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Genflow to become Europe’s first longevity biotech IPO

The company is developing novel therapeutics targeting aging in humans and dogs by using genetically modified adeno-associated virus (AAV) vectors to deliver copies of the SIRT6 gene variant found in centenarians. SIRT6 has already been shown to have significant capabilities to repair DNA damage, and Genflow’s aim is to show that it can also improve healthspan and, potentially, increase lifespan. “Our business model is to develop our lead compound, GF-1002, that has already yielded encouraging pre-clinical results,” Leire told us. “We are currently undertaking pre-clinical trials which are expected to take approximately two years.


SIRT6 targeting longevity biotech announces intention to float on the London Stock Exchange, with IPO later this month.

‘Dark genome’ offers insight into bipolar and schizophrenia

𝙀𝙫𝙤𝙡𝙪𝙩𝙞𝙤𝙣𝙖𝙧𝙮 𝙗𝙞𝙤𝙡𝙤𝙜𝙞𝙨𝙩𝙨 𝙝𝙖𝙫𝙚 𝙩𝙧𝙤𝙪𝙗𝙡𝙚 𝙚𝙭𝙥𝙡𝙖𝙞𝙣𝙞𝙣𝙜 𝙬𝙝𝙮 𝙨𝙘𝙝𝙞𝙯𝙤𝙥𝙝𝙧𝙚𝙣𝙞𝙖 𝙖𝙣𝙙 𝙗𝙞𝙥𝙤𝙡𝙖𝙧 𝙙𝙞𝙨𝙤𝙧𝙙𝙚𝙧 — 𝙬𝙝𝙞𝙘𝙝 𝙖𝙧𝙚 𝙝𝙞𝙜𝙝𝙡𝙮 𝙝𝙚𝙧𝙞𝙩𝙖𝙗𝙡𝙚 𝙘𝙤𝙣𝙙𝙞𝙩𝙞𝙤𝙣𝙨 — 𝙥𝙚𝙧𝙨𝙞𝙨𝙩 𝙞𝙣 𝙥𝙤𝙥𝙪𝙡𝙖𝙩𝙞𝙤𝙣𝙨 𝙙𝙚𝙨𝙥𝙞𝙩𝙚 𝙝𝙖𝙧𝙢𝙞𝙣𝙜 𝙧𝙚𝙥𝙧𝙤𝙙𝙪𝙘𝙩𝙞𝙫𝙚 𝙛𝙞𝙩𝙣𝙚𝙨𝙨.

𝙍𝙚𝙨𝙚𝙖𝙧𝙘𝙝𝙚𝙧𝙨 𝙢𝙖𝙮 𝙝𝙖𝙫𝙚 𝙛𝙤𝙪𝙣𝙙 𝙖𝙣 𝙚𝙭𝙥𝙡𝙖𝙣𝙖𝙩𝙞𝙤𝙣 𝙞𝙣 𝙧𝙚𝙘𝙚𝙣𝙩𝙡𝙮 𝙚𝙫𝙤𝙡𝙫𝙚𝙙 𝙧𝙚𝙜𝙞𝙤𝙣𝙨 𝙤𝙛 𝙩𝙝𝙚 𝙝𝙪𝙢𝙖𝙣 𝙜𝙚𝙣𝙤𝙢𝙚 𝙩𝙝𝙖𝙩 𝙖𝙧𝙚 𝙣𝙤𝙩 𝙪𝙨𝙪𝙖𝙡𝙡𝙮 𝙧𝙚𝙘𝙤𝙜𝙣𝙞𝙯𝙚𝙙 𝙖𝙨 𝙜𝙚𝙣𝙚𝙨 𝙗𝙪𝙩 𝙘𝙖𝙣 𝙨𝙩𝙞𝙡𝙡 𝙘𝙤𝙙𝙚 𝙛𝙤𝙧 𝙥𝙧𝙤𝙩𝙚𝙞𝙣𝙨.

𝙏𝙝𝙞𝙨 “𝙙𝙖𝙧𝙠 𝙜𝙚𝙣𝙤𝙢𝙚” 𝙢𝙖𝙮 𝙜𝙚𝙣𝙚𝙧𝙖𝙩𝙚 𝙥𝙧𝙤𝙩𝙚𝙞𝙣𝙨 𝙩𝙝𝙖𝙩 𝙖𝙧𝙚 𝙫𝙞𝙩𝙖… See more.

The Neuro-Network.

