Lifeboat Foundation

Genome editing technologies have revolutionized biomedical science, providing a fast and easy way to modify genes. However, the technique allowing scientists to carryout the most precise edits, doesn’t work in cells that are no longer dividing — which includes most neurons in the brain. This technology had limited use in brain research, until now. Research Fellow Jun Nishiyama, M.D., Ph.D., Research Scientist, Takayasu Mikuni, M.D., Ph.D., and Scientific Director, Ryohei Yasuda, Ph.D. at the Max Planck Florida Institute for Neuroscience (MPFI) have developed a new tool that, for the first time, allows precise genome editing in mature neurons, opening up vast new possibilities in neuroscience research.

This novel and powerful tool utilizes the newly discovered gene editing technology of CRISPR-Cas9, a viral defense mechanism originally found in bacteria. When placed inside a cell such as a neuron, the CRISPR-Cas9 system acts to damage DNA in a specifically targeted place. The cell then subsequently repairs this damage using predominantly two opposing methods; one being non-homologous end joining (NHEJ), which tends to be error prone, and homology directed repair (HDR), which is very precise and capable of undergoing specified gene insertions. HDR is the more desired method, allowing researchers flexibility to add, modify, or delete genes depending on the intended purpose.

Coaxing cells in the brain to preferentially make use of the HDR DNA repair mechanism has been rather challenging. HDR was originally thought to only be available as a repair route for actively proliferating cells in the body. When precursor brain cells mature into neurons, they are referred to as post-mitotic or nondividing cells, making the mature brain largely inaccessible to HDR — or so researchers previously thought. The team has now shown that it is possible for post-mitotic neurons of the brain to actively undergo HDR, terming the strategy “vSLENDR (viral mediated single-cell labeling of endogenous proteins by CRISPR-Cas9-mediated homology-directed repair).” The critical key to the success of this process is the combined use of CRISPR-Cas9 and a virus.

Researchers have developed a technique that enables gene editing on neurons — something previously thought to be impossible. This new tool will present amazing new opportunities for neuroscience research.

Technologies designed for editing the human genome are transforming biomedical science and providing us with relatively simple ways to modify and edit genes. However, precision editing has not been possible for cells that have stopped dividing, including mature neurons. This has meant that gene editing has been of limited use in neurological research — until now. Researchers at the Max Planck Florida Institute for Neuroscience (MPFI) have created a new tool that allows, for the first time ever, precise genome editing in mature neurons. This relieves previous constraints and presents amazing new opportunities for neuroscience research.

Speaking of concerns, I’m a bit concerned that the discussion about what might go wrong or how to prevent this or that hypothetical problem might draw attention away from another, possibly even more important question: Why do we strive to make rejuvenation a reality? There’s not much point in doing something if it doesn’t yield any benefits, especially if that something requires as much hard work as this cause does; so, what are the expected benefits of rejuvenation?

The benefits are many; some are obvious, and some are less so. The ones I’ll discuss in this article are the ones I see as obvious—tangible, immediate benefits for the people undergoing rejuvenation.

Exercise is a sensible part of any personal health strategy, and a new study suggests that even low levels of walking are associated with lower mortality compared to inactivity[1].

U.S. public health guidelines recommend that adults engage in at least 150 minutes of moderate or 75 minutes of intense exercise per week. However, surveys show that only half of U.S. adults actually reach this ideal target level of activity. Worse than that, older adults are even less likely to reach these recommendations, with only 42% of people between the ages of 65 and 74 and 28% of people age 75 or over meeting this goal.

Walking is a great choice for exercise, as it is low impact, convenient, free to do, and requires no special equipment. It is the most common kind of physical activity and is associated with a lower risk of heart disease and diabetes. While there are many studies that have focused on moderate to intense physical activity and mortality, there are considerably fewer studies looking at walking.

Company will use algorithm similar to new Go champ to find proteins.

I often hear the claim that death is a statistical certainty. This is my mathematical take at why this is not true, assuming the defeat of ageing, and no, being immortal is not required.

If a fully rejuvenated person was hit by a train at full speed, I can promise you they would stand the same pathetically low chances of ever being reassembled into a single, barely functional piece as any non-rejuvenated person of any age. Keeping that in mind, if anyone tried to sell me rejuvenation as ‘immortality’, rest assured I would demand to see the manager right away.

On a different yet unexpectedly related note, if I had a nickel for every time I heard or read something along the lines of ‘death is inevitable because probability’, I could donate so much money to LEAF the IRS would start thinking they’re a bit too well off for a charity.

Continue reading “Mathematics, rejuvenation, and immortality walk into a bar…” »

Whenever the topic of increasing human lifespan is discussed the concern is sometimes raised that a longer life would mean a life spent frail and decrepit. This is sometimes known as the Tithonus error and shows a fundamental misunderstanding of the aims of rejuvenation biotechnology. The concern is based on the ancient Greek myth of Tithonus which might be thought of as a cautionary tale warning seekers of an eternal life of its alleged inherent dangers.

This is the second part of our ongoing series of articles that discuss the Hallmarks of Aging. Published in 2013, the paper divides aging into a number of distinct categories (“hallmarks”) of damage to explain how the aging process works and how it causes age-related diseases[1].

Today, we will be looking at one of the primary hallmarks, epigenetic alterations.

Describes the epigenetic role in aging, cancer and disease as well as drugs that are targeting the epigenome.

Our epigenome plays a role in aging and also in diseases like cancer and diabetes. Scientists have developed epigenome-targeting cancer drugs.