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Life Extension – Lifeboat News: The Blog – Page 154
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Category: life extension – Page 154

A team of researchers affiliated with multiple institutions in Canada has found that obesity in young mice can lead to inflammatory disease later in life even if the mouse is no longer overweight. In their paper published in the journal Science, the group describes studying early life obesity in test mice and the development of age-related macular degeneration. Kevin Mangum and Katherine Gallagher with the University of Michigan have published a Perspectives piece in the same journal issue outlining the research.

Age-related (AMD) in older people can lead to permanent blindness. Prior research has shown obesity plays a major role in its development. Other research has also shown that AMD is a neuroinflammatory condition. It is believed that the inflammation in the eyes is related to obesity, but the exact connection has not been identified. In this new effort, the researchers sought to find the connection by studying obesity and macular degeneration in mice.

The work involved feeding a and studying the impact on adipose tissue macrophages (types of white blood cells that are part of the immune system). They found that obesity in mice led to epigenetic changes in the macrophages that resulted in an increase in expression of genes that incite an inflammatory response. They also found that the increased expression continued even after the test mice were put on a reduced diet that allowed them to return to their normal weight.

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The transport of mercury ions across intestinal epithelial cells can be studied for toxicology assessments by using animal models and static cell cultures. However, the concepts do not reliably replicate conditions of the human gut microenvironment to monitor in situ cell physiology. As a result, the mechanism of mercury transport in the human intestine is still unknown.

In a new report now published in Nature Microsystems and Nanoengineering, Li Wang and a research team in and in China developed a gut-on-a-chip instrument integrated with transepithelial electrical resistance (TEER) sensors and electrochemical sensors.

They proposed to explore the dynamic concept to simulate the physical intestinal barrier and mirror biological transport and adsorption mechanisms of mercury ions. The scientists recreated the cellular microenvironment by applying fluid shear stress and cyclic mechanical strain.

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Great advice here. I follow much of it; my diet is good though there is a little bit of processed stuff in it. I do not drink or smoke. Interesting that Dr Stanfield has a rapamycin human trial going.

We have the tools available today to have a healthy 105-year lifespan, and I’ll summarise it all in this video. Plus at the end we’ll go through the emerging therapies in the longevity space that will push us towards a healthy 120-year lifespan.

My full supplement stack: https://drstanfield.com/my-supplements/

Continue reading “How To Have A HEALTHY 105-Year Lifespan (Soon 120-Years)” | >

Powered by data produced by its AI-driven discovery platform, clinical-stage biotech BioAge Labs is rapidly developing a pipeline of therapies to extend healthy lifespan by targeting the molecular causes of aging. Having raised more than $120 million in funding, and with multiple clinical trials already under its belt, the company is focused on building a broad pipeline of potential longevity therapies in three main areas: muscle, immune, and brain aging.

Longevity. Technology: There are few companies in the longevity biotech field that appear to be executing on their vision as quickly and consistently as BioAge. When the company wowed the sector with a $90 million funding round in 2020, talk of multiple imminent clinical trials may have sounded optimistic to some, but BioAge has delivered on its promise time and again. Beyond the trials already underway, the company’s much-vaunted AI discovery platform also appears to be churning out the data, this year spawning a new programme exploring the potential of NLRP3 inhibitors in brain aging. To learn more, we caught up with BioAge co-founder and CEO Kristen Fortney.

Looking back at 2022, Fortney says it has been “immensely gratifying” to see so many new companies and investors coming into the longevity field.

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In this #webinar, Dr Vincenzo Sorrentino from the Department of Biochemistry and Healthy Longevity Translational Research Programme at the Yong Loo Lin School of Medicine, shared about his research on the relationship between metabolism, nutrition and proteostasis and their impact on health and ageing, and engaged in discussion about the role of mitochondrial proteostasis in ageing and related diseases.

Register for upcoming #HealthyLongevity #webinar sessions at https://nus-sg.zoom.us/webinar/register/7916395807744/WN__sypkX6ZSomc7cGAkK3LbA

#NUSMedicine #webinarseries.

References:

Continue reading “Targeting the mitochondria-proteostasis connection in ageing and disease | Dr Vincenzo Sorrentino” | >

Aging appears to progress similarly across species, from worms and flies to mice and humans, and involves pathways related to early development. Guest Linda Partridge talks with Gordon while visiting the Buck Institute to discuss the evolutionary trade offs of aging mechanisms, the role of nutrient-sensing pathways, and how we might get the most benefit from preventative interventions in midlife.

Linda Partridge, born in 1950 in Bath, England, studied and graduated in biology at the University of Oxford. After three years of postdoctoral research at the University of York, she was Demonstrator, Lecturer, Reader and finally Professor at the University of Edinburgh. After many years in Scotland, in 1994 she became Professor of Biometry, University College London. She is both a founding director of the new Max Planck Institute for Biology of Ageing in Cologne and Director of the UCL Institute of Healthy Ageing. Linda Partridge’s research is directed to understanding both how the rate of aging evolves in nature and the mechanisms by which healthy lifespan can be extended in laboratory model organisms. Her work has focussed in particular on the role of nutrient-sensing pathways, such as the insulin/insulin-like growth factor signaling pathway, and on dietary restriction.

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Interesting interview about the future of Ageing with leading expert with Aubrey De Grey.

This week we interview the phenomenal Aubrey De Grey, the world’s foremost authority on longevity and developing strategies to slow or eliminate aging altogether. The author of The Mitochondrial Free Radical Theory of Aging (1999) and Ending Aging (2007), De Grey is probably best known for the concept of Longevity Escape Velocity, a view that soon medical technology will enable human beings to prevent age-related deterioration, and eventually eliminated aging entirely.

The future of Ageing with Aubrey De Grey.

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Our DNA is made up of genes that vary drastically in size. In humans, genes can be as short as a few hundred molecules known as bases or as long as two million bases. These genes carry instructions for constructing proteins and other information crucial to keeping the body running. Now a new study suggests that longer genes become less active than shorter genes as we grow older. And understanding this phenomenon could reveal new ways of countering the aging process.

Luís Amaral, a professor of chemical and biological engineering at Northwestern University, says he and his colleagues did not initially set out to examine gene length. Some of Amaral’s collaborators at Northwestern had been trying to pinpoint alterations in gene expression—the process through which the information in a piece of DNA is used to form a functional product, such as a protein or piece of genetic material called RNA—as mice aged. But they were struggling to identify consistent changes. “It seemed like almost everything was random,” Amaral says.

Then, at the suggestion of Thomas Stoeger, a postdoctoral scholar In Amaral’s lab, the team decided to consider shifts in gene length. Prior studies had hinted that there might be such a large-scale change in gene activity with age—showing, for example, that the amount of RNA declines over time and that disruptions to transcription (the process through which RNA copies, or transcripts, are formed from DNA templates) can have a greater impact on longer genes than shorter ones.

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