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The secret to longevity is already in the animals around us.


Some species live unexpectedly long lives. By studying how they do it, researchers hope to pinpoint factors affecting human longevity.

By Bob Holmes.

Life, for most of us, ends far too soon — hence the effort by biomedical researchers to find ways to delay the aging process and extend our stay on Earth. But there’s a paradox at the heart of the science of aging: The vast majority of research focuses on fruit flies, nematode worms and laboratory mice, because they’re easy to work with and lots of genetic tools are available. And yet, a major reason that geneticists chose these species in the first place is because they have short lifespans. In effect, we’ve been learning about longevity from organisms that are the least successful at the game.

Scientists said the findings indicated that the virus likely recently jumped from animals to humans, but stressed that additional studies are necessary.


Scientists have reportedly discovered a new kind of coronavirus that is believed to have originated in dogs – in what may be the eighth unique form of the bug known to cause disease in humans.

Researchers in a study published in the Clinical Infectious Diseases journal said their findings from patients hospitalized with pneumonia in 2017–2018 underscored the public health threat of animal coronaviruses, Reuters reported.

They said they had tested nasal swab samples taken from 301 pneumonia patients at a hospital in the east Malaysian state of Sarawak.

In our ongoing search to continuously improve our health, we occasionally pay lip service to the bacteria that live inside our gut. Normally this concern rarely manifests as anything more than occasionally remembering to buy some of those small bottles of pro-biotic yoghurts while shopping for your…


Recent discoveries have led to the conclusion that the gut plays an important role in cognitive function, with a large amount of research into understanding what is known as the gut-brain axis, which is the collective name given to the biochemical signalling pathways which take place between the gastrointestinal tract and the central nervous system. With an ever-increasing understanding of this pathway, along with an expanded understand of the gut flora (which was found to decline with age), researchers started to ask how the gut flora are involved in the ageing process.

In order to test how exactly ageing gut flora effects the gut-brain axis, researchers at the University of East Anglia conducted a faecal transplant from elderly mice into younger mice. Following this transplant, the young mice were then put through a serious of tests to assess their cognitive abilities. The younger mice showed significant changes in their microbial profiles, as well as significantly impaired capacity for spatial learning, as well as a decreased capacity for memorisation. These mice also showed an altered expression of proteins associated with neurotransmission and neuroplasticity, along with changes in the mice’s hippocampus, which is responsible for allowing the mice to memories new information, as well as recalling previous memories.

This research has successfully proven a link between the changing microbiome of the gut and protein expression within the central nervous system. This discovery is exceptionally good news, as not only is the problem potentially fairly easy to fix (with an aforementioned faecal transplant), but it also provides clues as to how we might compensate for this age related change in the gut microbiome with medication tailors to mimic the role of a young microbiome. Either way, the discovery has opened the door to a number of exciting prospects for regenerative medicine, along with maybe highlighting the fact that we should really start considering our gut bacteria as more than just a collection of microorganisms, and more of a collection of symbiotic organisms that benefit us in ways that we are only just beginning to understand.

To begin with, why do we use mice in medical and biological research? The answer to this question is fairly straight forward. Mice are cheap, they grow quickly, and the public rarely object to experimentations involving mice. However, mice offer something that is far more important than simple pragmatism, as despite being significantly smaller and externally dissimilar to humans, our two species share an awful lot of similarities. Almost every gene found within mice share functions with genes found within humans, with many genes being essentially identical (with the obvious exception of genetic variation found within all species). This means that anatomically mice are remarkably similar to humans.

Now, this is where for the sake of clarity it would be best to break down biomedical research into two categories. Physiological research and pharmaceutical research, as the success of the mouse model should probably be judges separately depending upon the research that is being carried out. Separating the question of the usefulness of the mouse model down into these two categories also solves the function of more accurately focusing the ire of its critics.

The usefulness of the mouse model in the field of physiological research is largely unquestioned at this point. We have quite literally filled entire textbooks with the information we have gained from studying mice, especially in the field of genetics and pathology. The similarities between humans and mice are so prevalent that it is in fact possible to create functioning human/mouse hybrids, known as ‘genetically engineered mouse models’ or ‘GEMMs’. Essentially, GEMMs are mice that have had the mouse version of a particular gene replaced with its human equivalent. This is an exceptionally powerful tool for medical research, and has led to numerous medical breakthroughs, including most notably our current treatment of acute promyelocytic leukaemia (APL), which was created using GEMMs.

