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Fight Aging! 12/15/2019 09:08
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: https://www.fightaging.org/newsletter/ 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: https://www.fightaging.org/services/ Contents Cancer Survivors have Double the Risk of Suffering a Later Stroke Calorie Restriction
Fight Aging! 12/13/2019 16:11
The back and forth over whether regular aspirin use is beneficial continues with the publication of results from analysis of a large patient population that show a 15% reduction in all cause mortality in patients using aspirin. This contradicts the much smaller (but still large in and of itself) ASPREE clinical trial, in which patients using aspirin exhibited a small increase in mortality in comparison to their peers. As in that earlier study, the data here strongly suggests that benefits and risks vary with patient characteristics, such as whether or not a patient is overweight. Aspirin is thought to be a weak calorie restriction mimetic, in that it can produce benefits via upregulation of autophagy to some degree, but it also reduces infl.
Fight Aging! 12/13/2019 06:22
This review paper looks at the present range of strategies adopted by the research and development communities in their efforts to target senescent cells. The accumulation of senescent cells is a contributing cause of aging; many animal studies have demonstrated reversal of aspects of age-related disease via clearance of senescent cells, particularly for those conditions in which chronic inflammation plays an important role. Senescent cells are comparatively few in number even in later life, but cause harm via secreted signals, a potent mix of proteins and vesicles known as the senescence-associated secretory phenotype (SASP). The SASP drives inflammation, changes the behavior of nearby cells for the worse, and destructively remodels surrou.
Fight Aging! 12/13/2019 06:11
The accumulation of senescent cells is a cause of aging, which is why a great deal of effort is presently going towards the development of senolytic therapies capable of selectively destroying these unwanted cells. Very little is known about the dynamics of senescent cells in old age, however. We know that older individuals have more senescent cells at any given moment in time, but is this because a small fraction of the many senescent cells created every day manage to linger persistently for years, resistant to the efforts of the immune system to remove them, or because clearance processes, while they will eventually destroy all senescent cells, are slowed to the point at which they cannot keep up? This open access paper suggests the secon.
Fight Aging! 12/12/2019 15:48
Age-related neurodegeneration is characterized by rising levels of various protein aggregates in the brain. A few of the many thousands of proteins in the body can become misfolded in ways that encourage other molecules of the same protein to also misfold in the same way, forming structures that spread and precipitate into solid deposits. These aggregates are accompanied by a halo of surrounding biochemistry that is toxic to neurons, disrupting function in the brain and killing vital cells, causing loss of cognitive function and ultimately death. In recent years, increasing attention has been given to the role of cerebrospinal fluid drainage in maintaining the brain. The circulation of cerebrospinal fluid is not a closed system, but one tha.
Fight Aging! 12/12/2019 06:22
Researchers here use data on cholesterol and health assessed in a large patient population over a 40 year period in order to determine how the risk of suffering atherosclerosis by age 75 varies with cholesterol levels assessed in the 30s and 40s. It is no surprise that higher cholesterol levels mean a greater risk of atherosclerosis, the development of fatty lesions that narrow and weaken blood vessels. The condition is one in which the macrophage cells responsible for removing these unwanted lipids from blood vessel walls are made dysfunctional by rising levels of oxidized cholesterol. The more cholesterol in the blood stream, the more oxidized cholesterol, all other things being equal. Using data for individuals without prevalent cardiova.
Fight Aging! 12/12/2019 06:11
Why do genetically identical nematode worms raised in the same environment exhibit a distribution in life span? Researchers here suggest that differences in oxidative stress in early life are an important contributing factor, perhaps steering metabolism in some of these simple organisms towards greater resistance to the rising oxidative stress of aging. So a form of hormetic effect, perhaps. Does this have much relevance to higher animals such as our own, however? It would be challenging to separate out early life effects of this nature from the environmental differences across the whole of life, given the existing human epidemiological data. We might consider lines of research into childhood exposure to persistent viruses such as cytomegal.
Fight Aging! 12/11/2019 15:46
The lymphatic system is a parallel circulatory system responsible for moving fluid, immune cells, and a range of vital molecules around the body. It is of particular importance to immune function, allowing components of the immune system to carry messages from place to place in the body, and communicate and coordinate the immune response at the hubs known as lymph nodes. Like all tissues in the body, the lymphatic system is negatively impacted by aging, and this has widespread detrimental effects throughout the body and brain. For example, lymph nodes become disrupted in structure and function by the presence of senescent cells and consequent fibrosis as tissue maintenance runs awry in the face of the senescence-associated secretory phenoty.
Fight Aging! 12/11/2019 06:22
Cells enter a state of senescence in response to reaching the Hayflick limit, or to a toxic environment, or potentially cancerous mutational damage. Near all senescent cells self-destruct, or are destroyed by the immune system. Some linger, however, and when present in even comparatively small numbers relative to normal cells, these senescent cells cause considerable harm via their inflammatory secretions. Thus the targeted destruction of senescent cells via senolytic therapies has been shown to extend healthy life and reverse numerous aspects of aging in mice. Human trials of senolytic treatments are presently underway, and have produced promising initial results. Researchers here do the public service of combing through the existing liter.
