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For the first time, Senckenberg scientist Mónica Solórzano-Kraemer, together with lead authors David Peris and Kathrin Janssen of the University of Bonn and additional colleagues from Spain and Norway, successfully extracted genetic material from insects that were embedded in six- and two-year-old resin samples. DNA—in particular, DNA from extinct animals—is an important tool in the identification of species. In the future, the researchers plan to use their new methods on older resin inclusions, as well. The study was published today in the scientific journal PLOS ONE.

The idea of extracting DNA from resin-embedded organisms inevitably invokes memories of the blockbuster “Jurassic Park.”

“However, we have no intention of raising dinosaurs,” says Dr. Mónica Solórzano-Kraemer of the Senckenberg Research Institute and Natural History Museum. “Rather, our current study is a structured attempt to determine how long the DNA of insects enclosed in resinous materials can be preserved.”

Not too much here, but longevity research fans might like.


Time may be our worst enemy, and aging its most powerful weapon. Our hair turns gray, our strength wanes, and a slew of age-related diseases represent what is happening at the cellular and molecular levels. Aging affects all the cells in our body’s different tissues, and understanding its impact would be of great value in fighting this eternal enemy of all ephemeral life forms.

The key is to first observe and measure. In a paper published in Cell Reports, scientists led by Johan Auwerx at EPFL started by asking a simple question: how do the tissues of aging mice differ from those of mice that are mere adults?

To answer the question, the researchers used the multiple techniques to measure the expression of everyone one of the thousands of mouse’s genes, and to identify any underlying epigenetic differences. The researchers not only measured different layers of information, but they did it across three different tissues: liver, heart, and muscle.

A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.

In a study, published in the journal eLife on Sept. 29, the researchers identified a factor that acts like a molecular switch in the of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goose bumps, an ability that is lost in adult human scars.

“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”

David Sinclair wants to slow down and ultimately reverse aging. Sinclair sees aging as a disease and he is convinced aging is caused by epigenetic changes, abnormalities that occur when the body’s cells process extra or missing pieces of DNA. This results in the loss of the information that keeps our cells healthy. This information also tells the cells which genes to read. David Sinclair’s book: “Lifespan, why we age and why we don’t have to”, he describes the results of his research, theories and scientific philosophy as well as the potential consequences of the significant progress in genetic technologies.

At present, researchers are only just beginning to understand the biological basis of aging even in relatively simple and short-lived organisms such as yeast. Sinclair however, makes a convincing argument for why the life-extension technologies will eventually offer possibilities of life prolongation using genetic engineering.

He and his team recently developed two artificial intelligence algorithms that predict biological age in mice and when they will die. This will pave the way for similar machine learning models in people.
The loss of epigenetic information is likely the root cause of aging. By analogy, If DNA is the digital information on a compact disc, then aging is due to scratches. What we are searching for, is the polish.

Every time a cell divides, the DNA strands at the ends of your chromosomes replicate in order to copy all the genetic information to each new cell, and this process is not perfect. Over time, however, the ends of your chromosomes can become scrambled.

However, the progress in genetic engineering has proved that these changes can be reversed even at the cellular level, and it is possible to restore the information in our cells, thus improving the functioning of our organs and slowing the aging process.

#Aging #DavidSinclair #Lifespan

#DigitalTheology #TheologyofDigitalPhysics #PhenomenalConsciousness #CosmicSelf #HolographicPrinciple #DigitalPhysics #theology #pantheism #consciousness


Since we live in a world which isn’t random, but organized at every level, a role for consciousness seems unavoidable. The ‘digital theologian’ shows us compelling evidence from quantum mechanics, mathematics and computer sciences, which not only aligns with a philosophical worldview of the Primacy of Consciousness, but which also assigns a role to information as its modus operandi.

It is quantum mechanics which appears to connect the Universe as a whole to consciousness. A whole, which is more than the sum of its parts and irreducible to mere assumptions deriving from the anatomizing dissection into mental confabulations. Drawing from the holographic principle, perceptroniums and noocentrism, Alex provides crucial keys to unlock the mystery of consciousness to show us how our local consciousness can arise from a non-local cosmic consciousness network.

Carefully building his fortress of arguments, Alex gathers his building bricks from various areas of scientific exploration, ranging from the role of language and tools in the development of our consciousness, the physics of time and epigenetics. Traditional Darwinism and reductive materialism become so challenged, that we become bound to agree with Terence McKenna’s statement that “object fetishism is completely bankrupt.” All these threads are then skillfully woven into the irresistible attractor and only logical conclusion, or Digital Pantheism and Omega Point Cosmology. And with this thus synthesized Apotheosis, Vikoulov brings the architecture of his chef-d’oeuvre to full fruition.

Summary: PLCG2-P522R, a genetic variant that protects against Alzheimer’s disease, enhances key functions of immune cells.

Source: University of Eastern Finland

A new study conducted by researchers at the University of Eastern Finland found that the PLCG2-P522R genetic variant, which protects against Alzheimer’s disease, enhances several key functions of immune cells. The results obtained in the study highlight the importance of immune cells as a target of future development of new therapies for Alzheimer’s disease.

11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.

Lil bits of info on DNA methylation, clocks.


Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7–8 million years ago when our ancestors branched away from the lineage of chimps.

Slower ticker

There are tens of thousands of genes in the human genome, but that doesn’t mean all of them are active. For instance, through the methylation of DNA across certain sites of the genetic sequence, genes are locked in the “off” position. These modifications, known as epigenetic changes (‘epi’ means ‘above’ in Greek), do not alter the DNA sequence itself but, rather, simply regulate the activity of genes.

Very interesting!

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“The plan was to scan patients’ genomes—in particular, a set of 13 genes involved in interferon immunity against influenza. In healthy people, interferon molecules act as the body’s security system. They detect invading viruses and bacteria and sound the alarm, which brings other immune defenders to the scene.

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Casanova’s team has previously discovered [genetic mutations](https://medicalxpress.com/tags/genetic+mutations/) that hinder interferon production and function. People with these mutations are more vulnerable to certain pathogens, including those that cause influenza. Finding similar mutations in people with COVID-19, the team thought, could help doctors identify patients at risk of developing severe forms of the disease. It could also point to new directions for treatment, he says.”

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“As the researchers began analyzing patient samples, they started to uncover harmful mutations, in people young and old. The team found that 23 out of 659 patients studied carried errors in genes involved in producing antiviral interferons.”

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“That thought sparked a new idea. Maybe other patients with severe COVID-19 also lacked interferons—but for a different reason. Maybe some patients’ bodies were harming these molecules themselves.”

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Toronto scientists have mapped the genes allowing cancer cells to avoid getting killed by the immune system in a finding that paves the way for the development of immunotherapies that would be effective for larger patient populations and across different tumour types.

“Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments but the reality is that they only generate durable responses in a fraction of patients and not for all tumour types,” says Jason Moffat, a professor of molecular genetics in the Donnelly Centre for Cellular and Biomolecular Research at the University of Toronto who led the work.

The study also revealed the need for to take into account the genetic composition of tumours because of mutations in the cancer cells that can potentially make the disease worse in response to treatment, often referred to as cancer resistance mutations.