Circa 2017


What is the best way to preserve music for future generations to enjoy? Store it in DNA, of course.

That is exactly what Twist Biosciences, which pioneers high-quality DNA synthesis, has facilitated in collaboration with the University of Washington and Microsoft. Two iconic performances – from the iconic Montreux Jazz Festival, one Deep Purple’s playing of Smoke on the Water, and Tutu by Miles Davis, have been ‘encoded onto DNA and read back with 100 percent accuracy.

Legendary music composer and producer, Quincy Jones, said it “absolutely makes my soul smile” to know that the “beauty and history of the Montreux Jazz Festival” has been preserved in this way.

There’s some really interesting CRISPR news out today, and it’s likely to be a forerunner of much more news to come. A research team has demonstrated what looks like robust, long-lasting effects in a primate model after one injection of the CRISPR enzymatic machinery. There have been plenty of rodent reports on various forms of CRISPR, and there are some human trials underway, but these is the first primate numbers that I’m aware of.

The gene they chose to inactivate is PCSK9, which has been a hot topic in drug discovery for some years now. It’s a target validated by several converging lines of evidence from the human population (see the “History” section of that first link). People with overactive PCSK9 have high LDL lipoproteins and cholesterol, and people with mutations that make it inactive have extremely low LDL and seem to be protected from a lot of cardiovascular disease. There are several drugs and drug candidates out there targeting the protein, as well there might be.

It’s a good proof-of-concept, then, because we know exactly what the effects of turning down the expression of active PCSK9 should look like. It’s also got the major advantage of being mostly a liver target – as I’ve mentioned several times on the blog already, many therapies aimed at gene editing or RNA manipulation have a pharmacokinetic complication. The formulations used to get such agents intact into the body (and in a form that they can penetrate cells) tend to get combed out pretty thoroughly by the liver – which after all, is (among other things) in the business of policing the bloodstream for weird, unrecognized stuff that is then targeted for demolition by hepatocytes. Your entire bloodstream goes sluicing through the liver constantly; you’re not going to able to dodge it if your therapy is out there in the circulation. It happens to our small-molecule drugs all the time: hepatic “first pass” metabolism is almost always a factor to reckon with.

The harmfulness of pesticides to beneficial organisms is one of the most serious concerns in agriculture. Therefore scientists are eagerly looking for new, more environmentally friendly and species-specific solutions. Researchers at the Estonian University of Life Sciences, Ghent and the University of Maastricht took a long step forward in this regard.

The detrimental impact of pesticides on non-target organisms is one of the most urgent concerns in current agriculture. Double-stranded RNAs (dsRNAs) represent the most species-specific class of pesticides to date, potentially allowing control of a target pest without effecting other species. The unprecedented target-specificity of dsRNA is due to its nucleotide sequence-specific mode of action that results in post-transcriptional gene silencing, or RNA interference (RNAi), in the target species. The development and field use of dsRNAs, via both the insertion of transgenes into the plant genome and the application of dsRNA sprays, is a rapidly growing area of research. Simultaneously, there exists the growing prospect of harnessing RNAi within integrated pest management schemes.

Using the pollen beetle (Brassicogethes aeneus) and its host crop oilseed rape (Brassica napus) as a model crop-pest system, a team of researchers collectively from Estonian University of Life Sciences, Ghent University and Maastricht University examined how RNAi efficacy depends on duration of dietary exposure to dsRNA. To this end, the authors applied dsRNA (specifically designed to induce RNAi in the pollen beetle) to oilseed rape flowers, and analyzed RNAi-induced mortality between insects chronically fed dsRNA and insects fed dsRNA for 3 days. Most notably, their data suggest that, with chronic dietary exposure to dsRNA, reduced dsRNA concentrations can be applied in order to achieve a similar effect compared to short-term (e.g. 3 days) exposure to higher concentrations. This observation has important implications for optimizing dsRNA spray approaches to managing crop pests.

