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Fight Aging! 06/04/2020 06:22
The processes of autophagy recycle damaged and unwanted structures and proteins in cells. Increased autophagy is involved in the beneficial response to calorie restriction and numerous other mild forms of stress. A range of potential approaches to upregulate autophagy have been explored by the research community, but few have made much progress towards the clinic. It is entirely possible that increased autophagy is more beneficial in some tissues than in others - or to put it another way, perhaps some tissues are much more impaired than others by age-related loss of autophagy. Some of the most impressive data has centered on improved autophagy in the aging liver via LAMP2A upregulation, showing sizable increases in function. Again, these de.
Fight Aging! 06/04/2020 06:02
The ubiquitin-proteasome system is one of the ways in which cells remove damaged and unwanted proteins. Proteins are tagged with ubiquitin, which allows them to enter a proteasome and be broken down into component parts for reuse. Increased proteasomal activity has been shown to be beneficial in short-lived laboratory species, with the understanding that this is because cells will maintain a lower level of damaged components, leading to improved function and lesser degrees of downstream damage. As researchers note here, cells upregulate activity of the ubiquitin-proteasome system in response to mild stress, such as that produced by exercise. This is one of the ways in which exercise produces benefits to health and function. Physical activit.
Fight Aging! 06/03/2020 17:28
In today's open access paper, the authors survey the work of the past decade in the use of proteomics to assess the consequences of cellular senescence. Senescent cells accumulate with age, but even in late age they remain a tiny fraction of all cells. The harms caused by the long-term presence of senescent cells occur because these cells secrete a potent mix of inflammatory signals, growth factors, and other molecules that rouse the immune system, promote fibrosis and other dysfunctions in tissue maintenance, encourage other cells to also become senescent, and so forth. This senescence-associated secretory phenotype is actually beneficial in the short term: it assists in wound healing and suppression of cancer, for example. As for so many
Fight Aging! 06/03/2020 06:22
Autophagy is the name given to a collection of processes responsible for recycling damaged or otherwise unwanted structures and proteins in the cell. With age, autophagy becomes less efficient. Many individual mechanisms falter, and the end result is that cells become more cluttered with damaged parts and harmful proteins. Scaled up across entire organs, this has a meaningful contribution to the progression of aging and age-related disease. Interestingly, increased or more efficient autophagy appears to be a centrally important mechanism in the benefits to health and longevity provided by calorie restriction and a range of other interventions that mildly stress cells. Accordingly, there is a great deal of interest in the research community
Fight Aging! 06/03/2020 06:15
Evidence strongly suggests that the global faltering of mitochondrial function throughout the body with advancing age has a lot to do with a decline in the effectiveness of mitophagy. Mitochondria are the power plants of the cell, a herd of hundreds swarming and replicating like bacteria in every cell to produce the chemical energy store molecule ATP. Mitophagy is the specialized form of autophagy that destroys worn and damaged mitochondria, recycling their component parts. Without it, cells would become overtaken by broken, malfunctioning mitochondria. Mitochondrial dysfunction leads to too little ATP, but also higher levels of harmful oxidative molecules that stress cells. In energy-hungry tissues such as muscle, the heart, the brain, los.
Fight Aging! 06/02/2020 15:03
Aging as we understand it is almost a universal phenomenon in animals. Clearly there is something advantageous in evolutionary terms in having disposable individuals carry the immortal germline forward in time. One possibility is that aging is an emergent property of the fact that selection pressure is always going to fall more heavily on younger individuals, and thus evolution favors change in the direction of biological systems that are highly effective in youth but fall apart later on. Resources directed towards long-term maintenance subtract from resources directed towards immediate reproductive success. It is a brutal zero-sum race to the bottom, driven by the mortality of predation and a hostile environment. Younger individuals contri.
