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Category: life extension – Page 344

Scientists Discover Small Proteins Regulate the Aging Process

The attachment of the small protein ubiquitin to other proteins (ubiquitination) regulates numerous biological processes, including signal transduction and metabolism / Scientists at the University of Cologne discover the link to aging and longevity.

Scientists have discovered that the protein ubiquitin plays an important role in the regulation of the aging process. Ubiquitin was previously known to control numerous processes, such as signal transduction and metabolism. Prof. Dr. David Vilchez and his colleagues at the CECAD Cluster of Excellence for Aging Research at the University of Cologne performed a comprehensive quantitative analysis of ubiquitin signatures during aging in the model organism Caenorhabditis elegans, a nematode worm which is broadly used for aging research.

This method — called ubiquitin proteomics — measures all changes in ubiquitination of proteins in the cell. The resulting data provide site-specific information and define quantitative changes in ubiquitin changes across all proteins in a cell during aging. A comparison with the total protein content of a cell (proteome) showed which changes have functional consequences in protein turnover and actual protein content during aging. The scientists thus discovered new regulators of lifespan and provide a comprehensive data set that helps to understand aging and longevity. The article, ‘Rewiring of the ubiquitinated proteome determines aging in C. elegans,‘has now been published in Nature.

Northwestern scientists discover remarkable longevity in a subset of mitochondrial proteins

Northwestern Medicine investigators have discovered that a subset of proteins in mitochondria of brain and heart cells are long-lived, supporting the long-term stability of mitochondrial complex architecture.

The study, published in the Journal of Cell Biology, was led by Jeffrey Savas, PhD, assistant professor in the Ken & Ruth Davee Department of Neurology’s Division of Behavioral Neurology, of Medicine the in Division of Nephrology and Hypertension, and of Pharmacology.

Previous work led by Savas discovered that nuclear pore complex proteins in post-mitotic neurons are exceptionally long-lived and persist for months in mouse and rat brains. These proteins, termed long-lived proteins, or LLPs, provide long-term stability and structure to the nuclear pore and subsequently to the nuclear envelope of neurons; however, this concept had never been considered for other intracellular organelles, until now.

Researchers reveal new insights on mechanism that could help treat muscle-related diseases

Investigators who previously developed a recipe for turning skin cells into primitive muscle-like cells that can be maintained indefinitely in the lab without losing the potential to become mature muscle have now uncovered how this recipe works and what molecular changes it triggers within cells. The research, which was led by scientists at Massachusetts General Hospital (MGH) and is published in Genes & Development, could allow clinicians to generate patient-matched muscle cells to help treat muscle injuries, aging-related muscle degeneration, or conditions such as muscular dystrophy.

It’s known that expression of a regulatory gene called MyoD is sufficient to directly convert into mature ; however, mature muscle do not divide and self-renew, and therefore they cannot be propagated for clinical purposes. “To address this shortcoming, we developed a system several years ago to convert skin cells into self-renewing muscle stem-like cells we coined induced myogenic progenitor cells, or iMPCs. Our system uses MyoD in combination with three chemicals we previously identified as facilitators of cell plasticity in other contexts,” explains senior author Konrad Hochedlinger, Ph.D., a principal investigator at the Center for Regenerative Medicine at MGH and a professor of medicine at Harvard Medical School.

In this latest study, Hochedlinger and his colleagues uncovered the details behind how this combination converts skin cells into iMPCs. They found that while MyoD expression alone causes skin cells to take on the identity of mature muscle cells, adding the three chemicals causes the skin cells to instead acquire a more primitive stem cell–like state. Importantly, iMPCs are molecularly highly similar to muscle tissue stem cells, and muscle cells derived from iMPCs are more stable and mature than muscle cells produced with MyoD expression alone.

Maya Abi Chahine, Program Manager, University for Seniors, American University of Beirut

“University Of The 3rd Age” — Seniors Staying Intellectually Challenged, Socially Engaged, And Physically And Mentally Healthy — Maya Abi Chahine, University for Seniors, American University of Beirut (AUB)

AUB (https://www.aub.edu.lb/seniors/Pages/default.aspx).

The University for Seniors is a new life-long learning initiative at AUB, the first of its kind in Lebanon and the Middle East. It gives older adults (who are 50 and above) the opportunity to share their wisdom and passion, to learn things they have always wanted to learn in a friendly academic environment and to interact socially with other seniors, AUB faculty and students.

Ms. Abi Chahine holds an MA in Public Policy & Ageing from King’s College London and is a passionate advocate and researcher in health, well being issues and third age learning. Her portfolio includes collaborations with UN agencies, including WHO, United Nations Population Fund, and International Labour Organization, as well as INGOs such as HelpAge International and universities in the UK.

