMID: 20559568

June 28, 2010
11:37 PM
596 views

Regeneration of Tooth Enamel: Cavities Healed in Mice

by Reason in Fight Aging!

Dental researchers are forging ahead with their branch of tissue engineering and regenerative medicine. It hasn't been long since engineered growth in situ of replacement teeth was demonstrated in rats, and now a research group has shown they can regenerate tooth enamel in mice, thereby healing cavities: A new peptide, embedded in a soft gel or a thin, flexible film and placed next to a cavity, encourages cells inside teeth to regenerate in about a month ... The gel or thin film contains a peptide known as MSH, or melanocyte-stimulating hormone. Previous experiments [showed] that MSH encourages bone regeneration. Bone and teeth are fairly similar, so the French scientists reasoned that if the MSH were applied to teeth, it should help healing as well. To test their theory, the French scientists applied either a film or gel, both of which contained MSH, to cavity-filled mice teeth. After about one month, the cavities had disappeared. You can also take a look at the research paper if interested, though it's fairly dense. It is an excellent example of what can be achieved where materials science meets biotechnology and the life sciences, and overall a very encouraging proof of concept. It is reasonable...... Read more »

Fioretti, F., Mendoza-Palomares, C., Helms, M., Al Alam, D., Richert, L., Arntz, Y., Rinckenbach, S., Garnier, F., Haïkel, Y., Gangloff, S.... (2010) Nanostructured Assemblies for Dental Application. ACS Nano, 4(6), 3277-3287. DOI: 10.1021/nn100713m

June 25, 2010
10:24 PM
586 views

Another Illustration as to Why There Will Be Many, Many Genetic Contributions to Longevity

by Reason in Fight Aging!

As I mentioned not so long ago, there will most likely prove to be a great many subtle and overlapping genetic variants of human longevity. However, very few of them will be important in the sense that they will lead to ways to significantly increase human life span through new medicine. The effective way to greatly increase human longevity is to learn to repair the biochemical damage of aging, not to tinker with metabolism to slow down the rate at which damage occurs. In any case, here is an excellent illustration as to why there will be thousands of genetic variations that contribute to human longevity: the effects on life expectancy of known single gene variants may be enhanced or diminished by other variations that do not themselves directly contribute to longevity. Combinations of genetic variants are probably just as important as single gene differences, in other words: The search for longevity-determining genes in human has largely neglected the operation of genetic interactions. We have identified a novel combination of common variants of three genes that has a marked association with human lifespan and healthy aging. ... Haplotype analysis was performed in three candidate genes, and the haplotype combinations were...... Read more »

Michal Jazwinski S, Kim S, Dai J, Li L, Bi X, Jiang JC, Arnold J, Batzer MA, Walker JA, Welsh DA.... (2010) HRAS1 and LASS1 with APOE are associated with human longevity and healthy aging. Aging cell. PMID: 20569235

June 18, 2010
10:44 PM
498 views

Naked Mole Rats Do Not Suffer From Cancer

by Reason in Fight Aging!

When it comes to wandering Methuselah's zoo in search of comparisons between species that might lead to greater understanding of human longevity - and how to increase it - the naked mole rat stands out as a prominent point of interest. It lives for something like nine times longer than some similar rodent species, and appears to have unusually resilient biochemistry for a mammal. Naked Mole-Rats and Negligible Senescence Built Differently, Down in the Membranes You might recall that different fatty acid or lipid composition in cell membranes was floated as a reason for the ninefold longevity of naked mole-rats over related rodent species. Plenty of oxidative stress in the older mole-rats, but little sign of biochemical damage resulting from it - in comparison to those other rodents long since aged to death, that is. Better, more damage-resistant building blocks down at the molecular level might be the cause. The concept of "better membranes" has a theory of aging to go along with it: the membrane pacemaker hypothesis. Follow that link if you care to find out more. Naked mole rats are not just very long-lived, however. They also appear to be immune to cancer. No naked mole rat has...... Read more »

Liang S, Mele J, Wu Y, Buffenstein R, & Hornsby PJ. (2010) Resistance to experimental tumorigenesis in cells of a long-lived mammal, the naked mole-rat (Heterocephalus glaber). Aging cell. PMID: 20550519

June 17, 2010
12:38 AM
513 views

Ash-2, Another Longevity Gene in Worms

by Reason in Fight Aging!

