Dear Future Centenarian,
You see them all around you…
Those with high IQs, lean muscular bodies, bodies and faces that keep on ticking and don’t seem to age, extraordinary athletes, super strength and endurance, movie star looks and on and on.
What are their advantages?
They hit the genetic lotto.
It’s not fair, is it? Weren’t we meant to be created equal? Well maybe freedom-wise. But our minds and bodies depend on the genetic luck of the draw.
Finally, researchers are coming up with a way to level the playing field with ways to control gene expressions. Of course the gifted can become even more gifted.
Yes, a rising tide elevates all boats.
Even today, we have gene therapies to make you stronger, give you more endurance, reverse aspects of aging, increase mitochondrial function – giving you more energy and more, sharpen your cognition and maybe even bump your IQ, possibly roto root your arteries, manage your hypertension… and cure many diseases such as Chronic Kidney Disease and maybe Alzheimer’s.
All with one simple injection which might last you a lifetime.
A leading-edge company offers some of these therapies TODAY. www.Integrated-Health-Systems.com.
And then there’s gene editing. You’ve probably heard of CRISPR which burst on the scene several years ago. Now it seems like there’s a new CRISPR breakthrough every month or two.
CRISPR technology is a simple yet powerful tool for editing genomes. It allows researchers to easily alter DNA sequences and modify gene function.
Its many potential applications include correcting genetic defects, treating and preventing the spread of diseases and improving crops.
It also holds promise for the treatment and prevention of aging and complex diseases, such as cancer, heart disease, mental illness, and human immunodeficiency virus (HIV) infection.
Not enough seats left
In the spirit of staying connected with others in the super longevity community, you are hereby invited to our annual Super Longevity Holiday Party and Seminar!
Sponsored by: Maximum Life Foundation, Alcor, Humanity+ and Gerontology Research Group.
Hosted by David Kekich and Dr. Kat Cotter
Meet up with old friends and make some new ones. The more the merrier!
Due to overcapacity, we had to turn people away last year. So, get your tickets now because we DID sell out then and are well ahead of last year’s pace!
We hope you can join us to kick off the holiday season. We look forward to seeing you!
Seminar: 4:00-6:00 PM with six 15-minute presentations
Holiday party: 6:00-9:00 PM with heavy hors d'oeuvres and open bar
Come for the seminar, the holiday party or both!
There is a guarded gate. Show the attendant your Eventbrite ticket or receipt.
Event to be held at the following:
Date: Saturday, December 7, 2019
Time: 4:00 PM to 9:00 PM (PST)
Location: The Clubhouse
at The Colony in Newport Beach
5100 Colony Plaza
Newport Beach, CA 92660
NLRP3 Knockout Extends Maximum Life Span by 29% in Mice
Today's open access research is an interesting demonstration of the importance of chronic inflammation in aging.
Researchers generate a mouse lineage in which the NLRP3 gene is deleted, and show that these mice live significantly longer, and in better health, as a result.
The protein produced from the NLRP3 gene is important in the innate immune response; it is a component part of one of the inflammasomes, protein complexes with a central role in regulation of the inflammatory response. NLRP3 appears important in the inflammatory signaling generated by senescent cells as well.
Evidence for Human Cell Division Rates to Decrease with Age
We humans exhibit a peak cancer incidence in old age, around the early 80s, after which cancer rates decline from that peak.
If aging is the continual accumulation of damage, then why do we observe this pattern of cancer incidence with age rather than a continual increase over time? It does not occur in mice, after all.
Researchers here provide evidence for the explanation to involve reduced rates of cell division in later life, which may be one of many evolutionary adaptations connected to the unusual longevity of our species when compared with other similarly sized mammals, and particularly other primates.
A Perspective on Longevity Biotech Investment from James Peyer of Kronos BioVentures
James Peyer, formerly of Apollo Ventures and now at the larger Kronos BioVentures, has a range of interesting views on the new and growing longevity biotechnology industry.
Apollo Ventures was one of the earlier longevity-focused funds to emerge from the comparatively small community of scientists, patient advocates, and investors enthusiastic to accelerate progress towards the treatment of aging as a medical condition.
Taking the Founders Pledge to Donate to Charity Following a Liquidity Event
If there is anything worse than bragging about one's charitable giving, it is bragging about the charitable giving one might accomplish in the future, should one turn out to have the funds to do so.
In a world in which establishing cultural norms wasn't so very important to success in non-profit fundraising, none of the audience here would know anything about my donations to the Methuselah Foundation and SENS Research Foundation, made over the years as we moved ever closer to the reality of therapies to treat and reverse aging.
But establishing cultural norms is in fact very important in this business of non-profit fundraising. Why does cancer research receive such a large amount of non-profit funding? That has a lot more to do with the culture of charitable giving, and the visibility of giving to cancer research programs, than with the merits of those programs and organizations, or the merits of defeating these medical conditions.
It is a great idea to fund effective cancer research, but I don't think that is why most donors give to the cause.
Senescent Cells in Blind Mole Rats do not Exhibit the Senescence-Associated Secretory Phenotype
Naked mole-rats live as much as nine times longer than similarly sized rodent species.