𝐂𝐥𝐮𝐞𝐬 𝐭𝐨 𝐨𝐫𝐢𝐠𝐢𝐧𝐬 𝐨𝐟 𝐛𝐢𝐩𝐨𝐥𝐚𝐫 𝐚𝐧𝐝 𝐬𝐜𝐡𝐢𝐳𝐨𝐩𝐡𝐫𝐞𝐧𝐢𝐚 𝐟𝐨𝐮𝐧𝐝 𝐢𝐧 ‘𝐝𝐚𝐫𝐤 𝐠𝐞𝐧𝐨𝐦𝐞’


The authors of a recent study on the genetics of schizophrenia and bipolar disorder identify a potential role for the so-called dark genome.

The Science Behind Why We Age | Lifespan with Dr. David Sinclair #1

Sinclair’s first episode. Enjoy.


In this episode, Dr. David Sinclair and co-host Matthew LaPlante discuss why we age. In doing so, they discuss organisms that have extreme longevity, the genes that control aging (mTOR, AMPK, Sirtuins), the role of sirtuin proteins as epigenetic regulators of aging, the process of “ex-differentiation” in which cells begin to lose their identity, and how all of this makes up the “Information Theory of Aging”, and the difference between “biological age” and “chronological age” and how we can measure biological age through DNA methylation clocks.

Thank you to our sponsors:
Athletic Greens — https://athleticgreens.com/sinclair.
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Our Patreon page:
https://www.patreon.com/davidsinclair.

Lifespan book:

Researchers Use Machine Learning To Repair Genetic Damage

DNA damage is constantly occurring in cells, either due to external sources or as a result of internal cellular metabolic reactions and physiological activities. Accurate repair of such DNA damages is critical to avoid mutations and chromosomal rearrangements linked to diseases including cancer, immunodeficiencies, neurodegeneration, and premature aging.

A team of researchers at Massachusetts General Hospital and the National Cancer Research Centre have identified a way to repair genetic damage and prevent DNA alterations using machine learning techniques.

The researchers state that it is possible to learn more about how cancer develops and how to fight it if we understand how DNA lesions originate and repair. Therefore, they hope that their discovery will help create better cancer treatments while also protecting our healthy cells.

Did aliens genetically engineer humans 780,000 years ago?

The first humans emerged on Earth about 4 million years ago, but new evidence from the study of human evolution has revealed compelling evidence that a small group of these hominins was genetically modified by ancient alien visitors to create the first Homo sapiens.

Researcher and author Daniella Fenton has thoroughly analyzed humanity’s earliest origins and its sudden acceleration in brain development nearly 800,000 years ago, and this research has led to a major revelation.

“Homo sapiens is the creation of ancient astronauts who came through a wormhole in the Pleiades star cluster more than 780,000 years ago.”

The Australian researcher, an expert in equine lineages and gene expression, discovered numerous genetic changes that mark humans as abnormal when compared to modern primate species, some so extreme that they are best explained by advanced genetic engineering.

Full Story:

Goldman Sachs asks in biotech research report: ‘Is curing patients a sustainable business model?’

“The potential to deliver ‘one shot cures’ is one of the most attractive aspects of gene therapy, genetically-engineered cell therapy and gene editing. However, such treatments offer a very different outlook with regard to recurring revenue versus chronic therapies,” analyst Salveen Richter wrote in the note to clients Tuesday. “While this proposition carries tremendous value for patients and society, it could represent a challenge for genome medicine developers looking for sustained cash flow.”

🤔


Goldman Sachs warns sales from the most successful disease treatments are difficult to maintain.

Provocative new findings suggest a surprising cause of Down syndrome: cells linked to aging

Down syndrome is the most common genetic disorder, impacting about 1 in 700 newborns around the world. At some point during their first hours and days of embryonic development, their dividing cells fail to properly wriggle a chromosome pair away from each other, leaving an extra copy where it shouldn’t be. Although scientists have known for more than six decades that this extra copy of chromosome 21 causes the cognitive impairment people with Down syndrome experience, exactly how it happens remains a matter of debate.


But in recent years, scientists using new RNA sequencing techniques to study cells from pairs of twins — one with Down syndrome and one without — have repeatedly turned up a curious pattern. It wasn’t just the genes on chromosome 21 that had been cranked way up in individuals with Down syndrome. Across every chromosome, gene expression had gone haywire. Something else was going on.

On Thursday, a team from the Massachusetts Institute of Technology reported in Cell Stem Cell that it may have found a surprising culprit: senescent cells, the same types implicated in many diseases of aging. The study was small and preliminary, and some experts want to see it replicated in samples from more individuals before buying into its interpretations. But they are nevertheless intriguing.

Scientists Pull Animal DNA Out of Thin Air

While doing their research, the teams had no knowledge of the other’s work, but after finding each other’s preprint proof-of-concept papers online, the two groups decided to submit their manuscripts for review together. “It’s insane that two groups did such similar studies in two places, but it’s also a very rare opportunity,” says Bohmann.

