Turning off a newly identified enzyme could reverse a natural aging process in cells.
Research findings by a KAIST team provide insight into the complex mechanism of cellular senescence and present a potential therapeutic strategy for reducing age-related diseases associated with the accumulation of senescent cells.
Simulations that model molecular interactions have identified an enzyme that could be targeted to reverse a natural aging process called cellular senescence. The findings were validated with laboratory experiments on skin cells and skin equivalent tissues, and published in the Proceedings of the National Academy of Sciences (PNAS).
Cellular reprogramming can reverse the aging that leads to a decline in the activities and functions of mesenchymal stem/stromal cells (MSCs). This is something that scientists have known for a while. But what they had not figured out is which molecular mechanisms are responsible for this reversal. A study released today in STEM CELLS appears to have solved this mystery. It not only enhances the knowledge of MSC aging and associated diseases, but also provides insight into developing pharmacological strategies to reduce or reverse the aging process.
The research team, made up of scientists at the University of Wisconsin-Madison, relied on cellular reprogramming — a commonly used approach to reverse cell aging — to establish a genetically identical young and old cell model for this study. “While agreeing with previous findings in MSC rejuvenation by cellular reprogramming, our study goes further to provide insight into how reprogrammed MSCs are regulated molecularly to ameliorate the cellular hallmarks of aging,” explained lead investigator, Wan-Ju Li, Ph.D., a faculty member in the Department of Orthopedics and Rehabilitation and the Department of Biomedical Engineering.
Kewl… ~~~ “Led by Associate Professor Alfredo Franco-Obregón from the NUS Institute for Health Innovation and Technology (iHealthtech), the team found that a protein known as TRPC1 responds to weak oscillating magnetic fields. Such a response is normally activated when the body exercises. This responsiveness to magnets could be used to stimulate muscle recovery, which could improve the life quality for patients with impaired mobility, in an increasingly aging society.”
As people age, they progressively lose muscle mass and strength, and this can lead to frailty and other age-related diseases. As the causes for the decline remain largely unknown, promoting muscle health is an area of great research interest. A recent study led by the researchers from NUS has shown how a molecule found in muscles responds to weak magnetic fields to promote muscle health.
Led by Associate Professor Alfredo Franco-Obregón from the NUS Institute for Health Innovation and Technology (iHealthtech), the team found that a protein known as TRPC1 responds to weak oscillating magnetic fields. Such a response is normally activated when the body exercises. This responsiveness to magnets could be used to stimulate muscle recovery, which could improve the life quality for patients with impaired mobility, in an increasingly aging society.
“The use of pulsed magnetic fields to simulate some of the effects of exercise will greatly benefit patients with muscle injury, stroke, and frailty as a result of advanced age,” said lead researcher Assoc Prof Franco-Obregón, who is also from the NUS Department of Surgery.
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They say age breeds wisdom. But can we grow personally and mature, while staying young and healthy? Can ageing be cured just like any other disease? We asked David Sinclair, professor of genetics at Harvard Medical School.
David Andrew Sinclair is an Australian biologist and Professor of Genetics best known for his research on the biology of lifespan extension and driving research towards treating diseases of aging.
Sinclair is Co-Director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School. Sinclair obtained a Bachelors of Science (Honours Class I) at the University of New South Wales, Sydney, and received the Australian Commonwealth Prize. In 1995, he received a Ph.D. in Molecular Genetics then worked as a postdoctoral researcher at the Massachusetts Institute of Technology with Leonard Guarente. Since 1999 he has been a tenured professor in the Genetics Department of Harvard Medical School.
Sinclair has received over 25 awards including The Australian Commonwealth Prize, A Helen Hay Whitney Fellowship, the Nathan Shock Award, a Leukemia and Lymphoma Fellow, a MERIT Awards from the National Institutes of Health, the Merck Prize, the Arminese Fellowship, the Genzyme Outstanding Achievement in Biomedical Science Award, an Ellison Medical Senior Fellow, the Bio-Innovator award, the Bright Sparks Award for Top Scientists under 40, The Denham Harman Award in Biogerontology, a medal from the Australian Society for Medical Research, and a TIME 100 honoree, TIME magazine’s list of the 100 “most influential people in the world” (2014).
We will be joined by Morgan Levine, Yale University, to discuss the recent article “Underlying Features of Epigenetic Aging Clocks” she co-authored.
The talk will compare and contrast existing epigenetic clocks and describe how they can be deconstructed to facilitate our understanding of causes and consequences of epigenetic aging.
