July 12th our special one-day biotech and business conference launches in New York City. This event brings together some of the leading experts in aging research and investment and promises to be an action-packed day.
For more information please visit: https://www.eventbrite.com/e/ending-age-related-diseases-investment-prospects-advances-in-research-tickets-45733391806
Video Creator: Jason Shulkin, Motion Graphics Artist. www.jasonshulkin.com
Scientists at Hollings Cancer Center at the Medical University of South Carolina have found that human lung cancer cells resist dying by controlling parts of the aging process, in results published online May 10th in the Journal of Biological Chemistry. The discovery could help us better understand aging and eventually could lead to new treatments for cancer.
Cancer becomes more common as people get older, but scientists are still searching for answers about why this happens. At Hollings Cancer Center, research into the connections between aging and cancer is led by Besim Ogretmen, Ph.D., SmartState Endowed Chair in Lipidomics and Drug Discovery. Ogretmen’s team found that cancer cells have specific ways to resist dying the way normal cells do. They do so by protecting the tips of their chromosomes, which hold our DNA, from age-related damage.
Ogretmen studies how cancer cells are different than normal cells to understand how cancer grows and spreads in the body. His work is part of an $8.9 million program project grant to research how alterations of lipid metabolism affect cancer therapy. The grant is helping fund a clinical trial of an anticancer medicine to inhibit cellular signaling that helps cancer survive. The drug was found to be useful against cancer in the research reported in the group’s new paper.
“I am extremely excited about the research involved in the current Scientific Reports article,” said Joseph I. Shapiro, M.D., senior author and dean of the Joan C. Edwards School of Medicine. “I believe that our team has not only implicated the NAKL discovered by our colleague, Dr. Zijian Xie, in the aging process but identified a novel therapeutic target as well as a specific pharmacological strategy to actually slow the aging process. Although it will be some time before we can test these concepts in human subjects, I am cautiously optimistic that clinical therapeutics will ultimately result.”
The team’s extensive year-long study first focused on aging mice who were given a western diet to stimulate oxidant stress to antagonize the NAKL. The western diet increased the functional and structural evidence for aging; however, the introduction of pNaKtide slowed these changes in the mice. The same results were then replicated when human dermal fibroblasts were exposed to different types of oxidant stress in vitro by stimulating the NAKL, increasing expression of senescence markers, and causing cell injury. With pNaKtide treatment, the researchers demonstrated that the negative attributes associated with aging were significantly dampened.
“Our data clearly suggest that the Na/K-ATPase oxidant amplification loop is intimately involved in the aging process and, if confirmed in human studies, might ultimately serve as a therapeutic target,” said first author Komal Sodhi, M.D., an associate professor of surgery and biomedical sciences at the Joan C. Edwards School of Medicine. “If the pNaKtide can be safely used in humans, it might be possible to study the applicability of that specific agent to the problem of clinical aging.”
Today, we have part one of a two-part interview with Dr. Michael Fossel, the driving force behind Telocyte, a new company focused on telomerase therapy for various diseases, and a strong advocate of telomerase therapy to treat human disease over the past three decades.
I interviewed Dr. Fossel as an individual thought leader in this field and not in his role representing Telocyte, so the opinions stated here are purely his own.
Born in 1950, Michael Fossel grew up in New York and lived in London, Palo Alto, San Francisco, Portland, and Denver. He graduated cum laude from Phillips Exeter Academy, received a joint B.A. and M.A. in psychology in four years from Wesleyan University in Connecticut, and, after completing a Ph.D. in neurobiology at Stanford University in 1978, went on to finish his M.D. at Stanford Medical School in two and a half years. He was awarded a National Science Foundation Fellowship and taught at Stanford University, where he began studying aging with an emphasis on premature aging syndromes. Dr. Fossel was a Clinical Professor of Medicine at Michigan State University for almost three decades and taught the Biology of Aging at Grand Valley State University.
TRX-1 inhibitor TXNIP might be implicated in increased oxidative stress as we age.
According to scientists at the German Cancer Research Center (Deutsches Krebsforschungszentrum, or DKFZ), the enzyme TXNIP, which inhibits the enzyme TRX-1, might be a regulator of aging and might be a viable candidate for future interventions against age-related diseases [1].
