Longevity InTime: Autonomous AI Institute. Anti-Aging Digital Health Immortality Transhumanist AI Channel
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Evolution of funeral industry for the rich: 4,500 - 5,000 years ago
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The hidden cost of aging: Why we need to take action now

Every day, billions are spent on healthcare, but only a fraction goes toward preventing the biggest health risk of all—aging itself. What if we told you that slowing down aging could prevent diseases like cancer, Alzheimer’s, and heart disease before they even start?

Scientists have already discovered ways to slow aging in animals, extending their lifespan by 30-50%. Some of these methods are now being tested in humans. But the biggest challenge? Almost no one is paying attention.

Imagine adding 10, 20, or even 30 years of healthy life—not just living longer, but living better. Yet, most people accept aging as inevitable when science is proving otherwise.

It’s time to change the conversation. Longevity isn’t just about adding years—it’s about making those years count. Are you ready to rethink aging?

Follow this channel for the latest updates on longevity, anti-aging breakthroughs, and how you can take control of your future health.
The review article describes a hypothesis according to which the drivers of epigenetic regulation in memory formation are mobile genetic elements that affect the expression of specific genes in the brain. In support of this hypothesis, the results of scientific studies on the regular activation of transposons in neuronal stem cells during neuronal differentiation are presented. These processes occur in the neurogenesis zone - the dentate gyrus of the hippocampus, where the greatest activity of mobile genetic elements and their insertions into loci near the genes expressed by neurons with their activation are determined. In experiments on changing the activity of histone acetyltransferase, inhibition of DNA methyltransferase and reverse transcriptase, the involvement of epigenetic factors and retroelements in the mechanisms of memory formation was shown. At the same time, a number of studies on different animals demonstrated the preservation of long-term memory without the participation of synaptic plasticity. The obtained data allow us to assume that transposons, which are highly sensitive genome sensors to various environmental and internal influences, form memory at the level of nuclear coding. This is reflected in the change in synaptic plasticity, which can explain the preservation of long-term memory after the elimination of synaptic connections in animals. This is confirmed by the facts of the origin of proteins directly involved in the formation of memory, including the transfer of genetic information through synapses between neurons (Arc protein), from mobile genetic elements. Transposons are sources of long non-coding RNA and microRNA, the role of which in memory consolidation has been described. Pathological activation of mobile genetic elements is a probable cause of neurodegenerative diseases with memory impairment. An analysis of the scientific literature allowed us to find data on changes in the expression of 40 microRNAs originating from transposons in Alzheimer's disease. For 24 of these microRNAs, the mechanisms of gene regulation involved in brain function have been described. It is suggested that the microRNAs we identified could become potential tools for regulating transposon activity in the brain to improve memory.

https://vavilov.elpub.ru/jour/article/view/4229
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Baobab from Madagascar aged 10 years old in Singapore’s Flower Dome

They live over 5,000 years. But none saw them die ;-)
This what everyone should do to save the planet!

And tracking yourself early with hundred of biomarkers will make your lifespan longer!!!

Cloud Forest, Singapore, 2025
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Join us on Longevity Founders in Singapore, starting tomorrow:

https://founderslongevity.co/sg/
Longevity InTime Founder speech in Singapore on the Longevity Founders event in Singapore, 28 of February 2025:
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