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Fight Aging! 08/16/2019 16:13
The most common age-related neurodegenerative conditions are associated with the build up of various protein aggregates, chemically altered or misfolded proteins that can form solid deposits in and around cells when in that state. These protein aggregates are characterized by the ability to spread and grow, acting as seeds for more aggregation. They include the well known amyloid-β and tau of Alzheimer's disease, the α-synuclein associated with Parkinson's disease, and so forth. In recent years researchers have been devoting ever more effort to investigations of a less well known protein aggregate, TDP-43, associated with ALS and frontotemporal lobar degeneration. Today's open access paper is representative of work taking place to understan.
Fight Aging! 08/16/2019 06:22
Cells that enter a senescent state have many purposes in the body. They are involved in both wound healing and cancer suppression, for example. Senescence also serves to remove somatic cells that reach the Hayflick limit on replication. Senescent cells secrete a potent mix of signals to rouse the immune system and encourage local tissue regrowth and remodeling. This is all useful in the short term, where senescent cells accomplish the immediate task at hand and then self-destruct or are destroyed by immune cells. Wounds are healed, and potentially cancerous cells destroyed. Yet cellular senescence is a cause of aging. The problems arise due to the tiny fraction of senescent cells that evade destruction and linger in the body in increasing n.
Fight Aging! 08/16/2019 06:11
Inhibition of mTOR, and specifically of the mTORC1 protein complex these days, while trying to avoid inhibition of the mTORC2 complex, is a strategy for modestly slowing aging. It is what I would consider a good example of a worse strategy, in that it aims to adjust the operation of metabolism to make it more resilient to the damage of aging, rather than attempting to repair the damage of aging. It will thus produce benefits to health and longevity that are small in the grand scheme of what is possible. This is true of near all of the initiatives arising from the study of the metabolic response to calorie restriction and other stresses, in which cell maintenance processes such as autophagy are upregulated to beneficial […]
Fight Aging! 08/15/2019 15:28
Loss of the myelin layer that sheathes nerves is the proximate cause of severe conditions such as multiple sclerosis, but this sort of loss occurs to a lesser degree in the course of normal aging, and contributes to cognitive decline. In today's open access research materials, scientists draw a line of cause and effect between (a) increasing stiffness of the brain tissue that hosts niches where stem cells reside, (b) dysfunction of those stem cells mediated by the specific stiffness-sensing mechanism of Piezo1, a process that may exist in other stem cell populations as well, © the loss of myelin-generating cells normally produced by the stem cells, and (d) the consequent degradation of myelin and nervous system function. Without looking int.
Fight Aging! 08/15/2019 06:11
It is good to see that more of the promising technical approaches to aspects of aging, originally put forward by people in the SENS rejuvenation research network some years ago, are now making solid progress towards commercial implementation. The LIFT, or GIFT, approach to cancer therapy involves the transplantation of suitably aggressive leukocyte or granulocyte immune cells from a donor. At the time it was first demonstrated to be highly effective in mice, more than a decade ago, the underlying mechanisms were not well explored, and that always makes it hard to obtain further support from scientific funding institutions. This is despite the point that the approach has the potential to be a near universal cancer therapy, applicable to most.
Fight Aging! 08/14/2019 06:22
This open access review examines what is known of the role of fibroblast growth factors in mechanisms relevant to skin aging, such as loss of collagen and elastin from the extracellular matrix. This type of paper always makes for an interesting read, and fully mapping the cellular metabolism of aging is the right goal from a fundamental science perspective. When it comes to near term intervention in the aging process, this sort of examination is less helpful, however. Yes, growth factor expression levels change in aging skin cells, and that has consequential effects. But this is in and of itself far removed from the underlying causes of degenerative aging. It is itself a consequence and not a cause. The most efficient way forward is to […]
Fight Aging! 08/14/2019 06:11
Cancer cells abuse signals used elsewhere in normal mammalian biochemistry to prevent immune cells from destroying other cells, such as CD47. Interfering in these "don't eat me" signals has produced significant gains in the development of effective cancer therapies that can target multiple types of cancer. Here, researchers describe a newly discovered "don't eat me" signal, CD24, that should allow this class of cancer therapy to be expanded to target cancers that have proved resilient to existing implementations. This and related lines of work that lead to more general anti-cancer platforms are one of the reasons why young people today should have little concern over cancer in their old age yet to come. It will be near entirely a controllab.
Fight Aging! 08/13/2019 16:22
Every type of tissue is supported by its own dedicated stem cell population, delivering a supply of daughter somatic cells that replace losses and maintain tissue function. Unfortunately, stem cell function declines with age. This has numerous causes, all of which descend from the underlying accumulation of molecular damage outlined in the SENS research proposals for rejuvenation biotechnologies. Downstream of those causes, stem cells become less active due to some combination of internal damage, damage to their niche of supporting cells, and changes in the signaling environment. The latter two classes of issue appear more influential in the best studied stem cell populations, such as the satellite cells of muscle tissue. Thus most research.
Fight Aging! 08/13/2019 06:22
HDAC inhibitors are a comparatively poorly understood category of drugs that act to modestly slow aging in short-lived laboratory species. As such, they most likely function through some form of upregulation of cellular stress responses, thus activating cellular maintenance processes that lead to improved cell and tissue function. That said, the chain of cause and effect leading from the known mechanism of action to that stress response upregulation is not clearly mapped. As for all approaches that slow aging via stress response mechanisms, we should remember that the effects on life span in short-lived species are much larger, relatively speaking, than those in long-lived species such as our own, even when the short term effects on the ope.