Aging, DNA Repair, And Clinical Innovation — Dr. Morten Scheibye-Knudsen — University of Copenhagen.


Dr. Morten Scheibye-Knudsen is an Associate Professor at the Department of Cellular and Molecular Medicine, and at the Center for Healthy Aging (CEHA), at the University of Copenhagen.

Dr. Scheibye-Knudsen did his MD at the University of Copenhagen and worked briefly as a physician in Denmark and Greenland before turning to science. He did his post-doctoral fellowship at Vilhelm Bohr’s lab at the National Institute on Aging, National Institutes of Health, USA, where he utilized state-of-the art approaches to understand how DNA damage contributes to aging, discovering that neurodegeneration in several premature aging diseases is partly caused by hyperactivation of a DNA damage responsive enzyme called polyADP-ribose polymerase 1 (PARP1). This activation leads to loss of vital metabolites such as Nicotinamide Adenine Dinucleotide (NAD+) and acetyl-CoA. Importantly, this discovery facilitated the realization that we can intervene in the aging process by inhibiting PARP1, augmenting NAD+ levels and increasing acetyl-CoA.

In his own lab Dr. Scheibye-Knudsen continues to focus on understanding aging by combining machine learning based approaches with wet-lab analyses with the goal of developing interventions for age-associated diseases and perhaps aging itself.

Dr. Scheibye-Knudsen is Chief Editor, Frontiers in Aging, and an Advisory Board Member of the Longevity Vision Fund and Molecule Protocol.

Do we need to revisit this? 🤔


Airborne transmission by droplets and aerosols is important for the spread of viruses. Face masks are a well-established preventive measure, but their effectiveness for mitigating SARS-CoV-2 transmission is still under debate. We show that variations in mask efficacy can be explained by different regimes of virus abundance and related to population-average infection probability and reproduction number. For SARS-CoV-2, the viral load of infectious individuals can vary by orders of magnitude. We find that most environments and contacts are under conditions of low virus abundance (virus-limited) where surgical masks are effective at preventing virus spread. More advanced masks and other protective equipment are required in potentially virus-rich indoor environments including medical centers and hospitals. Masks are particularly effective in combination with other preventive measures like ventilation and distancing.

Airborne transmission is one of the main pathways for the transmission of respiratory viruses, including the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (1). Wearing face masks has been widely advocated to mitigate transmission. Masks are thought to protect people in two ways: source control reducing the emission and spread of respiratory viruses through airborne droplets and aerosols, and wearer protection reducing the inhalation of airborne respiratory viruses.

The effectiveness of masks, however, is still under debate. Compared to N95/FFP2 respirators which have very low particle penetration rates (around ~5%), surgical and similar masks exhibit higher and more variable penetration rates (around ~30–70%) (2, 3). Given the large number of particles emitted upon respiration and especially upon sneezing or coughing , the number of respiratory particles that may penetrate masks is substantial, which is one of the main reasons leading to doubts about their efficacy in preventing infections. Moreover, randomized clinical trials show inconsistent or inconclusive results, with some studies reporting only a marginal benefit or no effect of mask use (5, 6). Thus, surgical and similar masks are often considered to be ineffective. On the other hand, observational data show that regions or facilities with a higher percentage of the population wearing masks have better control of the coronavirus disease 2019 (COVID-19) (7–9).

Famed longevity pioneer Aubrey de Grey, Chief Science Officer of SENS Research Foundation, joins Geoffrey Woo, Founder and Chairman of Health Via Modern Nutrition Inc., for an enlightening conversation about advances in longevity, the investments and technologies that extend life, and the challenges and opportunities of a world in which people live longer. He walks us through his damage repair therapies with a focus on rejuvenation, prevention, and wearable technologies. Filmed on May 17, 2021. To continue the discussion with fellow Real Vision members on this interview, click here to visit the Exchange: https://rvtv.io/2T7nqZL

Key Learnings: Longevity escape velocity, which is a term de Grey coined, is the idea in which life expectancy is extended longer than the time that is passing, and he estimates a 50% chance that aging could be brought under medical control in as little as 15 years’ time. To learn more about SENS’ research and advancements, please visit their site here: https://www.sens.org/.