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This study explores age-related gene expression changes in mouse sweat glands, shedding light on aging processes.

"Groundbreaking deep proteomic method reveals new insights into human skeletal muscle aging - a must-read in Aging-US!"

💘 'Promo sm'

I have a tnfrsf13b deficiency....variant....homozygous.....taci deficiency....what would that mean for glycosylation?

"Exploring the role of FoxO6 in hepatic steatosis sheds light on aging-related conditions. Fascinating insights from Aging-US."

"Dive into the latest research on combating cellular aging with PR55α and Protein Phosphatase 2A in Aging-US."

"Slow Aging" continued progress. Avi/Healthy Chef A Fx VA : What happens to "Natural Killer Cells" for Senior Citizens among us (Age Group : 65+) ??

Mayb the problem is with D. Cancer patients are known to undergo more rapid aging, which I think is partly ascribed to the chemo drugs. Has Q been done on it's own or in combo with F.?

But maybe the shortened telomeres are a result of the lack of CLPP rather than the other way around. Or maybe i misread this.

Please make this happen soon and make it available to every hospital in the world so we can all be immortal and happy for the rest of eternity.

⚡️🙏

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david sinclair is my favorite i am one of his biggest fans will you please keep me updated on david sinclair's eternal youth chemicals because i want the pill when it is ready and safe hope it comes soon looks very promising but i need proof it works in humans

Pleas bring this medication soon

What about when they switch to ketones for fuel.

My life is entirely dedicated for every life specific for human life, love you all❤

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But then what about aging-related phenomena such as thymic atrophy starting at puberty, or osteoporosis, being highly influenced by hormones, diet, lifestyle, etc.? The np theory is very interesting but it's too reductive, in my opinion.

Will testosterone pellets affect glycan age and if so .. younger or older ?

Dr. Blagosklonny is a true Scientist and a pioneer anti-aging!

Skąd wpadliś cię na te składniki ? To wygląda na kampanię reklamową wybranych sumlementów diety. A gdzie można zobaczyć tych odmłodzonych myszy ? Forskalina jako panaceja plus kwasek walerianowy. Nie wierzę. Choćby podali zdjęcza komórek, jesli ich trudno nagrać. No i sama koncepcja " informacyjnej teorii starzenia" brzmi niesolidnie. Uważam, że to zwykła ukryta reklama suplimentów diety. Inaczej dowody byłyby udokumentowane . Nauka bez dowodów- to nie nauka, a tylko religia.

What is the mechanism? How does it work?

Great interview

Love it 🔥

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Promo SM

We need to donate blood, if we can😊

How then does long term use of hormonal birth control affect glycon aging? Do women who have been on birth control for many years enter menopause sooner or later than women who do not use hormonal birth control?

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Links to paper would be great.

It's very hard to understand. Please add subtitles.

How does NMN work with Fisetin and other senescent cells?

Super excited to see my hard work translated into this visual video. I am the proud first author of this research article

Thank you

Just so everyone knows. He doesbt respond to phone calls, doesnt answer my emails and based on the redaction watch interview, the Elesevier attorneys advised him to not address or acknowlege the reasons his study should be jerked!!!!! Anyone else would have been fined and unpublished. With a moratorium of a year, i guess you can modify the rules and get an unethical approval. Janice Carmiencke

ty

Continuing to follow - Love your research and break throughs on cell science .

I heard rapamayacin and acarbose at 50 mg extends life 20 percent in males

Thinking about using grim age to file for social security.

Thank you, 🤓

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This video was great. Packed to the brim with good information and yet easy to understand

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Excellent discussion!

Have you looked at homocysteine potentially being a common factor in the majority of the severe effects of SARS-COV-2? As it was erroneously dismissed in 2005 as being merely a marker of chronic diseases such as athrosclerosis and CVD rather than a major causative agent it became almost medical dogma to ignore it. Research in the past 15 years however has firmly established elevated blood homocysteine as a cause for every single pre-existing condition you mention that makes one more likely to suffer severe effects or death from covid. While their is a paucity of research on Hyperhomocysteinemia it is worth doing a quick pubmed search on 'homocysteine AND covid' and 'hyperhomocysteinemia AND covid'. Covid infection has been shown to raise blood homocysteine levels as it depletes the body of methyl donors, and other research had shown a linear relationship between rising homocysteine levels and severity of infection. Also the higher your blood homocysteine post-covid the more likely you are to develop Long-COVID. Although my science degree was in environmental management I have basically been forced to research homocysteine fairly thoroughly as I suffer from a rare condition called Hyperhomocysteinemia Accelerated Atherosclerosis. Unfortunately I'm also ApoE3/4 and around 2015, in my mid-50s, I believe my genetically high homocysteine switched off the functionality of my ApoE3 rendering me equivalent to ApoE4/4. I'm fortunate to have made it into my 60s as have some signs of classic Homocystinuria such as pectus excavatum, severe childhood myopia, and developing osteoarthritis and osteoporosis in my mid-30s but also symptoms of later onset Hyperhomocysteinemia such as arthrosclerotic and now possibly early-onset dementia. It's probably only due to the one-meal-a-day low calorie mainly lacto-ovo-vegetarian diet I've been on since 1990 that I'm still here. While longevity would be nice after requiring three heart operations and a femoral artery stent since July 2020 due to the extensive homocysteine-driven damage done to my endothelial layer I'd be happy just slowing it down to normal atherosclerosis speed. This fairly recent research from 2019 gives a clear outline of the current proposed pathways through which elevated blood homocysteine causes damage to the endothelial layer, as well as increasing thrombosis risk. Homocysteine both disrupts methylation and increases acetylation and basically speeds up the aging process. Some of the effects, like the increase in NF-kB, are countered by both intermittent fasting and metformin. Note: as metformin suppresses absorption of B12 it can lead to raised blood homocysteine levels, which could be why 65% of diabetics actually die of heart disease. Hyperhomocysteinemia disrupts glucose processing and increases both AGE and ROS, and I would have thought the 'longevity community' as well as covid researchers would have a much greater interest in homocysteine than they currently seem to. Having a simple blood homocysteine test and then ensuring its around 5 to 10 umol/L would be the most beneficial preventative measure one could take to avoid the majority of 'age related disease'. Unfortunately I learnt too late from direct experience that once it has initiated these diseases then lowering blood homocysteine does nothing as by then it has caused potentially irreversible epigenetic and metabolic changes. The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art www.ncbi.nlm.nih.gov/pmc/articles/PMC6412520/

Click here for the transcript of this video interview: aging-us.net/2022/06/15/interview-mtor-driven-aging-and-rapamycin/

Please add subtitles.

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