Ms. Abi Chahine has 21 years of experience in setting-up and managing programs in the fields of public health, gerontology and education, notably universities. Throughout her multifaceted career, she developed skills in establishing and restructuring programs, by spearheading strategies, setting institutionalization mechanisms and driving daily operations that ensured customers and collaborators’ satisfaction and expansion.

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Beware the ‘molecular parasites’ involved in aging and disease

If you’ve ever seen a petunia with artfully variegated petals, then you’ve seen transposons at work. The flower’s showy color patterns are due to transposable elements, or DNA sequences that can move locations within a genome. Yet when it comes to transposons’ effects on humans, the results might not be as lovely or desirable.

As researchers learn more about these so-called mobile genetic elements, they’ve found increasing evidence that transposons influence and even promote aging and like cancer as well as neurogenerative and autoimmune disorders, says John Sedivy, a professor of biology and director of the Center on the Biology of Aging at Brown. Sedivy is the corresponding author of a new review article in Nature that discusses the latest thinking and research around transposons.

“Let’s put it this way: These things can be pretty dangerous,” said Sedivy. “If they are uncontrolled, and there are many examples of that, transposons can have profound consequences on most forms of life that we know of.”

E5 On Dogs Project: Validating The 54% Reduction In Epigenetic Age | Dr Greg Fahy Episode 8

The Conboys are looking at human trials soon but not with E5. it will be interesting to see how their trial compares to this E5 dog trial.

In this video Dr. Fahy shares his opinion on some of the up and coming anti-aging therapies, including NAD boosters, Hyperbaric Oxygen Chambers and senolytics.

Intervene Immune website:

Intro page


Contact to join the trial or invest.

Contact Us

Dr. Greg Fahy is a world renowned cryobiologist and is also the chief science officer, and co-founder, of Intervene Immune, a company which pioneers treatments for thymus regeneration and age-related immune system decline. Dr. Fahy Designed and led the pilot TRIIM trial which first time showing both thymus rejuvenation and reversal of human epigenetic age. He is now running the follow up phase II trial TRIIM-X with the aim of confirming and extending the results.

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Gene therapy uses SIRT6 variant found in centenarians

“So many genes are involved in DNA maintenance, FOXO3 for example, which is very interesting, but it cannot be a therapeutic target because it will trigger a lot of other things,” he explains. “SIRT6 is coding for only one protein and, because it’s a small protein, the cargo size is not too big and it can be easily delivered into cells, so it’s possible to use it as a gene therapy target.”

Some of the other factors that play in Genflow’s favour, says Leire, are that the world has reached a better understanding of the biology of aging, but also that gene therapy has also progressed well over the years.

CRISPR Development Makes Stem Cells “Invisible” to Immune System Without Immunosuppressants

Quick vid and a reminder of the 4th conference of Lifespan.io is this weekend.

Gene editing can make stem cells invisible to the immune system, making it possible to carry out cell therapy transplants without suppressing the patients’ immune response. Scientists in the US and Germany used immune engineering to develop universal cell products that could be used in all transplant patients. The idea is to create stem cells that evade the immune system; these hypoimmune stem cells are then used to generate cells of the desired type that can be transplanted into any patient without the need for immunosuppression, since the cells won’t elicit an immune response. They used CRISPR-Cas9 to knock out two genes involved in the major histocompatibility complex, which is used for self/non-self discrimination. They also increased the expression of a protein that acts as a “don’t eat me” signal to protect cells from macrophages. Together, these changes made the stem cells look less foreign and avoid clearance by macrophages. The team then differentiated endothelial cells and cardiomyocytes from the engineered stem cells, and they used these to treat three different diseases in mice. Cell therapy treatments using the hypoimmune cells were effective in rescuing hindlimbs from vascular blockage, preventing lung damage in an engineered mouse model, and maintaining heart function following a myocardial infarction. Immunosuppression poses obvious risks to a patient, and generating custom cells for transplant therapy is often prohibitively expensive. The development of universal donor cells that can be used as therapeutics could bring the cost down significantly, making cellular therapeutics available to many more patients in a much safer way.

SOURCES AND FURTHER READING
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Engineering Cells to Avoid Immune Detection in Transplants: https://www.lifespan.io/news/engineering-cells-to-avoid-immu…ansplants/

“Hypoimmune induced pluripotent stem cell–derived cell therapeutics treat cardiovascular and pulmonary diseases in immunocompetent allogeneic mice” paper: https://www.pnas.org/content/118/28/e2022091118

LSN episode on Intellia Therapeutics’ clinical trial of NTLA-2001 — https://youtu.be/WKOPTfGqMPA

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