Toggle light / dark theme

The human trial of plasma dilution started in Russia last week. The lead researcher is checking how the biomarkers of aging will change in response to 110% plasma replacement during the therapy, and the difference between the group with albumin addition and without albumin. The trial is open to both Russian citizens and people from other countries. It is a hybrid model where part of the expenditures is paid by the volunteers, and part is provided by the patron of the research. This model allowed to get the trial started in record time — less than 9 months from conception to the start date.

The research group wants to test plasmapheresis in combination with other longevity therapies next to see if plasma dilution prior to the other therapy can enhance the results.


Are you interested in longevity news? Come over to https://youtube.com/x10show for more!

In The Last Generation to Die, we explore the difficult conversation of what is to be done for the elderly who might miss out on the benefits of enhanced longevity. But if these companies somehow achieved their goal, however farfetched, that conversation would become moot.

Would you want to resurrect a lost loved one if given the opportunity?

In this video, Drs Irina and Mike Conboy talk about their theory of why we age and introduce Neutral Blood Exchange, which came from their original parabiosis experiments documented in a 2005 paper.

Our guests today are Drs. Irina and Michael Conboy of the Department of Bioengineering at the University of California Berkeley. their discovery of the rejuvenating effects of young blood through parabiosis in a seminal paper published in Nature in 2005 paved the way for a thriving field of rejuvenation biology. The Conboy lab currently focuses on broad rejuvenation of tissue maintenance and repair, stem cell niche engineering, elucidating the mechanisms underlying muscle stem cell aging, directed organogenesis, and making CRISPR a therapeutic reality.

Papers mentioned in this video.
Plasma dilution improves cognition and attenuates neuroinflammation in old mice.
https://pubmed.ncbi.nlm.nih.gov/33191466/
Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin.
https://pubmed.ncbi.nlm.nih.gov/32474458/
Rejuvenation of aged progenitor cells by exposure to a young systemic environment.
https://pubmed.ncbi.nlm.nih.gov/15716955/

************************************************************

Great exclusive interview by longevity expert, PhD. Professor, Systems Biology. Director, Chronic Metabolic and Rare Diseases Systems Biology Initiative (ChroMe RaDSBIn) facebook.com/LifetimeTrustnet/posts/1021975448543419


Dr. Ancha Baranova interview on longevity and Covid technologies.

She discovered many biomarkers for chronic liver diseases, cancer and other illnesses, a biosynthesis of the melanin in human adipose, two novel properties of cell-free DNA, and a variety of novel functions for known biomolecules.

The findings, published in Nature Communications, could have important implications for human health: minis have been found at every type of synapse studied so far, and defects in miniature neurotransmission have been linked to range of neurodevelopmental disorders in children. Figuring out how a reduction in miniature neurotransmission changes the structure of synapses, and how that in turn affects behavior, could help to better understand neurodegenerative disorders and other brain conditions.


Summary: Study reveals how miniature release events help to keep neurons intact and preserve motor neuron function in aging insects.

Source: EPFL

Neurons communicate through rapid electrical signals that regulate the release of neurotransmitters, the brain’s chemical messengers. Once transmitted across a neuron, electrical signals cause the juncture with another neuron, known as a synapse, to release droplets filled with neurotransmitters that pass the information on to the next neuron. This type of neuron-to-neuron communication is known as evoked neurotransmission.

Replacing Aging — Dr. Jean M. Hebert, Ph.D. Albert Einstein College of Medicine.


Dr. Jean M. Hebert, Ph.D. (https://einsteinmed.org/faculty/9069/jean-hebert/) is Professor in the Department of Genetics and in the Dominick P. Purpura Department of Neuroscience, at Albert Einstein College of Medicine.

He’s also the author of the book Replacing Aging, which describes how regenerative medicine will beat aging.

Pulsechain has raised $25000, 000 for antiaging medical research after 5 days of a 14 day fundraiser. You must follow the SENS.org PulseChain instructions. Sacrifices to SENS.org during the sacrifice phase earn 25% less points compared to sacrifices at Pulse.info. SENS.org can also accept stocks and bank wires. Once the sacrifice phase is over, the total sacrifice points for each sacrificer’s address’s points (at the same metamask address) are totaled up across all the supported chains and the SENS.org report. This creates a list of sacrificers ranked by total points from largest to smallest.

SENS Research Foundation has been working to develop, promote, and ensure widespread access to therapies that cure and prevent the diseases and disabilities of aging by comprehensively repairing the damage that builds up in our bodies over time. SENS is redefining the way the world researches and treats age-related ill health, while inspiring the next generation of biomedical scientists. Aubrey dr Grey and SENS have been the leading proponents of repairing aging damage to reverse aging effects. They have been leading the research effort for aging damage repair for over 20 years.

The Crypto world has been very supportive of SENS and antiaging research. In 2018, SENS received a $2.4 million Ethereum donation from Vitalik Buterin, the co-founder of Ethereum and the co-founder of Bitcoin Magazine.

Encouraging Mid Trial data update! Great to know Dr. Katcher is applying for IRB approval for their human clinical trial for E5.


In this video we provide an update on Dr. Katcher’s experiment where he is treating rats with E5 (formerly called Elixer) on a regular schedule to see how long they will live for. Dr Katcher’s team have kindly provided some intermediate updates that we share in the video.
0:00 — 00:50 Introduction.
00:51 — 04:02 Project Background/Overview.
04:03 — Project Update.

Papers referred to in this newsletter.

NYU Abu Dhabi (NYUAD) researchers have uncovered a code that sets the genome of the liver to account for the remarkable ability for this organ to regenerate. This finding offers new insight into how the specific genes that promote regeneration can be activated when part of the liver is removed. These findings have the potential to inform the development of a new form of regenerative medicine that could help non-regenerative organs regrow in mice and humans.

While other animals can regenerate most organs, humans, mice, and other mammals can only regenerate their liver in response to an injury or when a piece is removed. NYUAD researchers hypothesized that the that drive in the liver would be controlled by a specific code that allows them to be activated in response to injury or resection. They home in on the epigenome, which is the modifications on the DNA that alter the gene expression, as opposed to changing the itself.

Using a mouse liver model, the team of NYUAD researchers, led by Professor of Biology Kirsten Sadler Edepli, identified the elements of the present in quiescent liver cells—cells that are currently not replicating but have the ability to proliferate under the right conditions—that activate to regenerate. Genes involved in liver cell proliferation are silenced in livers that are not regenerating, but the surprising finding was that they reside in parts of the genome where most genes are active. The researchers found that these pro-regenerative genes were marked with a specific modification—H3K27me3. During regeneration, H3K27me3 is depleted from these genes, enabling their dynamic expression and driving proliferation.