Lifeboat Foundation

An international group of scientists studied the effects of 17 different lifespan-extending interventions on gene activity in mice and discovered genetic biomarkers of longevity. The results of their study were published in the journal Cell Metabolism.

Nowadays, dozens of interventions are known that extend the lifespan of various living organisms ranging from yeast to mammals. They include chemical compounds (e.g. rapamycin), genetic interventions (e.g. mutations associated with disruption of growth hormone synthesis), and diets (e.g. caloric restriction). Some targets of these interventions have been discovered. However, there is still no clear understanding of the systemic molecular mechanisms leading to lifespan extension.

A group of scientists from Skoltech, Moscow State University and Harvard University decided to fill this gap and identify crucial molecular processes associated with longevity. To do so, they looked at the effects of various lifespan-extending interventions on the activity of genes in a mouse, a commonly used model organism closely related to humans.

In a recent study, a team from the Neurobiota Research Center in Korea has discovered that reducing gut dysbiosis partially alleviates the cognitive impairment associated with Alzheimer’s disease. This may seem puzzling, as the gut and the brain are separate and relatively distant organs, but this research makes sense in the context of chronic inflammation.

Inflammaging

Under normal circumstances, inflammation is a short-term measure in response to infection: immune cells are directed towards the inflamed area and handle the infection, and then the inflammation dies down. However, chronic inflammation causes harm to our organs; it is the main form of altered intercellular communication, which is one of the hallmarks of aging. The protein complex NF-kB, the master regulator of inflammation, is the main culprit of inflammaging, and it is specifically discussed in this paper.

How about some life extension optimism to start your day?

People 50 and older have a lot to look forward to, according to Juvenescence’s Greg Bailey—mainly that we won’t be aging as fast or poorly as our parents. “Science fiction has become science,” said the UK-based anti-aging biotech’s CEO about the company’s completing its $100 million Series B round of financing last week. “I think the world is going to be shocked,” he said in an interview. In total, Juvenescence has now raised $165 million in just 18 months to fund longevity projects with the lofty goal of extending human lifespans to 150 years.

Cellular senescence, a permanent state of replicative arrest in otherwise proliferating cells, is a hallmark of ageing and has been linked to ageing-related diseases like cancer. Senescent cells have been shown to accumulate in tissues of aged organisms which in turn can lead to chronic inflammation. Many genes have been associated with cell senescence, yet a comprehensive understanding of cell senescence pathways is still lacking. To this end, we created CellAge (http://genomics.senescence.info/cells), a manually curated database of 279 human genes associated with cellular senescence, and performed various integrative and functional analyses. We observed that genes promoting cell senescence tend to be overexpressed with age in human tissues and are also significantly overrepresented in anti-longevity and tumour-suppressor gene databases. By contrast, genes inhibiting cell senescence overlapped with pro-longevity genes and oncogenes. Furthermore, an evolutionary analysis revealed a strong conservation of senescence-associated genes in mammals, but not in invertebrates. Using the CellAge genes as seed nodes, we also built protein-protein interaction and co-expression networks. Clusters in the networks were enriched for cell cycle and immunological processes. Network topological parameters also revealed novel potential senescence-associated regulators. We then used siRNAs and observed that of 26 candidates tested, 19 induced markers of senescence. Overall, our work provides a new resource for researchers to study cell senescence and our systems biology analyses provide new insights and novel genes regarding cell senescence.

• http://genomics.senescence.info/cells/

An international group of scientists studied the effects of 17 lifespan-extending interventions on gene activity in mice and discovered genetic biomarkers of longevity. The results of their study were published in the journal Cell Metabolism.

Nowadays, dozens of interventions are known that extend the lifespan of various living organisms ranging from yeast to mammals. They include chemical compounds (e.g. rapamycin), genetic interventions (e.g. mutations associated with disruption of growth hormone synthesis), and diets (e.g. caloric restriction). Some targets of these interventions have been discovered. However, there is still no clear understanding of the systemic molecular mechanisms leading to lifespan extension.

A group of scientists from Skoltech, Moscow State University and Harvard University decided to fill this gap and identify crucial molecular processes associated with longevity. To do so, they looked at the effects of various lifespan-extending interventions on the activity of genes in a mouse, a commonly used model organism closely related to humans.

It is a sure sign that the tide has turned when mainstream news outlets and magazines start publishing positive articles about aging research and the prospects of rejuvenation.

A refreshing change

Today, I want to highlight an article in MIT Technology Review in which the author, David Adam, gives a sensible and measured overview of what is happening in the field and manages to sidestep the usual negativity and misconceptions that often plague popular science pieces.

We are now on a collision course with the most significant event in the entire history of our planet comparable in criticality only to the emergence of life itself. This “Novacene” event would mark the technological maturity of human-machine civilization, as we are to inevitably transcend our biology, and even more importantly, we are to transcend our dimensionality by achieving the so-called Simulation Singularity.

Most of us are familiar with the concept of the Technological Singularity. While those terms can be often used interchangeably, the ’Intelligence Supernova’ adds a slightly different connotation — it means the Omega Point of Homo sapiens — the convergent point of exponential technologies and on a civilizational scale, progressively morphing into one Global Mind and a phase transition of humanity termed in the book ’The Syntellect Emergence’. This convergent point would signify no less than Self-Transcendence, in other words, engineered godhood.

Within the next few decades, we’ll witness accelerating changes so profound and swift that the linear progression of human history would eventuate as the Intelligence Supernova of astronomical significance, the “implosion” of all knowledge of man and “transcension” outside the dimensionality of “human” universe.

The ability to edit genes in living organisms offers the opportunity to treat a plethora of inherited diseases. However, many types of gene-editing tools are unable to target critical areas of DNA, and creating such a technology has been difficult as living tissue contains diverse types of cells.

Now, Salk Institute researchers have developed a new tool—dubbed SATI—to edit the mouse genome, enabling the team to target a broad range of mutations and cell types. The new genome-editing technology, described in Cell Research on August 23, 2019, could be expanded for use in a broad range of gene mutation conditions such as Huntington’s disease and the rare premature aging syndrome, progeria.

“This study has shown that SATI is a powerful tool for genome editing,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases.”

In new research published in Psychoneuroendocrinology, scientists have shown that loving-kindness meditation has a positive impact at the cellular level. The study examined how different types of meditation influenced telomere length, an indicator of physiological aging.

Telomeres are the end caps of DNA on our chromosomes, which help in DNA replication and get shorter over time.

“Chronological age and biological age are not identical. The former is measured in years, whereas the latter is often indexed by telomere length,” the authors of the new study explained. “Telomeres progressively shorten with cell division (i.e., aging) in general, but may also be replenished, or lengthened, by the enzyme telomerase.”