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.
Biology The Unity and Diversity of Life (12th Edition)
Yet we live in an age of biotechnology and rapid, revolutionary progress. It is unthinkable that immunology, genetics, gene therapies, and advanced medical applications of the life sciences can continue to coexist with the fact that we can't get rid of a few simple bacterial species that are causing us considerable harm. Sooner or later the research community will bring all undesirable bacteria under medical control. For some years now, a number of dental research groups have been working on potential methods of permanently excluding the bacteria that cause periodontitis and other inflammatory damage to gums, teeth, and the underlying bone. This has proven to be slow going, unfortunately. Nonetheless there have been signs of progress of late. To pick an example from earlier this year, one research team has managed to rouse the innate immune system into attacking and destroying bacterial species that cause gum disease, reversing the progression of periodontitis. Similarly, the research linked below takes the form of a vaccine, training the immune system to attack one of the problem molecules produced by the Porphyromonas gingivalis bacteria that contribute to periodontitis. The dental research community tends to have a faster time to market and less of a regulatory burden than the rest of the broader medical community, so we might expect to see something along these lines reaching clinics within the next few years.
One of the most pressing aspects of stem cell biology is that the activity of stem cell populations decline with age, something that so far appears to be largely a matter of signaling when it comes to muscle stem cells. That may or may not universally true for other types of stem and progenitor cell. Certainly stem cell populations and their supporting niche cells suffer the molecular damage of aging just like other cells do. Nonetheless, in the case of muscle stem cells there are numerous studies demonstrating restored stem cell activity in old animals via various forms of intervention. Thus there is considerable interest in the research community when it comes to building a map of the biochemistry of this stem cell decline, and then building therapies to put these stem cells back to work. Loss of muscle mass and strength, and ability to regenerate from injury, is an important component of age-related frailty. If that can be reduced by overriding the reactions of cells to rising levels of damage, and without significantly raising the risk of cancer, then perhaps some good can be done here even in advance of methods of repairing the underlying damage that causes aging. I'd much rather see more work on rejuvenation through repair rather than forcing damaged cells into youthful patterns of behavior, but the latter is clearly going to happen regardless of my opinions on the matter: a fair number of research teams are headed in that direction. Stem cell research as a whole is set on a collision course with the issue of stem cell decline in aging, as a sizable majority of the therapies one would want to want to build using stem cell research are for age-related conditions. Solving the issues of failing stem cells in an old tissue environment must happen at some point in order for researchers to achieve their goals.
I mentioned CellAge some weeks ago; a new entry to the collection of companies and research groups interested in developing the means to safely identify and remove senescent cells from old tissues. A few days later one of those companies, UNITY Biotechnology, announced a sizable 116 million venture round, which certainly put the field on the map for anyone who wasn't paying attention up until that point. In contrast, CellAge are taking a less commercial path for now, by raising funds from the broader community of supporters and intending to make some of the tools they create freely available to the field. Why are senescent cells important? Because they are a cause of aging, and removing them is a narrowly focused form of rejuvenation, shown to restore function and extend healthy life in animal studies. An increasing number of senescent cells linger in our bodies as we age, secreting signals that harm tissue structures, produce chronic inflammation, and alter the behavior of nearby cells for the worse. Senescent cells also participate more directly in some disease processes, such as the growth of fatty deposits, weakening and blocking blood vessels, that takes place in atherosclerosis. By the time that senescent cells come to make up 1% of the cell population in an organ, their presence causes noticeable dysfunction and contributes significantly to the progression of all of the common age-related diseases.
Recently it has been demonstrated that senescent cells (cells which have ceased to replicate due to stress or replicative capacity exhaustion) are linked to many age-related diseases. Furthermore, removing senescent cells from mice has been recently shown to drastically increase mouse healthspan, the period of life free of serious diseases. CellAge, together with a leading synthetic biology partner, Synpromics, are poised to develop a technology allowing for the identification and removal of harmful senescent cells. Our breakthrough technology will benefit both the scientific community and the general public.
As many worthwhile efforts go, we didn't push CellAge into existence just because we wanted to start a company. I have been following ageing research for very long time and so I was aware what is happening in the field. At the same time, I emerged myself into synthetic biology where I am doing my PhD now. For a while, I have been exposed to these different fields and at some point things just connected. Recent publications on mouse models showed that there is a great promise in removing senescent cells and from my own end, some exciting technological opportunities presented themselves from the synthetic biology side. So CellAge is really a result of many coincidence that led to this project. After I discussed these ideas with more experienced people, some of whom are our advisors now, I came to realize that there is a real opportunity here and we took it!
The immune system declines with age, as the proportion of its cells capable of responding to new threats falls, autoimmunity increases, and the system as a whole enters a state of constant, rising inflammation. The failure of the immune system speeds other forms of damage and dysfunction in aging, as immune cells are responsible for killing potentially harmful cells, such as those that become senescent or precancerous. The immune system also plays important roles in a variety of essential processes, such as wound healing and maintenance of brain tissues. Clearing out the causes of immune system decline will be a necessary part of any future toolkit of rejuvenation therapies. The open access paper linked here is an illustration of the importance of immune function in aging, as markers of its decline correlate with age and remaining life expectancy:
Since numerous inflammatory factors are increased in aged hematopoietic tissues, and inflammation- and aging-associated hematopoietic changes share common cellular and molecular alterations, it is reasonable to speculate that low-grade inflammation might be involved in hematopoietic aging with reduced fitness of both adaptive and innate immune cells. Given that some hematopoietic phenotypes during inflammation and aging arise from functional alterations in HSCs and progenitor cells (HSPCs), it would be worthwhile to elucidate the underlying common mechanisms. Future research could yield meaningful insights into cell-intrinsic changes in HSPC quantity and quality, e.g., how aspects of HSPC population dynamics such as functional heterogeneity and population size change, whether all subsets of HSCs with a distinct lineage output respond equally to inflammatory stimuli or only the minor fraction is responsive, how the self-renewal and differentiation capacities of HSC are altered on a per-cell basis, and molecular changes in cellular signaling, such as alterations in cellular metabolism, transcriptional networks, epigenetic modifications, and genomic instability. It is also essential to understand to what extent inflammaging-associated cell-extrinsic factors influence HSPC biology, including signals derived from the BM niche, tissue damage/repair, infection, obesity, or the microbiome. In addition, the fundamental task that remains is identification of the factors initially triggering the process of hematopoietic inflammaging. Inflammation- or aging-related external stimuli appear to force quiescent HSCs to proliferate and impair their self-renewal and differentiation capacities, as suggested by evidence that HSC cycling in response to chemotherapy administration or hematopoietic stress accelerates the manifestation of aging phenotypes. These data suggest that the central features of HSCs aging might be attributable to accumulation of a proliferative history that is closely associated with perturbed self-renewal and differentiation.
Minot State celebrates Mother Language Day Fri. Feb. 17, 2017 12:00 AM Minot State University will host a community celebration of multilingualism, diversity and culture Tuesday (Feb. 21) at 1:30 p.m. in the... Read More
A course in the history of western civilization is an excellent opportunity for students to develop and master skills of reading, analysis, discussion, and writing which will be useful for a lifetime. The aim of this course is not to fill the student's mind with a mass of useless, quickly forgotten facts. Instead, in this course we will emphasize three skills: 1) careful and critical reading; 2) effective discussion, analysis and reasoning; and 3) clear and accurate written presentation. To build these skills, in each class meeting we will discuss primary sources - direct evidence from the past. 2ff7e9595c
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