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Fight Aging!



Reports from the front line in the fight against aging. The science of healthy life extension. Activism and advocacy for longer, healthier lives.



Last Build Date: Sun, 28 May 2017 13:40:05 +0000

 



Fight Aging! Newsletter, May 29th 2017

Sun, 28 May 2017 13:40:05 +0000

Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more. This content is published under the Creative Commons Attribution 3.0 license. You are encouraged to republish and rewrite it in any way you see fit, the only requirements being that […]



The Problem with Focusing on Healthspan

Fri, 26 May 2017 21:21:29 +0000

There are numerous ways to go about advocacy for the cause of treating aging as a medical condition, for the production of therapies to address the aging process. One might focus on talking about extended health, or the goal of greatly increased longevity, or the details of aging as a novel target for medicine, or discard aging as a topic in favor of the development of cures for common, well-recognized age-related diseases - something that can only be achieved through addressing the causes of aging, but many people are more receptive to treating age-related disease rather than treating aging, no matter that these must be one and the same in the end. The advocates, researchers, and supporters in our small community are largely here because […]



It Might be Possible to Prevent Cellular Senescence from Occurring at All

Fri, 26 May 2017 13:18:31 +0000

Cellular senescence is a cause of aging. Enormous numbers of cells become senescent day in and day out, entering a state in which they secrete damaging signals that disrupt surrounding tissue. Near all self-destruct or are quickly destroyed by the immune system. It is the very few that linger and build up in tissues over the years that act to produce chronic inflammation, fibrosis, and ultimately age-related disease. Current approaches to the problem aim at killing these errant cells, finishing the job that was left uncompleted by natural processes, and turning back this aspect of aging. As this research makes apparent, it may be possible in the near term to take the alternative approach of completely preventing senescence from occurring in the first place. Is […]



Another Example of a Human Genetic Variant that Lowers Blood Lipids and thus Reduces Heart Disease Risk

Fri, 26 May 2017 12:34:11 +0000

In recent years researchers have discovered a couple of human gene variants that dramatically reduce blood lipid levels, in ANGPTL4 and ASGR1, which in turn reduces the risk of cardiovascular disease by slowing the development of atherosclerosis. The atherosclerotic lesions that form in blood vessel walls are seeded by oxidatively damaged blood lipids, and so lower lipid levels mean less seeding, all other things being equal. The research here presents another such gene variant, though by the sound of it one that has a lesser effect and isn't as widespread across populations. A genetic variant that protects the heart against cardiovascular disease has been discovered in an isolated Greek population, who are known to live long and healthy lives despite having a diet rich in […]



Patterns of Aging in Both Normal and Longevity Mutant Nematodes

Thu, 25 May 2017 23:20:56 +0000

If you've been following efforts to slow aging in laboratory animals for any great length of time, then you should find the open access paper I'll point out today to be quite interesting - though note that the full text is PDF only at the time of writing. As a general rule, it is a lot harder to dissect the statistical shape of aging for a population than it is to just put numbers to mean and maximum life span. Measuring health to any useful level of detail is far more labor intensive than counting the study animals who are still alive. This means that there is actually comparatively little information on the numerous methods of slightly slowing aging when it comes to what exactly […]



Stem Cells versus Inflammation in Tendon Regeneration

Thu, 25 May 2017 12:58:37 +0000

Tendon tissue is one of many tissue types in mammals that is reluctant to heal completely following injury. Better methods of regeneration are desired, here as elsewhere in the body, and stem cell therapies show a great deal of promise in this regard. The most reliable of current stem cell therapy approaches, those with the greatest expectation of benefits to result for the patient, appear to work largely through a reduction in chronic inflammation. It is interesting to see that hold up in the case of tendons and their supporting stem cell populations. New research suggests that tendon stem cells (TSCs) may be able to significantly improve tendon healing by regulating inflammation, which contributes to scar-like tendon healing and chronic matrix degradation. This has implications […]



Speculation on a Role for ATP in Age-Related Protein Aggregation

Thu, 25 May 2017 12:37:00 +0000

Researchers here suggest that ATP, the chemical energy store molecule produced by mitochondria, also serves to keep proteins soluble in the cell. This might help to explain the well known correlation between age-related mitochondrial dysfunction and age-related neurodegenerative diseases involving protein aggregates that build up in brain tissue. If mitochondria are producing less ATP, that may in turn accelerate the seeding of solid aggregates, and the consequent harm they produce. At this stage, the research is interesting but still fairly speculative when it comes to the degree to which this chemistry is relevant in disease states, however. Adenosine triphosphate (ATP) performs many jobs in a cell. It carries energy, serves as a signaling molecule, and is the source of adenosine in DNA and RNA. But […]



In Essence, All Aging Research Revolves around the Science and Advocacy of SENS, the Strategies for Engineered Negligible Senescence

Thu, 25 May 2017 01:41:42 +0000

Today's popular science article for consideration is the usual mix of frustrating and interesting remarks that result when various researchers are convinced to talk to the press on the subject of SENS rejuvenation research. I in no way exaggerate when I say that all approaches to the research of aging, all of the intent in aging research, all of the fundamental disagreements in the field, ultimately revolve around SENS, the Strategies for Engineered Negligible Senescence. The advocacy and the science of SENS are the moral and technological sun in this solar system, for all that many of those orbiting it apparently would rather things were otherwise. Is the point of aging research to cure aging, rejuvenate the old, and greatly extend healthy human life spans? […]



Assessing the Prevalence of Sarcopenia

Wed, 24 May 2017 13:04:09 +0000

Sarcopenia is the name given to the characteristic loss of muscle mass and strength that accompanies aging, though formal definitions under development tend towards including only those with the greatest degree of loss. This is something of a political problem in the research and medical community; the tendency to describe some level of aging as normal and therefore not treatable, while classifying greater degrees of exactly the same process and symptoms as a disease. Along with the failure of the immune system and loss of bone strength, sarcopenia is one of the most evident forms of age-related frailty. A good many research groups are involved in the attempt to find ways to slow or reverse this decline, most of which are focused on mechanisms of […]



A View of How Senescent Cells Disrupt Tissue Regeneration

Wed, 24 May 2017 12:36:24 +0000

Normal tissue regeneration is disrupted in various ways in later life, such as the tendency for increased fibrosis, scar tissue formation rather than normal regrowth. Researchers here theorize on the role of growing numbers of lingering senescent cells in this age-related loss of function, a complex situation because the transient creation of senescent cells, soon destroyed, is an important part of the normal wound healing process. Despite their positive function in that scenario, the accumulation of long-lasting senescent cells is nonetheless one of the root causes of aging. These cells produce a harmful effect on surrounding tissue through the potent mix of signals they generate, known as the senescence-associated secretory phenotype (SASP), which drives chronic inflammation, among other items. The inability of adult tissues to […]