The fact the groups took different paths to find a similar result is particularly compelling, says Mark Johnson, who studies eDNA and Texas Tech University and was not involved in the work. “It’s really exciting looking at how both of these papers, done independently of each other, have produced, really, the same results,” says Johnson. “It adds that extra little bit of validation that what we’re seeing is real.” While hopeful about the future of airborne eDNA, Johnson notes huge leaps need to be made before the techniques used in the zoo can be applied in the field. Collecting eDNA in the wild adds a host of new variables, and enclosed spaces like caves may accumulate genetic material differently than open areas like grasslands. “The next step is to take it from the zoo into the natural environment and see what we find there,” says Johnson.

Clare and Bohmann anticipate that one of the best applications of airborne DNA could be to measure biodiversity in difficult-to-access places, such as burrows and caves. Fabian Roger, an eDNA researcher at ETH in Switzerland, is eager to see how the work could be applied to studying insects. “We have very little ways of monitoring them other than catching and killing them,” says Roger, who was not involved in the recent work. Using eDNA to detect insect species from a sample of air instead of trapping them could rapidly advance entomology research. The technique could also clue scientists into the presence or spread of an invasive species. Like Clare and Bohmann, Roger doesn’t see airborne eDNA as a replacement for traditional monitoring methods, but as another tool they can use. “Biodiversity science is sort of an all-hands-on-deck situation. It’s not one over the other, or one or the other,” says Roger.

Omicron might have come from a mouse, but what kind of mouse?

Researchers from the Chinese Academy of Sciences in Beijing recently reported intriguing new evidence for a possible mouse origin of the Omicron variant. Their paper, posted on the BioRxiv preprint server, was quickly picked up and published a few days later by the Journal of Genetics and Genomics, and defies the prevailing theory which claims that the polymutant spike sequence of Omicron must have evolved under protracted infection in a severely immunocompromised patient.

Their main idea is that a mouse could have somehow been infected with the human virus by “reverse zoonotic transfer,” whereupon the virus evolved all or many of its 45 novel mutations, and then subsequently was transferred back to humans. While this theory might explain why Omicron appears so anomalous when plotted on a phylogenetic tree against the usual suspects, there is one major problem: The mouse homolog of the human ACE2 receptor (hACE2), which the virus typically uses to gain entry into , has little affinity for the standard issue SARS-CoV-2 spike protein.

So little in fact, that in order to study the virus in this preferred research animal, scientists must artificially introduce hACE2 in order to create mice that show any significant respiratory distress upon infection. These are made in several ways, each showing unique tissue tropisms, penetrance and correspondingly different effects. Researchers have conducted knock-in experiments in which the human hACE2 sequence is integrated into the and induced under the control of a number of different promoters. Adenoviruses can also be used to infect cells and create replicating plasmids that propagate the hACE2 code.

Dr. Maximina Yun, Ph.D. — Unlocking Secrets Of Salamander Regeneration For Regenerative Therapies

Unlocking The Secrets Of Salamander Regeneration For Regenerative Therapies — Dr. Maximina Yun, Ph.D., CRTD / Center for Regenerative Therapies TU Dresden, Technische Universität Dresden.


Dr. Maximina Yun, Ph.D. (https://tu-dresden.de/cmcb/crtd/forschungsgruppen/crtd-forsc…oup-leader) is Research Group Leader at the Center for Regenerative Therapies Dresden (CRTD), Technical University Dresden, jointly affiliated with Max Planck Institute for Molecular Cell Biology and Genetics (MPI-CBG).

Dr. Yun and her group (https://tu-dresden.de/cmcb/crtd/forschungsgruppen/crtd-forschungsgruppen/yun) study the cellular and molecular basis of regeneration of complex structures with the help of salamanders (like newts and axolotls) and these vertebrates exceptional regenerative abilities, which in contrast to humans, are capable of regenerating complex tissues, and even entire organs, to a remarkable extent. Therefore, they offer unique insights into what molecular mechanisms must be in place for achieving quasi-perfect regeneration.

Research in the Yun group focuses on three main areas: describing cellular and molecular mechanisms driving regeneration (Mechanisms underlying the plasticity of the differentiated state), their connection with cellular aging (Role and regulation of senescence in regeneration), and the role that the immune system plays in regenerative context.

The research in the Yun group combines advanced molecular biology methods with state-of-the-art microscopy. Most recently the group has established Salamander-Eci, a novel method that enables the three-dimensional visualization of salamander tissues for a more comprehensive understanding of regenerative processes.

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