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Though mitochondrial dysfunction is a known marker of aging and neurodegenerative diseases, the exact mechanism behind it remains unknown. Our study suggests that the decay of SIRT6 levels during aging [18] and in Alzheimer’s disease [18, 23, 46] could be a key mechanism causing the deterioration of mitochondrial functions. The changes induced by the SIRT6 knockout that we observe at the metabolite level support this claim: metabolites related to mitochondrial energy system pathways (in particular, OXPHOS and TCA cycle) are significantly overrepresented among differentially abundant metabolites. In line with the discussed mitochondrial dysfunction in aging, all these metabolites are downregulated in the SIRT6-KO samples. Importantly, the dramatic decline of one of them, NAD+, was also associated with pro-senescence mechanisms in various species [47, 48], as well as with limited neuroprotective activity of sirtuins [49].

Accordingly, the vast majority of differentially expressed mitochondria-related genes were downregulated in our gene expression analysis. As they were strongly enriched with mitochondrial respiratory chain complexes, we measured the mitochondrial membrane potential and mitochondrial content in SIRT6-KO cells because reduced gene expression might indicate the loss of mitochondria. Both measured characteristics were significantly decreased, validating the suggested impairment of mitochondrial oxidative phosphorylation and mitochondrial biogenesis in SIRT6-deficient brains. Interestingly, the average decrease of mtDNA gene expression (~19.7%) in SIRT6-KO was in good agreement with the corresponding reduction of mitochondrial content (21.8%), suggesting impaired mitochondrial biogenesis as a primary cause of the observed transcriptional dysregulation in mitochondria upon SIRT6 knockout.

Concordantly, the impaired membrane potential upon SIRT6-KO can be partially rescued by restoring SIRT3 and SIRT4 levels, which were significantly downregulated in SIRT6-deficient brains. Both of them are localized in mitochondria and impact mitochondrial pathways related to redox homeostasis and cellular metabolism [38] and have important roles in mitochondria metabolism ROS balance and lifespan [50,51,52]. The analysis of our and publicly available gene expression data [39] confirms that SIRT6 transcriptionally regulates SIRT3 and SIRT4. Our analysis further indicates that SIRT6 regulates mitochondrial gene expression through the transcription factor YY1. We have previously shown that SIRT6 and YY1 form a complex that regulates many shared target genes [24]. Our analysis of YY1 ChIP-seq data [53] suggests that SIRT6 and YY1 regulate mitochondrial processes coordinately.

Potentially huge. Effecting blood plasma via a pill. This is of course a mice experiment and they are working to see if the process happens in humans too.


Some wealthy elites prefer young blood plasma transfusions for anti-aging purposes. There are suggestions that the body’s organs are rejuvenated by young blood. However, a recent study from Columbia University in New York suggests that anti-inflammatory drugs can rejuvenate the body and possibly extend the human lifespan by decades, negating the need for blood transfusions to turn back the body’s clock.

According to Emmanuelle Passegué, Ph.D., director of the Columbia Stem Cell Initiative, who has been researching how blood changes with age, “an aging blood system, because it’s a vector for a lot of proteins, cytokines, and cells, has a lot of bad consequences for the organism,”

The Methuselah Foundation is a non-profit medical charity focused on extending the healthy human lifespan by making 90 the new 50 by 2030. Our goal is to accelerate results in the longevity field, as well as the biotechnology, regenerative medicine, life sciences sectors. We incubate and sponsor mission-relevant ventures, fund research, and support projects and prizes.

The Methuselah Foundation is a non-profit medical charity focused on extending the healthy human lifespan by making 90 the new 50 by 2030. Our goal is to accelerate results in the longevity field, as well as the biotechnology, regenerative medicine, life sciences sectors. We incubate and sponsor mission-relevant ventures, fund research, and support projects and prizes.

University of Chicago scientists have discovered a new wrinkle in our understanding of how our genes work. The team, led by Chuan He, the UChicago John T. Wilson Distinguished Service Professor of Chemistry, Biochemistry and Molecular Biology, shed light on a longstanding puzzle involved in a common way our genes are modified that is known as RNA methylation.

Published Jan. 27 in Science, the finding could have implications for for disease, as well as our picture of gene expression, development, and evolution.

For more than a decade, Chuan He’s laboratory has been focused on trying to unravel the puzzle of a phenomenon called RNA methylation, which we are increasingly understanding plays a key role in our bodies and lives—everything from cancer to PTSD to aging.

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This is an in-depth interview with scientist, author and expert on longevity science, Dr Andrew Steele. We discuss what ageing even is, whether it should be regarded as a disease, how we differ from other animals, where the research is, what treatments look promising, health and economic policy, and what the future looks like.

So please for Tech news and views from the perspective of building a humane and sustainable economic system, check them all out!
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Episode 24 discusses:
Ben Zion and Dr. Hale discuss the two most exceptional 21st century projects (beyond those to do with building a humane and sustainable economic system, which should have rightly been achieved in the 20th century) namely Universal Superlongevity and Human-Centered-Artificial-Superintelligence, and the noble work of Ageless Partners in the life extension arena.(continued in ep. 25)

Prof. Ian Hale, the autism author and broadcaster, is a member of the World Academy of Medical Science and Director of Research for Ageless Partners’ radical new rejuvenation project.

He’s an associate of both the Moscow Institute of Science & Technology & the Russian Academy of Science.

I have started uploading them primarily to YouTube, this is a sneak preview, and it will be uploaded there next week–
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These are the molecular machines inside your body that make cell division possible. Animation by Drew Berry at the Walter and Eliza Hall Institute of Medical Research. http://wehi.tv.

Special thanks to Patreon supporters:
Joshua Abenir, Tony Fadell, Donal Botkin, Jeff Straathof, Zach Mueller, Ron Neal, Nathan Hansen.

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Every day in an adult human roughly 50–70 billion of your cells die. They may be damaged, stressed, or just plain old — this is normal, in fact it’s called programmed cell death.

To make up for that loss, right now, inside your body, billions of cells are dividing, creating new cells.

And cell division, also called mitosis, requires an army of tiny molecular machines. DNA is a good place to start — the double helix molecule that we always talk about.