Fight Aging! 06/02/2020 06:22
Exercise is known to improve outcomes in heart failure patients, but there is a limit as to the data that can be obtained on mechanisms of action from human patients. Here researchers use a mouse model of heart failure to show that exercise doesn't impact the harmful presence of fibrosis in heart tissue, but does increase capillary density. The density of capillaries in tissues throughout the body declines with age, and this progressive loss is probably quite important in a number of aspects of aging, particularly in tissues that have high energy demands, such as the heart. That fibrosis isn't affected suggests that exercise doesn't do much to reduce the burden of cellular senescence, however, given that senescent cells are strongly implica.
Fight Aging! 06/02/2020 06:11
One possible expansion of present immunotherapies for Alzheimer's disease is to more specifically track and target oligomeric forms of amyloid-β. Efforts to reduce amyloid-β in the brain have, after many years of failure, started to succeed in that goal in human trials, but patients are not exhibiting benefits as a result. It remains to be seen whether or not this is because amyloid-β is a trigger for other self-sustaining pathological mechanisms, such as cellular senescence of supporting cells in the brain, and thus removing it does little good once Alzheimer's is underway. An alternative view is that perhaps the wrong forms of amyloid-β are being targeted by existing approaches, and a more specific therapy would achieve better results. Re.
Fight Aging! 06/01/2020 15:22
There is evidence for particulate air pollution to raise the risk of age-related diseases via mechanisms such as increased levels of chronic inflammation. While the burden of age-related disease varies widely from region to region, establishing the relative weight of specific contributions is a challenge. Poverty, particulate air pollution, high rates of chronic infection, and other environmental factors thought likely to lead to a greater risk of age-related disease all tend to overlap to some degree. Thus while there are plausible mechanisms for particulate air pollution to spur chronic inflammation and thus speed the onset of age-related disease, and these mechanisms are well-demonstrated in laboratory animals, one cannot rule out the po.
Fight Aging! 06/01/2020 06:22
BCL-xL is a mitochondrial protein that acts to suppress the programmed cell death response of apoptosis, and is overexpressed in some cancers, as well as in senescent cells. Thus small molecules that bind to BCL-xL have been used as chemotherapeutics and more recently as senolytics that selectively destroy senescent cells. That removal of senescent cells is a legitimate rejuvenation therapy that quite literally turns back aging in animal models has caused greater attention to be given to BCL-2 family proteins and their role in allowing cells to hold back apoptosis. Separately, as noted here, evidence shows that BCL-xL is a longevity-associated protein, which is interesting, to say the least. This may or may not have anything to do with supp.
Fight Aging! 06/01/2020 06:11
In most species, including our own, females live longer than males. Why this is the case is likely one of those simple questions that lacks a simple answer. At the root of it all are evolutionary pressures relating to sex-specific differences in mating strategy, but that says little about how and why an emergent property such as sex-specific life span differences actually emerges. Researchers here find a great deal of variation from species to species in the degree of the female longevity advantage, complicating the picture. The researchers compiled demographic data for more than 130 wild mammal populations and were able to estimate the average longevity and the rate of increase in the risk of dying as a function of age for both sexes. The
Fight Aging! 05/31/2020 08:24
Fight Aging! publishes news and commentary relevant to the goal of ending all age-related disease, to be achieved by bringing the mechanisms of aging under the control of modern medicine. This weekly newsletter is sent to thousands of interested subscribers. To subscribe or unsubscribe from the newsletter, please visit: Longevity Industry Consulting Services Reason, the founder of Fight Aging! and Repair Biotechnologies, offers strategic consulting services to investors, entrepreneurs, and others interested in the longevity industry and its complexities. To find out more: Contents Secreted Stem Cell Factors as a Treatment for Male-Pattern Baldness Vaccination as a L.
