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Category: life extension

10% longer.

Reduced food intake, known as dietary restriction, leads to a longer lifespan in many animals and can improve health in humans. However, the molecular mechanisms underlying the positive effects of dietary restriction are still unclear. Researchers from the Max Planck Institute for Biology of Aging have now found one possible explanation in fruit flies: they identified a protein named Sestrin that mediates the beneficial effects of dietary restriction. By increasing the amount of Sestrin in flies, researchers were able to extend their lifespan and at the same time these flies were protected against the lifespan-shortening effects of a protein-rich diet. The researchers could further show that Sestrin plays a key role in stem cells in the fly gut thereby improving the health of the fly.

The health benefits of have long been known. Recently, it has become clear that restriction of certain food components, especially proteins and their individual building blocks, the , is more important for the organism’s response to dietary restriction than general calorie reduction. On the , one particular well-known signaling pathway, named TOR pathway, is important for longevity.

“We wanted to know which factor is responsible for measuring nutrients in the cell, especially amino acids, and how this factor affects the TOR pathway,” explains Jiongming Lu, researcher in the department of Linda Partridge at the Max Planck Institute for Biology of Aging. “We focused on a protein called Sestrin, which was suggested to sense amino acids. However, no one has ever demonstrated amino acid sensing function of Sestrin in a living being.” Therefore, Lu and his colleagues focused on the role of Sestrin in the model organism Drosophila melanogaster, commonly known as fruit fly.

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Important that people read this given how much this spread.

If you have been following the mainstream media recently, you have probably seen a story about hyperbaric oxygen treatment and claims that it can reverse aging. Unfortunately, the media hype surrounding the results is nothing like the reality of the actual research paper, and this is another example of how shoddy journalism harms our field.

Welcome to the media circus

Back in July, we talked about how hyperbaric oxygen therapy may reduce age-related cognitive decline in older people, which was based on the results of another study. A new publication from the same team of Israeli scientists led by Prof. Shai Efrati has further explored these original findings, and while the results are interesting, the media hype and marketing surrounding those results is frankly ridiculous and entirely unwarranted.

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Stem cells hold so much potential for regenerative medicine, it is understandable that so many people should be so impatient to see all that potential realized. But people, the desperately ill among them, need to recognize that stem cells aren’t talismans. In unregulated clinical settings, stem cells can be worthless or even harmful. That’s the bad news. The good news is that stem cells are giving up their profound but decidedly unmagical secrets.

What stem cells lose in mystery, they gain in practicality. They are to be seen as manageable biological units that can, given the right preparation, perform myriad therapeutic applications, less as miracle workers and more as drudges that accept reprogramming and subsequently perform their assigned tasks. They may also sacrifice some of their protean identity, turning into cells that are less stemmy but more effective (and safer) as therapeutic agents. Stemminess may even by bypassed completely, as when cells of one type are directly transdifferentiated into cells of another type.

Even as the preparation of stem cell therapeutics becomes more sophisticated, it is becoming more streamlined, more industrialized. Helping to advance both trends—greater refinement, greater manufacturability—is a new generation of biotech startups. Several of these startups are described in this article. By commercializing the latest stem cell technologies, these startups mean to add to the list of FDA-approved cell-based treatments.

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The replacement of lost neurons is a holy grail for neuroscience. A new promising approach is the conversion of glial cells into new neurons. Improving the efficiency of this conversion or reprogramming after brain injury is an important step towards developing reliable regenerative medicine therapies. Researchers at Helmholtz Zentrum München and Ludwig Maximilians University Munich (LMU) have identified a hurdle towards an efficient conversion: the cell metabolism. By expressing neuron-enriched mitochondrial proteins at an early stage of the direct reprogramming process, the researchers achieved a four times higher conversion rate and simultaneously increased the speed of reprogramming.

Neurons (nerve cells) have very important functions in the brain such as information processing. Many brain diseases, injuries and neurodegenerative processes, are characterized by the loss of neurons that are not replaced. Approaches in regenerative medicine therefore aim to reconstitute the neurons by transplantation, stem cell differentiation or direct conversion of endogenous non-neuronal cell types into functional neurons.

