Interventions that may slow ageing include drugs (e.g., rapamycin, metformin), supplements (e.g., nicotinamide riboside, nicotinamide mononucleotide), lifestyle interventions (e.g., exercise) and diets (e.g., fasting)

Thanks to advances in modern medicine over the past century, the world’s population has experienced a marked increase in longevity. However, disparities exist that lead to groups with both shorter lifespan and significantly diminished health, especially in the aged. Unequal access to proper nutrition, healthcare services, and information to make informed health and nutrition decisions all contribute to these concerns. This in turn has hastened the ageing process in some and adversely affected others’ ability to age healthfully. Many in developing as well as developed societies are plagued with the dichotomy of simultaneous calorie excess and nutrient inadequacy. This has resulted in mental and physical deterioration, increased non-communicable disease rates, lost productivity and quality of life, and increased medical costs. While adequate nutrition is fundamental to good health, it remains unclear what impact various dietary interventions may have on improving healthspan and quality of life with age. With a rapidly ageing global population, there is an urgent need for innovative approaches to health promotion as individual’s age. Successful research, education, and interventions should include the development of both qualitative and quantitative biomarkers and other tools which can measure improvements in physiological integrity throughout life. Data-driven health policy shifts should be aimed at reducing the socio-economic inequalities that lead to premature ageing. A framework for progress has been proposed and published by the World Health Organization in its Global Strategy and Action Plan on Ageing and Health. This symposium focused on the impact of nutrition on this framework, stressing the need to better understand an individual’s balance of intrinsic capacity and functional abilities at various life stages, and the impact this balance has on their mental and physical health in the environments they inhabit.

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Today would have been the 99th birthday of Ms. Henrietta Lacks, a woman whose remarkable DNA led to countless cures, patents and discoveries:

“I was wrong,” Church now admits.

A startup he cofounded, eGenesis, had made news for its ambitious plans to use CRISPR gene-editing technology to modify pigs so their organs could be safely transplanted into humans without being rejected. That could solve a critical shortage of human organs available for transplant.

But no human test has yet been carried out. Instead, the company is currently testing organs from its pigs in monkeys at Massachusetts General Hospital in Boston. The experiments are being led by the hospital’s chief of transplant surgery, James Markmann.

Can the origin of life be explained with quantum mechanics? And if so, are there quantum algorithms that could encode life itself?

We’re a little closer to finding out the answers to those big questions thanks to new research carried out with an IBM supercomputer.

Encoding behaviours related to self-replication, mutation, interaction between individuals, and (inevitably) death, a newly created quantum algorithm has been used to show that quantum computers can indeed mimic some of the patterns of biology in the real world.

Meet Zhong Zhong and Hua Hua, the first monkeys to ever be cloned .

A new technique developed by MIT physicists could someday provide a way to custom-design multilayered nanoparticles with desired properties, potentially for use in displays, cloaking systems, or biomedical devices. It may also help physicists tackle a variety of thorny research problems, in ways that could in some cases be orders of magnitude faster than existing methods.

The innovation uses computational neural networks, a form of artificial intelligence, to “learn” how a nanoparticle’s structure affects its behavior, in this case the way it scatters different colors of light, based on thousands of training examples. Then, having learned the relationship, the program can essentially be run backward to design a particle with a desired set of light-scattering properties—a process called inverse design.

The findings are being reported in the journal Science Advances, in a paper by MIT senior John Peurifoy, research affiliate Yichen Shen, graduate student Li Jing, professor of physics Marin Soljacic, and five others.

Chemically induced pluripotent stem cells (CiPSCs) may provide an alternative and attractive source for stem cell-based therapy. Sufficient telomere lengths are critical for unlimited self-renewal and genomic stability of pluripotent stem cells. Dynamics and mechanisms of telomere reprogramming of CiPSCs remain elusive. We show that CiPSCs acquire telomere lengthening with increasing passages after clonal formation. Both telomerase activity and recombination-based mechanisms are involved in the telomere elongation. Telomere lengths strongly indicate the degree of reprogramming, pluripotency, and differentiation capacity of CiPSCs. Nevertheless, telomere damage and shortening occur at a late stage of lengthy induction, limiting CiPSC formation. We find that histone crotonylation induced by crotonic acid can activate two-cell genes, including Zscan4; maintain telomeres; and promote CiPSC generation. Crotonylation decreases the abundance of heterochromatic H3K9me3 and HP1α at subtelomeres and Zscan4 loci. Taken together, telomere rejuvenation links to reprogramming and pluripotency of CiPSCs. Crotonylation facilitates telomere maintenance and enhances chemically induced reprogramming to pluripotency.

