Lifeboat Foundation

A new study shows that scientists might be able to not only slow the process of aging but actually reverse it, Benjamin Button-style.

Volunteers in a California study were given a cocktail of three common drugs for one year— a growth hormone and two diabetes medications. Scientists had been testing the drugs in the hope of regenerating the thymus gland.

But upon further analysis, they found that participants had lost an average of 2.5 years on their “epigenetic clock,” measured by analyzing marks on a person’s genomes, according to the journal Nature. Participants’ immune systems also showed signs of rejuvenation.

Telomeres are the protective caps of our chromosomes and play a central role in the aging process. Shorter telomeres are associated with chronic diseases and high stress levels can contribute to their shortening. A new study now shows that if telomeres change in their length, that change is also reflected in our brain structure. This association was identified by a team of scientists including Lara Puhlmann and Pascal Vrtička from the Max Planck Institute for Cognitive Brain Sciences in Leipzig together with Elissa Epel from the University of California and Tania Singer from the Social Neuroscience Lab in Berlin as part of Singer’s ReSource Project.

Telomeres are protective caps at the ends of chromosomes that become shorter with each cell division. If they become so short that the genes they protect could be damaged, the cell stops dividing and renewing. Consequently, the cell is increasingly unable to perform its functions. This mechanism is one of the ways in which we age.

Telomere length is therefore regarded as a marker for the biological age of a person—in contrast to their chronological age. For two people of the same chronological age, the person with shorter telomeres has an increased risk of developing age-related diseases such as Alzheimer’s or cancer, and even a shorter life expectancy.

“DNA is like a computer program but far, far more advanced than any software ever created.” Bill Gates wrote this in 1995, long before synthetic biology – a scientific discipline focused on reading, writing, and editing DNA – was being harnessed to program living cells. Today, the cost to order a custom DNA sequence has fallen faster than Moore’s law; perhaps that’s why the Microsoft founder is turning a significant part of his attention, and wallet, towards this exciting field.

Bill Gates is not the only tech founder billionaire that sees a parallel between bits and biology, either. Many other tech founders – the same people that made their money programming 1s and 0s – are now investing in biotech founders poised to make their own fortunes by programming A’s, T’s, G’s and C’s.

The industry has raised more than $12.3B in the last 10 years and last year, 98 synthetic biology companies collectively raised $3.8 billion, compared to just under $400 million total invested less than a decade ago. Synthetic biology companies are disrupting nearly every industry, from agriculture to medicine to cell-based meats. Engineered microorganisms are even being used to produce more sustainable fabrics and manufacture biofuels from recycled carbon emissions.

Imagine waking up every morning in a house that is just as alive as you are. With synthetic biology, your future home could be a living, breathing marvel of nature and biotechnology. Yes, it’s a bold ambition. But this kind of visionary thinking could be the key to achieving sustainability for modern cities.

Our current homes and cities are severely outdated. Dr. Rachel Armstrong, a synthetic biologist and experimental architect, says, “All our current buildings have something in common: they’re built using Victorian technologies.” Traditional design, manufacturing, and construction processes demand huge amounts of energy and resources, but the resulting buildings give nothing back. To make our future sustainable, we need dynamic structures that give as much as they take. We need to build with nature, not against it.

In nature, everything is connected. For the world’s tallest trees—the California redwoods— their lives depend on their connection to each other as well as on a host of symbiotic organisms. Winds and rain batter the California coast, so redwoods weave their roots together for stability, creating networks that can stretch hundreds of miles. The rains also leach nutrients from the soil. But fungi fill the shortage by breaking down dead organic matter into food for the living. A secondary network of mycelia—the root-like structures of the fungi—entwine with the tree roots to transport nutrients, water, and chemical communications throughout the forest. What if our future cities functioned like these symbiotic networks? What if our future homes were alive?

A recent review shows the current state of the industry with regards to using human pluripotent stem cells (hPSCs) to create cells that are useful for the study of, and therapies for, the human heart.

Pluripotent Stem Cells

Stem cells are the cells that form every other cell in the body, and adult humans naturally have native populations of stem cells to replace losses; the depletion of these reserves is stem cell exhaustion, which is one of the hallmarks of aging. To create stem cells from regular (somatic) cells, researchers use a technique called induced pluripotency, which creates induced pluripotent stem cells (iPSCs). However, purely naive, dedifferentiated pluripotent cells, which could create any cell in the body, are only of limited use and are not effective as a therapy. To form specific somatic cell lines, stem cells must first be differentiated into specific types.

Japan’s attractiveness to regenerative-medicine entrepreneurs is prompting other countries to look closely at its regulatory changes. There is undoubtedly a competition under way, and unless something is done, it risks becoming a race to the bottom.

Japan helped to bring stem-cell technology to the world. Its regulatory policies threaten its hard-won reputation.

Quantum computing has the potential to revolutionize technology, medicine, and science by providing faster and more efficient processors, sensors, and communication devices.

But transferring information and correcting errors within a quantum system remains a challenge to making effective quantum computers.

In a paper in the journal Nature, researchers from Purdue University and the University of Rochester, including John Nichol, an assistant professor of physics, and Rochester Ph.D. students Yadav P. Kandel and Haifeng Qiao, demonstrate their method of relaying information by transferring the state of electrons. The research brings scientists one step closer to creating fully functional quantum computers and is the latest example of Rochester’s initiative to better understand quantum behavior and develop novel quantum systems. The University recently received a $4 million grant from the Department of Energy to explore quantum materials.

Cells that become senescent irrevocably stop dividing under stress, spewing out a mix of inflammatory proteins that lead to chronic inflammation as more and more of the cells accumulate over time. Publishing in the September 24 edition of Cell Reports, researchers at the Buck Institute identified 44 specific senescence-associated proteins that are involved in blood clotting, marking the first time that cellular senescence has been associated with age-related blood clots.

“The incidence of venous thrombosis, which includes deep vein thrombosis and pulmonary embolism is extremely low until the age of 45, when it begins to rise rapidly. Over time it becomes a major risk factor for death. By 80, the condition affects five to six people per thousand individuals,” said Judith Campisi, PhD, Buck professor and senior co-author of the study. “Blood clots are also a serious side effect of chemotherapy, which sets off a cascade of senescence in those undergoing treatment. That’s why blood thinners, which carry their own risks, are often included in treatment protocols.”

Scientists in the Campisi lab and other labs around the world are working to develop senolytics, drugs which would clear senescent cells from the body, potentially providing treatment options for many age-related diseases that are either caused or linked to senescence. They include Alzheimer’s and Parkinson’s diseases, cardiovascular disease, osteoarthritis, macular degeneration, age-related cancers and sarcopenia, among others.