 Quantum computers have been growing in popularity because experts are hopeful that quantum computers may soon help us solve problems in just a few days that would currently take our best classical computers literally thousands of years to solve. So we'll explore how quantum computers could soon potentially dramatically accelerate longevity research. Next we'll show how a certain kind of stem cell can reverse some aspects of aging in neighboring cells. And finally we'll explore how the aged microenvironment in the body of older mice is linked to sarcopenia, which is the age-related loss of muscle mass. You'll find these stories in this episode of Lifespan News. Welcome to Lifespan News on X10, your source for longevity science updates. I'm your host, Brent Nally. We encourage you to check the description below for links to these stories. For our first story, can quantum computing dramatically accelerate new healthy longevity drug discovery? There's been considerable hype around quantum computers over the past few years, and the legitimate promise they hold. Unlike classical computers, quantum computers take advantage of the principles of quantum mechanics. In a classical computer, every bit can be in either of two states, either zero or one. Instead, a quantum computer doesn't deal with bits but with qubits, which can be in an indeterminate state of superposition of both zero or one until measured. The technical details are, well, too technical. But the important thing is that quantum computers are able to crack tough problems much faster than classical computers. Problems that could take a classical computer literally thousands of years to solve. Some of these problems are of interest for the longevity space, such as drug discovery. A drug is just a molecule that is expected to interact in certain ways with a biological system. And as such, it's closer to a quantum system than a macroscopic object. After all, molecules are nothing but atoms bonded together. Besides, at the tiny scales at which drugs operate, quantum effects that do not happen in the macroscopic world come into play. And accurate simulations of their interactions with their target are much harder to run on classical computers. Tech giants are all racing to produce better, faster, and more accurate quantum computers that can solve these and many other problems whose solution may change the world for the better. If you'd like to learn more, you'll find a link in the description below. Lifespan.io is excited to announce our fourth annual Ending Age-related diseases conference, which is scheduled to take place August 19th to 22nd, 2021. We'll be meeting virtually to hear the latest developments from the leading experts in rejuvenation biotechnology research. In addition to the scientific program, we'll provide interviews and panel discussions on the philosophy and practice of life extension, longevity journalism, and the relationship between bio-rejuvenation and blockchain. Register now before the early bird offer runs out, June 30th, 2021, at Lifespan.io Backslash Conference, which is also linked in the description below. Our next story is about how mesenchymal stem cells, or MSCs, promote the health of nearby cells. The researchers first tested embryonic cells derived from mice, measuring their viability along with their senescence biomarkers when co-cultured along with adipose-derived stem cells, or ADSCs. Being in the presence of ADSCs significantly decreased the well-known senescence biomarkers of SAB-GAL, P16, P53, and P21, and it also slowed down metabolism and changed the cell's metabolic profile. The researchers then used a fluorescent marker to show that these effects were the results of the cell's consumption of their own mitochondria. Co-culture with ADSCs boosted this process. Removing damaged mitochondria and thus increasing mitochondrial quality while reducing harmful reactive oxygen species, the team tested this idea using a mouse model of mitochondrial dysfunction. When given regular injections of ADSCs, these mice had increased mitophagy and cellular senescence like that of normal, wild-type mice. So it would be nice to see a study of ADSCs in aged wild-type mice. If ADSCs can be shown to work in that case, then the development of a treatment for humans would be the next logical step. If such a treatment were to pass human clinical trials, it would almost certainly assist in combating not only stem cell exhaustion, which is the original hallmark that stem cell therapies are meant to ameliorate, but would also reduce mitochondrial dysfunction and cellular senescence to other hallmarks of aging. A new longevity project is going live to the public today, June 29th, 2021. On-deck longevity biotech, or ODLB, is a continuous community for people to come together to build, join, or invest in revolutionary longevity biotechnology startups. ODLB is seeking the most talented and mission-driven people looking to build, join, or invest in longevity biotech companies with a strong focus on aspiring entrepreneurs, graduate students, and academics looking to start longevity companies. ODLB is scheduled to kick off the first cohort September 12th, 2021, and onboard three cohorts per year. Go to beondeck.com to learn more. There's also a link in the description below. For our final story, according to new research, sarcopenia is likely due to changes in the muscle microenvironment that reduce repair and regeneration. Muscular degradation with age is not the result of a decline in the intrinsic regenerative ability of muscles. Scientists are unsure why sarcopenia happens. Maybe it's because the exhaustion of muscle precursor cells with age makes the muscles unable to repair accumulated damage to muscle cells. Or it could be that there's no change in the intrinsic competence of muscle cells and that muscle damage goes unrepaired because of changes in the muscle microenvironment. So to figure out the answer, a team of U.S. researchers developed and used a system to graft muscle tissue from human cadavers into mice. By using tissue from cadavers of people from different ages, the team was able to evaluate the intrinsic regenerative ability of muscle cells at these ages. The transplants were equally successful regardless of whether the tissue came from the body of a 36-year-old or a 78-year-old. Donor tissue from cadavers of various ages integrated into the mouse host and began producing muscle within three weeks and continued for at least six weeks. In other words, the precursor cells in the elderly people retain the ability to generate muscle tissue. So the researchers argue that the most likely explanation for their failure to do this in elderly people is that the changes in the muscle microenvironment somehow reduce regenerative competence. That's all the news for this episode. Is there a recent life extension story that you think we should have covered but haven't yet? And what was your favorite story from this episode? Let us know what you think in the comments and we'll see you in the next episode.