Researchers at Helmholtz Zentrum München and LMU are pioneering the field of direct conversion of glial cells into neurons which they have originally discovered. Glia are the most abundant cell type in the brain and can proliferate upon injury. Currently, researchers are able to convert glia cells into neurons — but during the process many cells die. This means that only few glial cells convert into functional nerve cells, making the process inefficient.

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In the third episode of the Healthy Longevity webinar series, we hear from Dr Aubrey de Grey, Chief Science Officer of the SENS Research Foundation as he joins Prof Brian Kennedy for a science-backed and inspirational conversation on regenerative medicine and the implications of a population that lives longer and in good health.

Register for upcoming webinar episodes here: https://bit.ly/3jhe0SB.

#NUSMedicine #webinarseries

Disclaimer: The opinions and advice expressed in this webinar are those of the speakers and do not represent the views and opinions of the organizers and National University of Singapore or any of its subsidiaries or affiliates. The information provided in this webinar is for general information purposes only as part of a general discussion on public health. The information is not intended to be a substitute for professional medical advice, diagnoses or treatment; and cannot be relied on in place of consultation with your licensed healthcare provider.

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All of the proceedings of this webinar, including the presentation of scientific papers, are intended for limited publication only, and all property rights in the material presented, including common-law copyright, are expressly reserved to the speaker or NUS. No statement or presentation made is to be regarded as dedicated to the public domain. Any sound reproduction, transcript or other use of the material presented at this course without the permission of the speaker or NUS is prohibited to the full extent of common-law copyright in such material.

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A landmark study shows this age-old tech is the key.

The cure for aging has long been the Holy Grail of medicine. Emerging technologies, like the gene editing tool CRISPR, have opened the floodgates to what may be possible for the future of medical science. The key to slowing down aging, however, may lie in a simple and age-old technique.

Dive deeper. ➡ Read best-in-class health, tech, and science features, and get unlimited access to Pop Mech.

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Senescence in cancer cells

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Sometimes, too much of a good thing can turn out to be bad. This is certainly the case for the excessive cell growth found in cancer. But when cancers try to grow too fast, this excessive speed can cause a type of cellular aging that actually results in arrested growth. Scientists at Duke-NUS Medical School have now discovered that a well-known signaling pathway helps cancers grow by blocking the pro-growth signals from a second major cancer pathway.

Inhibiting Wnt signaling with ETC-159 reactivates the hyperactive RAS-MAPK , causing cells to led undergo senescence. Many cancers are driven by activating mutations in the RAS-MAPK signaling pathway which triggers a cascade of proteins that directs cells to grow, divide and migrate. Mutations in proteins involved in this cascade can turn on genes that make this process go into overdrive, causing cells to grow out of control and aggressively invade other parts of the body. However, too much RAS-MAPK signaling causes cancer cells to prematurely age, and eventually stop growing—a process called cellular senescence.

Publishing in Cancer Research, the Duke-NUS research team found that another important and well-known biochemical pathway, the Wnt (pronounced “wint”) signaling pathway, allows some cancers to grow by dampening RAS-MAPK signaling.

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This may be good news for those who have damaged joints due to sports or old age.

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Human knees are notoriously vulnerable to injury or wearing out with age, often culminating in the need for surgery. Now researchers have created new hybrid bioinks that can be used to 3D print structures to replace damaged cartilage in the knee.

The meniscus is the rubbery cartilage that forms a C-shaped cushion in your knee, preventing the bones of your upper and lower leg from rubbing against each other. This stuff is susceptible to damage from sports injuries, but can also wear out with age – and if it gets particularly bad, sometimes the only thing left to do is surgically remove some of the damaged meniscus.

For the new proof-of-concept study, researchers at the Wake Forest Institute for Regenerative Medicine (WFIRM) demonstrated a new method for 3D bioprinting that creates both the cartilage and the supporting structures. The team used the Integrated Tissue and Organ Printing System (ITOPS), which has been used in past studies to print complex tissues such as bones, muscles and even ears.

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