Fight Aging! 05/29/2020 15:28
One has to be cautious about studies in which metabolism is broken in some way, and symptoms of aging start to appear earlier as a result. Whether or not this has any relevance to normal aging is dependent on the fine details of the biochemistry involved, and can often be argued either way even by those with the most knowledge in the field. Aging is an accumulation of damage and dysfunction in cells and tissues. Many genetic alterations and toxins that disrupt cell metabolism will lead to damage and dysfunction, and thus conditions that appear similar to those of aging. But unless it is the same forms and distribution of damage, and it never is, there may well be little to learn that will help […]
Fight Aging! 05/29/2020 06:01
A few varieties of dwarf mice exhibit considerable longevity. They are produced via forms of mutation that disable portions of growth hormone metabolism, such as via growth hormone receptor knockout. Most research has thus focused on insulin signaling, IGF-1, and other pathways closely tied to growth hormone. Here, scientists instead focus on the behavior of fat tissue in these long-lived mouse lineages, suggesting that the significant differences they observe in the metabolism of visceral fat may contribute to the impact on aging. It is well known that visceral fat is metabolically active, and excess amounts create chronic inflammation through a number of mechanisms, including accelerated generation of senescent cells. That doesn't appear
Fight Aging! 05/28/2020 15:14
The Forever Healthy Foundation publishes a series of conservative risk-benefit analyses of presently available interventions that might prove beneficial in addressing aspects of aging. These range widely in proven effectiveness, quality of animal evidence, and theoretical utility. Some do not in any way attack the known root causes of aging. Some are still pending any sort of rigorous human trial data. Some have plenty of human data that strongly indicates small, unreliable effects at best. It is nonetheless a useful exercise to make clear which are which. In a world in which the "anti-aging" industry propagates all sorts of nonsense to sell their snake-oil products, there is a comparative lack of good, unbiased analysis of approaches that
Fight Aging! 05/28/2020 06:22
To what degree is increased blood flow to the brain the important mechanism mediating the beneficial effects of exercise on memory? Exercise improves memory both in the very short term, and over the long term. This may be as simple as increased blood flow delivering more of the nutrients and signals that spur brain tissue into greater activity, though there are other mechanisms to consider as well. The research here adds evidence for the effect to result from better blood flow to memory-related areas of the brain. Scientists have collected plenty of evidence linking exercise to brain health, with some research suggesting fitness may even improve memory. But what happens during exercise to trigger these benefits? New research that mapped bra.
Fight Aging! 05/28/2020 06:11
Researchers here investigate detailed measures of brain function over time, and correlate them with the level of physical activity. There is plenty of evidence for greater physical activity to slow cognitive decline with age and reduce the risk of dementia. Which of the many mechanisms involved are the most important is an open question: is it as simple as better vascular function to supply the brain with the nutrients it needs, or are more direct effects on neural mechanisms just as relevant? Although various studies have identified physical activity as a possible primary preventive protective factor for brain health, the mechanisms by which physical activity affect cognitive function are not fully understood. Until recently, it was though.
Fight Aging! 05/27/2020 15:50
Microglia are immune cells of the brain, analogous to macrophages in the rest of the body. They take on a broad range of tasks: chasing down pathogens; clearing up cell debris and molecular waste; assisting in regeneration and tissue maintenance; assisting neurons in remodeling of synapses. Microglia, like macrophages, can shift between behavior patterns in response to environmental circumstances, such as M1 (inflammatory and aggressive) and M2 (anti-inflammatory and regenerative). With advancing age, microglia become increasingly inflammatory: this may be the result of too much molecular waste, such as the amyloid-β associated with Alzheimer's disease, it may be the consequence of persistent infections such as herpeviruses, or there may be.
Fight Aging! 05/27/2020 06:22
Stochastic mutational damage to nuclear DNA occurs constantly in the body, and near all of it is quickly repaired. Most unrepaired damage occurs in DNA that isn't used, or the change has only has a small effect on cell metabolism, or occurs in a somatic cell that will replicate only a limited number of times. When mutations occur in stem cells or progenitor cells, however, they can spread widely through tissue, producing a pattern of mutations known as somatic mosaicism. It is thought that this can contribute to the progression of aging via a slowly growing disarray of cellular metabolism, particularly through the spread of more severe damage, such as aneuploidy, missing or additional chromosomes. That said, firm evidence for the size of th.

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