Aged population is increasing worldwide due to the aging process that is inevitable. Accordingly, longevity and healthy aging have been spotlighted to promote social contribution of aged population. Many studies in the past few decades have reported the process of aging and longevity, emphasizing the importance of maintaining genomic stability in exceptionally long-lived population. Underlying reason of longevity remains unclear due to its complexity involving multiple factors. With advances in sequencing technology and human genome-associated approaches, studies based on population-based genomic studies are increasing. In this review, we summarize recent longevity and healthy aging studies of human population focusing on DNA repair as a major factor in maintaining genome integrity. To keep pace with recent growth in genomic research, aging- and longevity-associated genomic databases are also briefly introduced. To suggest novel approaches to investigate longevity-associated genetic variants related to DNA repair using genomic databases, gene set analysis was conducted, focusing on DNA repair- and longevity-associated genes. Their biological networks were additionally analyzed to grasp major factors containing genetic variants of human longevity and healthy aging in DNA repair mechanisms. In summary, this review emphasizes DNA repair activity in human longevity and suggests approach to conduct DNA repair-associated genomic study on human healthy aging.

Aging is an inevitable process in human life. Many countries are rapidly transitioning to an aging society due to increasing life expectancy and advanced medical supports [1–3]. Over the last few decades, the advent of aging society is considered a crucial issue that may cause future decline in productivity of community [1, 4]. Many researchers have recently warned that urban environmental pollutants can cause physiological weakness and increase the risk of premature aging or chronic diseases in the elderly population [5–9]. Thus, interest in antiaging and healthy longevity is constantly increasing. “Active aging” or “successful aging” has been spotlighted as a strategy to promote social contribution of the elderly [10]. The definition of successful aging remains controversial.

Sought after guest speaker, Aubrey de Grey, has appeared on numerous popular programs including CBS 60 Minutes, BBC, TED and The Colbert Report to name just a few. Today, he joins The Future Tech Podcast, to share his vision on how we can improve the aging process through enhancing the human body’s capability of rejuvenation through cell immortality and pluripotency to human aging and age-related disease.

The. Vice President of New Technology and Discovery at AgeX Therapeutics, Aubrey de Grey, Ph.D., is also the Chief Science Officer of SENS Research Foundation, a California-based 501©(3) biomedical research charity that performs, and funds research devoted to battling the progression of aging.

In this fascinating discussion, Aubrey explains some of the obstacles that need to be overcome, including issues involving age-related tissue damage and stem cell decline which contribute to accelerating the aging process. He also discusses what AgeX is doing in stem cell research and in regenerative medicine that will improve not only the longevity of life, but also the quality and health of individuals throughout the aging process. He also touches on what he sees could be the future in the science of aging and treatments being worked on by the rejuvenation research community.

When I am 85, there will have been next to no senescent cells in my body for going on thirty years. I bear only a small fraction of the inflammatory burden of older people of past generations. I paid for the products of companies descended from Oisin Biotechnologies and Unity Biotechnology, every few years wiping away the accumulation of senescent cells, each new approach more effective than the last. Eventually, I took one of the permanent gene therapy options, made possible by biochemical discrimination between short-term beneficial senescence and long-term harmful senescence, and then there was little need for ongoing treatments. Artificial DNA machinery floats in every cell, a backup for the normal mechanisms of apoptosis, triggered by lingering senescence.

When I am 85, the senolytic DNA machinery will be far from the only addition to my cells. I underwent a half dozen gene therapies over the years. I picked the most useful of the many more that were available, starting once the price fell into the affordable-but-painful range, after the initial frenzy of high-cost treatments subsided into business as usual. My cholesterol transport system is enhanced to attack atherosclerotic lesions, my muscle maintenance and neurogenesis operate at levels far above what was once a normal range for my age, and my mitochondria are both enhanced in operation and well-protected against damage by additional copies of mitochondrial genes backed up elsewhere in the cell. Some of these additions were rendered moot by later advances in medicine, but they get the job done.