A short summary of what is known of their biochemistry is that they exhibit many of the molecular signs of aging found in other mammals, such as oxidative damage, presence of senescent cells, and so forth, but few to none of the consequences found in other mammals.
Naked mole rats stay fit and healthy and physiologically youthful right up until very late life. The near relative species of blind mole-rat has many of the same characteristics, although it is less well studied than naked mole-rats at the present time.
Early Detection of Misfolded Amyoid-? in the Blood Implies Greater Risk of Later Alzheimer's Disease
In recent years, a great deal of effort has been put towards means of assessing risk of Alzheimer's disease as early as possible in aging individuals.
The results here are an illustrative example of initiatives focused on amyloid-? in the blood: assays based on a blood sample are somewhat easier to develop than most of the other options; amyloid-? levels in the brain are known to increase slowly over time; and the presence of amyloid-? in the brain and bloodstream are in some form of dynamic equilibrium with one another.
The Collapse of Proteostasis in Later Stages of Aging
Proteostasis is the name given to successful maintenance of youthful levels of proteins and minimal protein damage in cells.
With age, the molecular damage of aging leads to changes in expression of proteins and dysfunction in cellular maintenance processes. The result is ever more damaged proteins and altered cellular behavior.
A Role for Acetylcholine in Sarcopenia
It has been suggested that some fraction of sarcopenia, an age-related loss of muscle mass and strength leading to frailty, is caused by dysfunction of neuromuscular junctions, the points of integration between muscle and nervous system.
This is as opposed to the more straightforward loss of stem cell function, leading to a lesser capacity for muscle growth and tissue maintenance. Acetylcholine has a prominent role in the function of neuromuscular junctions, and on this basis researchers here demonstrate that reduced levels of acetylcholine lead to both improvement in the structure of neuromuscular junctions and a slowing of the progression of sarcopenia in aged mice.
Low Dose Quercetin as a Geroprotector in Mice
Quercetin is used in combination with dasatinib as a senolytic treatment capable of selectively destroying senescent cells, but quercetin used by itself is not meaningfully senolytic.
Researchers here show that long term low dosage with quercetin modestly slows aspects of aging in mice, however, without extending life span. They evaluate a number of potential mechanisms, including possible reductions of the inflammatory signaling secreted by senescent cells.
Quercetin Coated Nanoparticles Shown to be Senolytic in Cell Cultures
Quercetin, while used in combination with dasatinib as a senolytic therapy capable of destroying senescent cells, is not meaningfully senolytic on its own.
One argument as to why this is the case is that compounds of this class are not very bioavailable - in other words that quercetin, suitably modified, or delivered in a different manner, would be senolytic enough to form a basis for therapy. Researchers here take the approach of coating nanoparticles with quercetin molecules, and find that the resulting particles can selectively kill senescent cells in cell culture, unlike quercetin alone.
This is a promising demonstration, particularly if we consider that it might be applied to the much more senolytic flavenoid fisetin, but it is always best to wait for animal data before becoming too excited by any given approach.
Senescent Cells Consume their Neighbors
The accumulation of lingering senescent cells is an important contributing cause of degenerative aging. In this intriguing report, researchers note that senescent cells resulting from chemotherapy treatment can consume neighboring cells in order to prolong their survival.
This is most likely the case for senescent cells in general, whatever their origin. This cellular cannibalism is probably detrimental to tissue function to some small degree, but, since senescent cells are always a tiny minority of all cells, even in old tissues, it is nowhere near as detrimental as the inflammatory signaling profile that accompanies cellular senescence.
Unless this consumption of nearby cells is absolutely vital to the survival of a large fraction of long-lived senescent cells, the mechanisms involved are unlikely to present a useful point of intervention.
Calorie Restriction Started in Old Age Does Not Extend Life in Mice
Researchers here establish that calorie restriction started in late life does not extend life in mice, contradicting older research results showing that it does to some degree.
This may be a difference resulting from mouse lineage or housing or diet prior to applying calorie restriction. The researchers here point to the behavior of fat tissue in the older mice as being important, so we might think that perhaps the mice in the two studies began calorie restriction with differing amounts of fat tissue.
Senescent Mesenchymal Stem Cells Contribute to Osteoarthritis
Cellular senescence is a significant contributing cause of osteoarthritis in old age, and senolytic therapies capable of selectively destroying senescent cells are presently undergoing clinical trials in osteoarthritic patients.
Researchers here investigate a specific population of senescent cells, the supporting mesenchymal stem cells found in and around joint tissue, and establish that they are important in the progression of osteoarthritis.
Microglial Neuroinflammation as a Cause of Tau Aggregation
Chronic inflammation in the brain is an important aspect of all neurodegenerative conditions. In particular, as discussed in this open access paper, there is good evidence for inflammatory and dysfunctional (and senescent) microglia to drive the tau protein aggregation characteristic of late stage Alzheimer's disease.
It remains to be seen as to how the research community will build on past years of research on this topic to develop therapies, but one of the best near term possibilities is the use of senolytic therapies such as the dasatinib and quercetin combination to selectively destroy senescent microglia in the aging brain.