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When we think about gene editing, the first thing we remember is the designer babies, and that it’s usually called unethical. But actually, gene editing (CRISPR) may be one of the most promising upcoming medical technologies. Learn why in this video.

Check out other videos from this series:
https://www.youtube.com/playlist?list=PLnWSi4zEceYXPCBYXZ9ZEV-9q44ebksoo.

0:00 — Opening scene.
0:20 — Gene editing is promising. Here’s why.
2:35 — Also, it can transform the beauty industry.
3:49 — How does gene editing work?
4:16 — My thoughts on that.
5:16 — End credits.

Text me: [email protected].

More than a million Americans undergo knee and hip replacements each year. It’s a last resort treatment for pain and mobility issues associated with osteoarthritis, a progressive disease caused by degeneration of the protective layer of cartilage that stops our bones grinding together when we sit, stand, write, or move around.

But what if doctors could intervene and repair damaged cartilage before surgery is needed?

For the first time, researchers at the Keck School of Medicine of USC have used a stem cell-based bio-implant to repair cartilage and delay joint degeneration in a large animal model. The work will now advance into humans with support from a $6 million grant from the California Institute of Regenerative Medicine (CIRM).

Researchers say they have found a growth hormone in the colon that helps damage DNA, which aides in the aging process. The finding could lead to new therapeutic approaches to aging-associated disorders like cancer.

Whereas circulating pituitary growth hormones decline with age, non-pituitary growth hormones, or npGH, increase with age. That means the colon tissue growth hormone helps initiate the first stages of tumor development and influence the aging process, Cedars-Sinai Medical Center researchers said in research published in the journal Cell Reports.

At the core of the issue is npGH blocking a certain protein from protecting DNA from damage. The protein, p53, is a tumor suppressor that helps repair DNA, but it can also awaken growth hormones.

Aging is a highly complex process with thousands of genes influencing our health, which poses a challenge for researchers looking to explain and target the underlying processes that lead to declining health. Researchers from the Babraham Institute’s Epigenetics research program have published a map of genetic interactions in C. elegans in iScience which can be used to identify new genes that influence lifespan and that have equivalent genes in humans.

Researchers use simple model organisms like the nematode worm C. elegans to gather information that can inform studies on human aging because many are shared or have counterparts in other species. However, there are some conceptual and that apply to the study of aging in model organisms. Dr. Casanueva, Group leader in the Epigenetics research program explains: “The way researchers usually study gene function is by disrupting its function and observing what happens. The disruption of some genes causes worms to live a very long-life. In this way, researchers have found the so-called ‘longevity-pathways.” However, the complexity underlying aging means that it is not enough to focus on individual genes. We need to study the overall organization of longevity by generating a systems-wide view.”

In collaboration with the physicist Marta Sales Pardo at University of Rovira i Virgili, Dr. Casanueva and her lab set out to cast a wider net when it comes to studying longevity genes. Together they created the largest network of gene regulatory interactions that are found in a long-lived type of C. elegans. In this network, the relationships between genes are represented by lines, and represented in different layers based on the flow of information between genes. The middle of the web represents the genes with the most influence, in this case, they receive complex input signals and de-code them, and connect to an output layer of genes. The researchers found that most key genes for longevity belong to transcription factors and metabolic genes.

Part 2


In this video Dr. Lustgarten goes into more detail on what he tracks and how he does the analysis of the results. He emphasizes the importance of running your own tests, to not only look at one biomarker but to then combine that marker with other biomarkers, looking for what is optimal for you.

Dr. Michael Lustgarten is a scientist at the Tufts University Human Nutrition Research Center on Aging in Boston, Massachusetts. His research currently focuses on the role of the gut microbiome and serum metabolome on muscle mass and function in older adults.

Karlsruhe, germany and novato, CA, USA

The Forever Healthy Foundation and the Buck Institute for Research on Aging today announced a new partnership to advance early-stage discoveries at the Institute that show promise to reverse physiologic aging in humans. The focus will be on cutting-edge research aimed at the repair of age-related damage at the cellular and molecular level, a hallmark of the aging process. Forever Healthy will commit up to $1 million per year for five years to drive this innovation. The funding aims to advance early-stage research with high translational potential in order to speed up the transition from lab to product.

German entrepreneur and longevity pioneer Michael Greve founded his humanitarian Forever Healthy initiative with the mission of accelerating the development of therapies to impede the aging process and the diseases that accompany it. This mission is in perfect alignment with the Buck Institute, the first independent biomedical facility in the world focused solely on the biology of aging.

The Neuro-Network.

𝐍𝐞𝐰 ‘𝐀𝐧𝐭𝐢-𝐀𝐠𝐢𝐧𝐠’ 𝐕𝐚𝐜𝐜𝐢𝐧𝐞 𝐇𝐚𝐬 𝐈𝐧𝐜𝐫𝐞𝐚𝐬𝐞𝐝 𝐌𝐨𝐮𝐬𝐞 𝐋𝐢𝐟𝐞 𝐒𝐩𝐚𝐧𝐬. 𝐖𝐨𝐮𝐥𝐝 𝐈𝐭 𝐖𝐨𝐫𝐤 𝐢𝐧 𝐇𝐮𝐦𝐚𝐧𝐬?

𝘼𝙣 𝙚𝙭𝙥𝙚𝙧𝙞𝙢𝙚𝙣𝙩𝙖𝙡 𝙫𝙖𝙘𝙘𝙞𝙣𝙚 𝙨𝙪𝙘𝙘𝙚𝙨𝙨𝙛𝙪𝙡𝙡𝙮 𝙚𝙡𝙞𝙢𝙞𝙣𝙖𝙩𝙚𝙙 𝙖𝙜𝙞𝙣𝙜 𝙘𝙚𝙡𝙡𝙨 𝙛𝙧𝙤𝙢 𝙩𝙝𝙚 𝙗𝙤𝙙𝙞𝙚𝙨 𝙤𝙛… See more.


An experimental vaccine successfully eliminated aging cells from the bodies of mice, helping to prolong the rodents’ lives and reverse some signs of age-related disease.