Study summary
KrioRus charges $36,000 to cryonize a corpse, or half that for just the head. The process is fairly straightforward: First, cryonicists drain the blood of the “patient,” and pump in a solution resembling antifreeze. The body goes into a cooling chamber beneath KrioRus’s 2,000-square-foot hangar in Sergiyev Posad, a suburb north of Moscow, for roughly a week. Then it’s immersed, head first, in a double-walled dewar of liquid nitrogen, where it hangs indefinitely until scientists figure out how to revive it. In this way, KrioRus has cryopreserved 61 people and 31 pets, including a cat, a goldfinch, and a chinchilla. At least 487 others have signed up.
“Maybe in five, 30, or 300 years, there will be a way to wake her again,” Riabinina says.
Riabinina’s story is among several that Italian photographer Giuseppe Nucci documents in -196: The Pioneers of Resurrection. His ethereal, atmospheric images respectfully capture the quest for immortality in Russia, home to a visionary gaggle of cosmists, cryonicists, and transhumanists who believe in a deathless future. They preach resurrection, wear high-tech cyber-suits, and deep-freeze the corpses of loved ones they hope to meet again.
“We are all scared of death,” Nucci says. “The idea that humans will one day defeat it is fascinating.”
A revolutionary new DNA tool could help take humanity a step closer to eternal life. The device (pictured) pioneers a new technique that makes it cheaper and easier to synthesise genes ‘overnight’, say scientists — a process that normally takes several days.
Scientists at the University of California at Berkeley said it could lead to ‘DNA printers’ in research labs that work like the 3D printers in many modern workshops.
‘If you’re a mechanical engineer, it’s really nice to have a 3D printer in your shop that can print out a part overnight so you can test it the next morning,’ said UC Berkeley graduate student Dan Arlow.
Humanity is made of individuals; preserving the life of individuals preserves humanity. Thus, life extension and the preservation of our species aren’t incompatible.
What is it that really matters: preserving individual lives or preserving humanity? Is it more important to grant individuals the option to live as long as they’d like in good health, or is it more important to ensure the preservation of our species? This sort of question isn’t unheard of in the context of discussions of pros and cons of rejuvenation biotechnology; at times, when presented with the possibility of indefinite lifespans, some people reply that focusing on the preservation of our species is more important. This observation is reminiscent of the “other priorities” objection, and one could respond to it in the same way. However, this issue is also worth examining from other angles.
Quick comeback: the two goals aren’t incompatible
A practical remark to make here is that preserving individual lives automatically preserves the human species because the species only exists as long as there are humans. Not everyone agrees that having a population of individuals that live indefinitely is “good for the species”—be it for fear of overpopulation or of cultural stagnation—but this concept is rather vaguely defined and not objectively measurable. However, here we are stepping into a different territory, one that has been explored in other articles, so we won’t go there in this one.
For the June edition of Journal Club, we will be taking a look at the recent paper entitled “Changes at the nuclear lamina alter binding of pioneer factor Foxa2 in aged liver”.
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https://onlinelibrary.wiley.com/doi/abs/10.1111/acel.12742
The exponential potential of longevity technologies.
Jim Mellon became a billionaire by pouncing on a wide variety of opportunities, from the dawn of business privatization in Russia to uranium mining in Africa and real estate in Germany. But all of that might eventually look small, he says, compared to the money to be made in the next decade or so from biotechnologies that will increase human longevity well past 100.
The British investor is so enthusiastic about these technologies that he co-authored a 2017 book about them, Juvenescence: Investing in the Age of Longevity, and launched a company, Juvenescence Ltd., to capitalize on them. “Juvenescence” is a real word — it’s the state of being youthful. Says Mellon, who is 61: “I’m hoping that this stuff works on me as well as on my portfolio.”
Juvenescence Ltd., which has raised $62.5 million from Mellon and some partners, has invested in or is close to confirming investments in nine biotech companies. He won’t discuss most of them. But one of the deals was an 11 percent stake in Insilico Medicine, a company applying machine-learning techniques to drug discovery. Insilico Medicine and Mellon’s company also formed a joint venture called Juvenescence AI to investigate the therapeutic properties of specific compounds. Mellon is particularly optimistic that this venture can develop a “senolytic” drug that helps the body clear out cells that have stopped dividing and can damage other cells.