Fight Aging! 08/13/2019 06:11
Researchers here process statistical data to suggest that major surgery in later life accelerates cognitive decline. It would be interesting to compare data on serious injuries rather than surgery, as one of the possible mechanisms underlying this effect is a greater presence of senescent cells than would otherwise be the case. Senescent cells produce systemic chronic inflammation, and that is important in the progression of age-related neurodegeneration. Senescent cells are also generated in the course of wound healing, such as recovery from surgery, and some small fraction will always linger, failing to self-destruct or to be cleared from the body by the immune system. Thus we might expect severe injuries and major surgeries to produce so.
Fight Aging! 08/12/2019 14:39
Adam Ford of Science, Technology, and the Future carried out a number of interviews while at Undoing Aging in Berlin earlier this year. The interview materials are steadily being processed and uploaded, and that just recently included this interview with Jim Mellon, billionaire investor and philanthropist, cofounder of Juvenescence, and a very down to earth fellow who is interested in improving the human condition by targeting aging with new biotechnologies. Accordingly, he has used his resources to put himself into a position to talk up the longevity industry, move research forward, and attract a great deal more funding for the next stage in the process of guiding the first treatments to slow and reverse aspects of aging from the laborator.
Fight Aging! 08/12/2019 06:22
Retrotransposons are genetic sequences that can copy themselves to new locations in the genome. This activity increases with age, for reasons that are still poorly understood, and it is an open question as to the degree to which this is important as a cause of tissue dysfunction with aging. The arguments for and against are much the same as those for stochastic mutation of nuclear DNA to be a meaningful contribution to degenerative aging, with the most compelling model being the one in which mutations in stem or progenitor cells can spread widely in a tissue through their descendant somatic cells. This open access paper is focused on assessing the growth in retrotransposon activity and the increasing burden of senescent cells with advancing.
Fight Aging! 08/12/2019 06:11
The gut microbiome is influential on the progression of health, perhaps to a similar degree as regular moderate exercise. Age-related changes in these microbial populations can promote chronic inflammation and tissue dysfunction, though the direction of causation is still up for debate when it comes to many of the details of the relationship between tissue and immune issues in the intestine and an altered gut microbiome. Nonetheless, less desirable microbes undertake activities that can raise the risk of cancer resulting from inflammation of the intestines, occurring in conditions such as inflammatory bowel disease. Researchers here demonstrate that suitable adjustment of microbial populations in mice can lower the incidence of cancer in th.
Fight Aging! 08/11/2019 07:15
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 An Interview with Reason at Undoing Aging 2019 The Potential of Senolytic Therapies to.
Fight Aging! 08/09/2019 16:22
A fair number of research groups are presently working on ways to force large numbers of cells in the body to adopt more youthful epigenetic profiles. Much of this research is an outgrowth of the discovery of induced pluripotency, the ability to reprogram any cell into a pluripotent stem cell that is largely indistinguishable from an embryonic stem cell, capable of generating any of the cell types in the body. This process also happens to reset many of the epigenetic markers of age that are found in cells in old tissues, alongside restoring mitochondrial function by clearing out damaged mitochondria, and a few other interesting changes. The article here focuses on one representative project, but readers here might be more familiar with the
Fight Aging! 08/09/2019 06:11
Researchers here suggest that infection plays an important role in cardiovascular disease in later life, and that the chronic inflammation of aging is a factor in allowing infection to cause significant harm to the heart. This is one of countless issues that could be mitigated through rejuvenation of the aging immune system, fixing the underlying issues that cause the immune system to become less functional and more inflammatory. These include atrophy of the thymus, the loss of thymic tissue where T cells of the adaptive immune system mature, loss of hematopoietic stem cell capacity, leading to reduced generation of new immune cells, the structural aging of lymph nodes, preventing immune cells from efficiently coordinating with one another,
Fight Aging! 08/08/2019 16:17
Today's open access paper is a review of present progress towards regenerative therapies that can reverse hearing loss. Progressive hearing loss is pervasive in old age, and accelerates considerable in the later stages of life. Hearing loss correlates with cognitive decline, and while it is plausible that this is because of degeneration of central nervous system function, there is also the consideration that loss of hearing isolates people and deprives them of interactions that stimulate brain activity. It is well demonstrated in mice that environment richness has a strong impact on the brain and its pace of aging. Much of the research into age-related hearing loss is focused on the sensory hair cells of the inner ear. These detect the pres.
Fight Aging! 08/08/2019 06:22
The open access editorial noted here serves as an introduction to some of the current thinking on the role of cytomegalovirus (CMV) in the age-related decline of the immune system. CMV infection is pervasive throughout the population, particularly in the old. This persistent viral infection cannot be effectively cleared by the immune system, and an ever greater percentage of immune cells become uselessly specialized to fight CMV. This leaves ever fewer immune cells ready to tackle other threats. This seems an important component of immune dysfunction, one that can perhaps be addressed by selectively destroying these immune cells to free up space for replacements. The research community is by no means unified on this view of CMV, however, as.
Fight Aging! 08/08/2019 06:17
Given the newfound acceptance of cellular senescence as an important cause of aging, many more research groups are assessing the impact of senescent cells in their research into aging. Here, the focus is on chromatin organization, a collection of nuclear structures and processes in the cell that appear to have some influence over the pace of aging over a lifetime. The researchers discover that the gene DGCR8 accelerates the appearance of senescent cells and dysfunction when mutated, and thus producing broken protein machinery, but slows the accumulation of lingering senescent cells when overexpressed in its correct form. This touches on some of the same machinery of the cell as the mir-122 findings discussed a few days ago, and that work is.

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