Researchers have been turning up quite the trove of longevity-influencing genes and processes in nematode worms of late. Here is the latest: Study identifies proteins that modulate life span in worms The gene with the most pronounced effect, Ash-2, makes a protein that functions as a methyltransferase - meaning it works together with other proteins to add a chemical tag called a methyl group to a component of a cell's DNA packaging machinery, which is known as a histone. The presence or absence of this tag affects whether the DNA remains wound up tightly like thread on a spool, or unfurls to allow its genes to be expressed. Inhibiting Ash-2 activity reduces the number of methyl tags on the histone, which keeps the DNA inaccessible and somehow extends the animal's life by as much as 30 percent. ... The researchers found that Ash-2 is highly expressed in the germline, or reproductive cells, as well as in newly formed eggs. These cells also had high levels of the methyl tag. When Greer blocked the expression of Ash-2 in worms that lacked normal reproductive cells, he found that this no longer extended worm life span, suggesting that an intact germline is necessary...... Read more »

Greer, E., Maures, T., Hauswirth, A., Green, E., Leeman, D., Maro, G., Han, S., Banko, M., Gozani, O., & Brunet, A. (2010) Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans. Nature. DOI: 10.1038/nature09195

June 12, 2010
12:26 AM
537 views

Structural Causes of Increasing Life Expectancy

by Reason in Fight Aging!

As I'm sure you're all aware by now, human life expectancy for both young and old in the most developed regions of the world is slowly increasing, and this has been the case for some time. As medical technology advances and our wealth grows, we benefit in ways that lead to less biochemical damage to the complex machinery of our body accumulated over the course of a lifetime - and thus a greater likelihood of living longer. That the medical and research establishments have achieved this ongoing benefit even in advance of any structured, deliberate, large-scale efforts to slow or (more preferably) repair the consequences of aging bodes well for the future. The scientific community should be able to achieve far more impressive results when they are actually trying to directly tackle aging. I noticed an open access paper today (PDF version included) that applies some mathematical wizardry so as to break out the most important structural contributions to increasing longevity. I think you'll find it interesting: The ongoing increase in life expectancy in developed countries is associated with changes in the shape of the survival curve. These changes can be characterized by two main, distinct components: (i) the decline...... Read more »

Rousson, V., & Paccaud, F. (2010) A set of indicators for decomposing the secular increase of life expectancy. Population Health Metrics, 8(1), 18. DOI: 10.1186/1478-7954-8-18

June 10, 2010
10:17 PM
515 views

Building the Foundation of Tomorrow's Immune System

by Reason in Fight Aging!

The human immune system of tomorrow will look, conceptually, a lot like today's software defenses: Scientists are making real inroads into replicating and controlling the cells and mechanisms of our immune system. Producing immune cells, directing their actions, deciphering the biochemistry of pathogens - all these pieces are waiting to be put together as a bioartificial immune system, many times more selective, efficient and resistant to damage than the basic version we're all equipped with. ... One might imagine the future providers of immune system technology looking a lot like today's providers of anti-virus software for your computers, harvesting information on potential infections and streaming update information to bioartificial antibody manufactories in your bloodstream. Wireless anti-virus nanotechnology in the blood may seem like a far future vision, but the first building blocks of that technology are already emerging from present day research. For example, it won't be long before clinics can assemble massive doses of artificial antibodies to order and then infuse them into your body. Antibodies are the immune system's weapons, molecules tailored to a specific threat that either directly kill attackers or flag them for ingestion and destruction by white blood cells. An infusion of antibodies produced in...... Read more »

Hoshino, Y., Koide, H., Urakami, T., Kanazawa, H., Kodama, T., Oku, N., & Shea, K. (2010) Recognition, Neutralization, and Clearance of Target Peptides in the Bloodstream of Living Mice by Molecularly Imprinted Polymer Nanoparticles: A Plastic Antibody. Journal of the American Chemical Society, 132(19), 6644-6645. DOI: 10.1021/ja102148f

June 10, 2010
09:13 AM
477 views

There Will Be Ten Thousand Subtle Gene Variants of Human Longevity

by Reason in Fight Aging!

There will be ten thousand subtle gene variants of human longevity. Or rather, these differences between individuals most likely exist now and will be steadily uncovered in the years ahead as the cost of DNA sequencing continues to fall. Most of these longevity-associated genetic variants will look much like this one: an association discovered by comparing long-lived people to average members of the population, and neither terribly exciting nor particularly exploitable: Cytokines are crucial for the regulation of inflammation development in humans. Many studies have shown that variations in cytokine genes might play a role in determining human longevity. This study examined the changes in the gene pool relevant to the -308 G/A polymorphism in the promoter region of the proinflammatory cytokine tumour necrosis factor (TNF)-alpha gene and the -1082 G/A polymorphism in the promoter region of anti-inflammatory cytokine interleukin (IL)-10 gene with aging and survival selection occurs in the Jordanian population. .. the IL-10 genotype and allele frequencies were significantly associated with longevity in men but not in women. We should expect to see subtle associations with human longevity in genes associated with processes known to be important in long-term health - such as the inflammatory response, or indeed...... Read more »

Khabour OF, & Barnawi JM. (2010) Association of longevity with IL-10 -1082 G/A and TNF-alpha-308 G/A polymorphisms. International journal of immunogenetics. PMID: 20518833

login

Reason

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

search

topics

dates

View

Language

Languages to Display

join us!

News