The 2020s are the nascent era of Drug discovery sped up by machine learning.
Category: life extension – Page 169
Researchers from Harvard Medical School found that it is the changes that affect the expression of the DNA â called epigenetics â that affect aging. The discovery may pave the way for more insights into how humans age.
The last few years have exceeded all expectations in terms of investment activity in longevity, but much more is needed to push the field forward. With more than 40 investments in the longevity field over the past three years, LongevityTech.fund is one of the worldâs most active longevity investment funds. The fundâs wide-ranging investment portfolio includes companies like BrainKey, Gerostate Alpha and Occuity.
LongevityTech.fund is now accepting new investors for its second fund, with a target fund size of $50 million up to a maximum of $100 million USD.
Longevity. Technology: LongevityTech.fund has built an impressive company portfolio that has seen no failures to date, with one IPO (longevity biotech Genflow Biosciences) and one company (longevity risk management firm Vesttoo) recently becoming the fundâs first unicorn (valued at more than $1 billion). To learn more about his views on the longevity market, we spoke to serial entrepreneur and investor Petr Sramek, LongevityTech.fundâs co-founder and managing partner.
Healthy mutant gene in super-fit people can reverse the decline of heart performance in the elderly, according to a study.
Injecting the genes of so-called âsuper-agersâ into failing heart cells regenerates them, making them function as if they were 10 years younger, scientists have found.
The discovery opens the door for heart failure to be treated or prevented by reprogramming damaged cells.
The hypertension drug rilmenidine has been shown to slow down aging in worms, an effect that in humans could hypothetically help us live longer and keep us healthier in our latter years.
Rilmenidine was picked for this latest study because past research has shown it mimics the effects of caloric restriction on a cellular level. Reducing available energy while maintaining nutrition within the body has been shown to extend lifespans in several animal models.
Whether this translates to human biology, or is a potential risk to our health, is a topic of ongoing debate. Finding ways to achieve the same benefits without the costs of extreme calorie cutting could lead to new ways to improve health in old age.
Bryan Johnson releases his rejuvenation protocol:
Blueprint is a public science experiment to determine whether itâs possible to stay the same biological age. This requires slowing down aging processes as much as possible and then reversing the aging that has happened. Currently my speed of aging is .76 (DunedinPACE). That means for every 365 days each year, I age 277 days. My goal is to remain the same age biologically for every 365 days that pass.
I openly share (for free!) my diet, exercise and other protocols so that others can benefit and try to improve upon what Iâm doing. I also openly share my health data as data is better than human opinion at guiding decision making. You can find everything here: https://blueprint.bryanjohnson.co/
This video is a whirlwind tour of what my daily life looks like as my team and I are on this adventure.
On the surface, Blueprint may seem like something about health, wellness and aging. To me, itâs a philosophy.
Health tests and reports suggest that Bryan Johnson, 45, has the heart of a 37-year-old and gets erections like a teenager, Bloomberg reported.
We spoke with Dr Morgan Levine 2 years ago concerning the remarkable results that she and a team that included Dr David Sinclair had in restoring vision in mice. In that experiment, published in the journal Nature, older mice had tighter optic nerves crushed causing blindness. Then, using a combination of 3 of the 4 Yamanaka cellular programing factors, they were able to restore the miceâs vision by signally the underlying DNA, rebuilding what had been thought to be permanently damaged cells. This was a remarkable result, as it was restoring a damaged organ, essentially a part of the brain, to its original healthy state. When I spoke to Dr Levine about the next step in her research, she mentioned it may be a more complex organ, such as a mouse liver.
But they went further. In the January issue of Cell, Sinclair published results of their ability to age an entire mouse. That is, to signal the epigenome to cause the underlying mouse DNA to behave as if it were much older. They were also able to do the reverse: to take an older mouse and, by signaling the epigenome, bring its cells and organs to the state of a younger mouse. This is a truly remarkable achievement, and it seems to prove Sinclairâs theory that all of our cells have within them a pristine copy of their DNA, and that aging and the disease associated with aging are the result of miscues from the epigenome. If these miscues can be corrected then the cell can be restored, not to a blank stem cell but to its original condition.
A gene called BPIFB4, discovered in a population of centenarians, could help to reverse the aging of human hearts.
Carriers of healthy mutant genes, including people in so-called âblue zonesâ of the world, often live to 100 years or more and remain in good health. Cardiovascular complications are also rarer in these individuals. Scientists now believe that a gene may help to keep their hearts young by protecting them against diseases linked to aging.
Recent experiments conducted in Boston labs have shown reverse aging results among mice and could show similar results in people.
The combined experiments â which were conducted during a span of 13 years â published Thursday (January 12) in the scientific journal Cell reported that old, blind mice regained eyesight, developed smarter brains and built healthier muscle and kidney tissue, challenging the theory that DNA was the only cause of aging, as it proved that chemical and structural changes to chromatin played a factor without altering genetic code.
The research showed that a breakdown in epigenetic information caused the mice to age and the restoration of the epigenome reversed aging effects.