Fight Aging! 12/11/2019 06:08
As this open access paper notes, a great deal of the present work on developing biomarkers of aging involves machine learning. Researchers are sifting and arranging health metrics, blood markers, and epigenetic data to find combinations that predict risk of disease and mortality. The aim at the end of the day is to determine a good measure of biological age, one that accounts for all of the burden of cellular and molecular damage that leads to death and dysfunction, and will thus be a good, rapid measure of effectiveness for rejuvenation therapies. The biggest challenge in this line of work at the present time is that researchers don't have a good understanding of what exactly is being measured by many of these potential biomarkers. It […]
Fight Aging! 12/10/2019 15:38
The practice of calorie restriction, eating 20-40% fewer calories while still obtaining an optimal intake of micronutrients, produces sweeping changes in the operation of cellular metabolism. It improves health and extends life span in near all species tested to date, though much more so in short-lived species than in long-lived species. The most important mechanism appears to be a boost to the operation of the cellular housekeeping processes of autophagy, more efficiently clearing out damaged components and unwanted molecular waste before they can cause further issues. That said, near every measure of aging is slowed by calorie restriction, so it is no surprise to see in today's open access paper that this slowing also applies to the detri.
Fight Aging! 12/10/2019 06:22
Neurodegenerative diseases are characterized by the formation of protein aggregates, misfolded proteins that encourage other molecules of the same protein to also misfold in the same way, forming solid deposits that damage and destroy brain cells. Researchers here suggest that the age-related decline in proteasomal function is a contributing factor. The proteasome is a structure that breaks down damaged or otherwise unwanted proteins in cells. While this form of cellular housekeeping does decline with age, and there is good evidence in lower animals for increased proteasomal function to slow aging, it is worth bearing in mind that the research here is based on deliberately breaking proteasomes by removing a crucial component protein. It is
Fight Aging! 12/10/2019 06:11
Numerous demonstrations of rejuvenation via clearance of senescent cells in recent years have led to a newfound and considerable enthusiasm for the study of the mechanisms of cellular senescence. Ever more funding in flowing into this part of the life sciences. That any new discovery might lead to a company, valuable intellectual property, a means to treat aging, is a considerable incentive forthe various research and funding ecosystems. The open access research noted here is a representative example of numerous projects presently underway. Cellular senescence is involved in modulating aging and aging-associated pathologies via the senescence-associated secretory phenotype (SASP). Growing evidence has implicated the accumulation of senescen.
Fight Aging! 12/09/2019 16:22
Surviving cancer comes with a well known loss of remaining life expectancy, roughly the same as being obese or a lifelong smoker. It is plausible that this is a consequence of the generation of large numbers of lingering senescent cells, resulting from radiotherapy and chemotherapy, still the dominant forms of cancer treatment. An increased burden of cellular senescence is certainly preferable to death by cancer, but these cells secrete a potent mix of inflammatory signals that disrupt tissue maintenance and immune function, encourage fibrosis, and increase the risk of numerous age-related conditions. Given that the accumulation of senescent cells is a cause of aging, increasing their presence might rightfully be regarded as an acceleration.
Fight Aging! 12/09/2019 06:11
Lymphopenia is the condition of having lower than normal levels of lymphocytes, a mix of cells of the adaptive and innate immune system, in blood samples. The immune system is of vital importance to health, and this is demonstrated here by data that shows raised mortality in the sizable fraction of older people with degrees of lymphopenia versus those without. Lymophocytes do not just respond to the presence of infectious pathogens, but also attack and destroy senescent cells and cancerous cells, among other important activities. A severely deficient immune system is a real threat to life, and as this work illustrates, even a modestly deficient immune system is something to worry about. The near future should see the advent of approaches to.
Fight Aging! 12/08/2019 09:59
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: https://www.fightaging.org/newsletter/ 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: https://www.fightaging.org/services/ Contents The Catalytic Antibody Approach to Amyloid Aggregation This Giving Tuesday, Support Re.
Fight Aging! 12/06/2019 15:44
Today's open access research on tryptophan and its role in age-related immune dysfunction is particularly interesting in the context of ongoing research into the changes that take place in gut microbiota with age. Other recent work has examined the way in which tryptophan production by gut microbes declines precipitously with age, as this is one of a number of compounds produced by bacteria, such as butyrate, indole, and proprionate, that are influential on long term health. It is a slow process, but researchers are uncovering the specific mechanisms linking age-related changes in gut microbe populations with declining health. The overall size of effect of gut microbes on heath might be in the same ballpark as that of exercise, but this is
Fight Aging! 12/06/2019 06:26
Nuclear DNA damage is considered a contributing cause of aging, though at this stage the research community is still proposing and debating processes by which this damage might cause metabolic dysfunction throughout the body. Mutations to nuclear DNA evidently increase cancer risk, but setting this aside, how does random damage to random cells contribute to the declines of age? There are a few possibilities; firstly that the vast majority of nuclear DNA damage, occurring as it does in somatic cells, or in unusued portions of the genome, is irrelevant. Harms are done when mutations affecting function occur in stem cells and progenitor cells, allowing that mutation to spread widely throughout a tissue. The second possibility, more recently pr.
Fight Aging! 12/06/2019 06:11
A sizable body of evidence, both mechanistic and epidemiological, supports the idea that exercise slows age-related cognitive decline. The report here is an example of the type, noting the results of a study in which some of the participants were assigned to an exercise program. The exercising participants exhibited a slower decline in cognitive function, particularly memory, in comparison to the others. This is a representative result: in general, the consensus in the scientific literature is that regular exercise is beneficial to cognitive function over the long term. Researchers theorized that the healthy lifestyle behaviors that slow the development of heart disease could reduce heart disease risk and also slow cognitive decline in olde.

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