Article Abstract:
Epigenetic clocks, developed using DNA methylation data, have been widely used to quantify biological aging in multiple tissues/cells. However, many existing epigenetic clocks are weakly correlated with each other, suggesting they may capture different biological processes. We utilize multi‐omics data from diverse human tissue/cells to identify shared features across eleven existing epigenetic clocks. Despite the striking lack of overlap in CpGs, multi‐omics analysis suggested five clocks (Horvath1, Horvath2, Levine, Hannum, and Lin) share transcriptional associations conserved across purified CD14+ monocytes and dorsolateral prefrontal cortex. The pathways enriched in the shared transcriptional association suggested links between epigenetic aging and metabolism, immunity, and autophagy. Results from in vitro experiments showed that two clocks (Levine and Lin) were accelerated in accordance with two hallmarks of aging—cellular senescence and mitochondrial dysfunction. Finally, using multi‐tissue data to deconstruct the epigenetic clock signals, we developed a meta‐clock that demonstrated improved prediction for mortality and robustly related to hallmarks of aging in vitro than single clocks.
Morgan’s Bio:
Morgan Levine is a ladder-rank Assistant Professor in the Department of Pathology at the Yale School of Medicine and a member of both the Yale Combined Program in Computational Biology and Bioinformatics, and the Yale Center for Research on Aging. Her work relies on an interdisciplinary approach, integrating theories and methods from statistical genetics, computational biology, and mathematical demography to develop biomarkers of aging for humans and animal models using high-dimensional omics data. As PI or co-Investigator on multiple NIH-, Foundation-, and University-funded projects, she has extensive experience using systems-level and machine learning approaches to track epigenetic, transcriptomic, and proteomic changes with aging and incorporate this information to develop measures of risk stratification for major chronic diseases, such as cancer and Alzheimer’s disease. Her work also involves development of systems-level outcome measures of aging, aimed at facilitating evaluation for geroprotective interventions. A number of the existing biological aging measures she has developed are being applied in both basic and observational research.
An Israeli study came out last week that has been described as rejuvenation via hyperbaric oxygen. I’m not taking it very seriously, and I owe you an explanation why.
According to new research from CCR scientists, embryonic stem cells have a unique way of protecting their telomeres, the structures at the ends of chromosomes that shorten with every cell division. A research team led by Eros Lazzerini Denchi, Ph.D., an NIH Stadtman investigator in CCR’s Laboratory of Genomic Integrity, has found that rather than treating exposed telomeres as damaged DNA as most cells do, embryonic stem cells call on genes typically used only during the earliest stage of development to stave off unwanted DNA repair. The team’s findings, which come from studies of mouse embryonic stem cells, are reported November 25, 2020, in Nature.
By revealing an unexpected way cells can protect their telomeres, the new findings may help explain a survival strategy employed by some cancer cells, which must find a way to circumvent growth limits imposed by the natural shortening of telomeres that occurs as we age.
Embryonic stem cells, which arise early in an embryo’s development, have a unique capacity to become virtually any of the body’s specialized cell types. Lazzerini Denchi and colleagues first discovered their unusual approach to protecting telomeres when they found that the cells can survive without a protein called TRF2, which binds to and protects chromosome tips. The protein is absolutely essential for hundreds of different types of cells. Without it, exposed chromosome tips trigger faulty activation of DNA damage repair pathways, which stitch the unprotected ends together. Chromosomes fuse together and cells lose the ability to divide. But when Lazzerini Denchi’s team removed TRF2 from embryonic stem cells, chromosomes maintained their integrity and the cells continued to proliferate.
These findings […] strongly suggest that high levels of iron in the blood reduces our healthy years of life, and keeping these levels in check could prevent age-related damage.
Genes linked to ageing that could help explain why some people age at different rates to others have been identified by scientists.
The international study using genetic data from more than a million people suggests that maintaining healthy levels of iron in the blood could be a key to ageing better and living longer.
The findings could accelerate the development of drugs to reduce age-related diseases, extend healthy years of life and increase the chances of living to old age free of disease, the researchers say.
The historic NASA Twins Study investigated identical twin astronauts Scott and Mark Kelly and provided new information on the health effects of spending time in space.
Colorado State University Professor Susan Bailey was one of more than 80 scientists across 12 universities who conducted research on the textbook experiment; Mark remained on Earth while Scott orbited high above for nearly one year. The massive effort was coordinated by NASA’s Human Research Program.
Bailey has continued her NASA research and now joins more than 200 investigators from dozens of academic, government, aerospace and industry groups to publish a package of 30 scientific papers in five Cell Press journals on Nov. 25.
Meta-analysis for the association between HDL with all-cause mortality risk has identified HDL levels 55 — 60 mg/dL range as optimal. However, that data includes subjects up to 85y-in the video, I present data for 85y — 115yr olds that additionally suggests HDL in the 55 — 60 mg/dL range as optimal. In addition, I show my own HDL data over the past 15 years (n=34), the correlation for HDL with my diet, and how I plan on consistently increasing my 15-year average HDL of ~44 mg/dL to the 50’s.
