“We are going backwards in time,” Prof. Shai Efrati said.
Category: life extension – Page 370
Can damage repair give us indefinite youth? | Dr Aubrey de Grey
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.
All Rights Reserved.
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.
It Sure Looks Like Humans Have Found a Way to Reverse Aging
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.
Getting it just right: The Goldilocks model of cancer
Senescence in cancer cells
~~~
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 pathway, 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.
Hybrid 3D-printing bioinks help repair damaged knee cartilage
This may be good news for those who have damaged joints due to sports or old age.
😃
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.
Near-infrared probe decodes telomere dynamics
A new synthetic probe offers a safe and straightforward approach for visualizing chromosome tips in living cells. The probe was designed by scientists at the Institute for Integrated Cell-Material Science (iCeMS) and colleagues at Kyoto University, and could advance research into aging and a wide range of diseases, including cancers. The details were published in the Journal of the American Chemical Society.
“Chromosome ends are constantly at risk of degradation and fusion, so they are protected by structures called telomeres, which are made of long repeating DNA sequences and bound proteins,” says iCeMS chemical biologist Hiroshi Sugiyama, who led the study. “If telomeres malfunction, they are unable to maintain chromosome stability, which can lead to diseases such as cancer. Also, telomeres normally shorten with each cell division until they reach their limit, causing cell death.”
Visualizing telomeres, especially their physical arrangements in real-time, is important for understanding their relevance to disease and aging. Several visualization approaches already exist, but they have disadvantages. For example, some can only observe telomeres in preserved, or fixed, cells. Others are time-consuming or involve harsh treatments that denature DNA.
Hyperbaric Oxygen Therapy: First Human Study Shows Reversal in Biology of Aging
TEL AVIV — November 18, 2020: In a scientifically verified approach, signalling an important breakthrough in the study of aging, Tel Aviv University and The Sagol Center for Hyperbaric Medicine and Research at Shamir Medical Center announced today that, for the first time in humans, two key biological hallmarks of aging, telomere length shortening, and accumulation of senescent cells, can be reversed. The prospective clinical trial, published in peer-reviewed Journal Aging, utilizes Hyperbaric Oxygen Therapy protocols to demonstrate cellular level improvement in healthy aging adults.
For the first-time a human study shows the reversal in the biology of aging including telomere shortening with Hyperbaric Oxygen Therapy.
Human ageing process biologically reversed in world first
Fantastic news for a change!
The ageing process has been biologically reversed for the first time by giving humans oxygen therapy in a pressurised chamber.
Scientists in Israel showed they could turn back the clock in two key areas of the body believed to be responsible for the frailty and ill-health that comes with growing older.
As people age, the protective caps at the ends of chromosomes – called telomeres – shorten, causing DNA to become damaged and cells to stop replicating. At the same time, “zombie” senescent cells build up in the body, preventing regeneration.
Chronic inflammation causes a reduction in NAD+
NAD+ (nicotinamide adenine dinucleotide), a key metabolite central to an efficient and healthy metabolism, declines with age. This previously unexplained phenomena is associated with numerous age-related diseases and has spawned the development of many nutritional supplements aimed at restoring NAD+ to more youthful levels. Publishing in Nature Metabolism, researchers at the Buck Institute have identified chronic inflammation as a driver of NAD+ decline. They show that an increasing burden of senescent cells, which is also implicated in the aging process, causes the degradation of NAD via the activation of CD38 (cyclic ADP ribose hydrolase) a protein that is found on the cell membranes both inside and on the surface of many immune cells.
“We are very excited to link two phenomena which have been separately associated with aging and age-related disease,” said Eric Verdin, MD, Buck Institute President and CEO and senior author of the paper. “The fact that NAD+ decline and chronic inflammation are intertwined provides a more holistic, systemic approach to aging and the discovery of CD38 macrophages as the mediator of the link between the two gives us a new target for therapeutic interventions.”