Lifeboat Foundation

Researchers at the Stanford University School of Medicine report in a new study that they found a way to help rats recover neurons in the brain’s center of learning and memory. They accomplished the feat by blocking a molecule that controls how efficiently genetic instructions are used to build proteins.

If the approach described in the study can be applied to humans, it may one day help patients who’ve suffered a stroke, cardiac arrest or major blood loss and are thus at higher risk of memory loss.

In the study, to be published online Aug. 19 in eNeuro, researchers induced extremely low blood pressure—as would happen when the heart stops beating—in rats. These rats lost neurons in a specific region of the hippocampus critical to learning and memory, but the researchers improved the animals’ recovery of the cells by injecting a molecule that blocks a microRNA: a short molecule that tweaks gene activation by preventing the conversion of genetic blueprints into proteins. Interestingly, the scientists found that a microRNA blockade potentially causes astrocytes—cells that support neurons and make up 50% of the cells in the brain—to turn into neurons.

Each Cyclops had a single eye because, legend has it, the mythical giants traded the other one with the god Hades in return for the ability to see into the future. But Hades tricked them: the only vision the Cyclopes were shown was the day they would die. They carried this knowledge through their lives as a burden—the unending torture of being forewarned and yet having no ability to do anything about it.

Since ancient times, aging has been viewed as simply inevitable, unstoppable, nature’s way. “Natural causes” have long been blamed for deaths among the old, even if they died of a recognized pathological condition. The medical writer Galen argued back in the second century AD that aging is a natural process.

His view, the acceptance that one can die simply of old age, has dominated ever since. We think of aging as the accumulation of all the other conditions that get more common as we get older—cancer, dementia, physical frailty. All that tells us, though, is that we’re going to sicken and die; it doesn’t give us a way to change it. We don’t have much more control over our destiny than a Cyclops.

Study finds that Alzheimer’s damage allows toxins to enter the brain, further harming neurons.

Today, we’re offering another discussion from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Today, we’re offering another talk from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Continue reading “Ronald Kohanski at Ending Age-Related Diseases 2019” »

Great discuss of time travel by Dr. Brain greene.

Machine interfaces today can link up brains to play tetris together. Like it’s not hard enough to find a place for the L-shaped block without another cerebrum trying to overrule you.

Let’s go farther: What if we could create a digital replica of your brain and upload and download it like a piece of software?

This feat, aka whole brain emulation (WBE), is still decades, perhaps more than a century away. Outside of the pure science challenge, it could make us confront some of the most daunting questions about what it means to be human, and where man ends and machine begins.

No one needs intelligence more than the military. That’s why the U.S. armed forces and intelligence services are working on a stunning array of pioneering brain development techniques that could one day make their way into civilian life. “The sophistication of our weapons and communications technologies in the Navy and elsewhere is growing dramatically,” says Harold Hawkins, a cognitive psychologist and the director of a program at the Office of Naval Research studying brain training. “To have intellectually stronger people to deal with these new systems is going to be critical.”

The Army, Navy and Air Force are all funding substantial research programs, but a $12 million program approved in January by the Intelligence Advanced Research Projects Activity (IARPA) is one of the largest. It will pay for the first year of a planned three-and-a-half-year program called Strengthening Human Adaptive Reasoning and Problem-solving (SHARP).

The SHARP program is studying techniques both ancient and avant-garde, from meditation to low-dose electrical stimulation of the brain, with an aim toward making intelligence analysts, well, more intelligent. Also on the drawing board are large-scale studies of computerized games that have shown promise in smaller studies for strengthening “working memory” — the critical-thinking ability to not simply remember facts and figures but to juggle and manipulate them. “If these interventions are actually doing what we think they’re doing,” says Adam Russell, a neuroscientist and the SHARP program’s manager at IARPA, “we should be able to demonstrate that with large numbers of participants, strong metrics and a real-world test battery.”

A team of scientists at UC San Francisco and the National Institutes of Health have achieved another CRISPR first, one which may fundamentally alter the way scientists study brain diseases.

In a paper published August 15 in the journal Neuron, the researchers describe a technique that uses a special version of CRISPR developed at UCSF to systematically alter the activity of genes in human neurons generated from stem cells, the first successful merger of stem cell-derived cell types and CRISPR screening technologies.

Though mutations and other genetic variants are known to be associated with an increased risk for many neurological diseases, technological bottlenecks have thwarted the efforts of scientists working to understand exactly how these genes cause disease.

Most people who’ve been jabbed by a needle know the drill: First the pierce, then the sharp, searing pain and an urge to pull away, or at least wince. While the exact circuitry behind this nearly universal reaction is not fully understood, scientists may have just found an important piece of the puzzle: a previously unknown sensory organ inside the skin.

Dubbed the nociceptive glio-neural complex, this structure is not quite like the typical picture of a complex organ like the heart or the spleen. Instead, it’s a simple organ made up of a network of cells called glial cells, which are already known to surround and support the body’s nerve cells. In this case, the glial cells form a mesh-like structure between the skin’s outer and inner layers, with filament-like protrusions that extend into the skin’s outer layer. (Also find out about a type of simple organ recently found in humans, called the interstitium.)

As the study team reports today in the journal Science, this humble organ seems to play a key role in the perception of mechanical pain—discomfort caused by pressure, pricking, and other impacts to the skin. Until now, individual cells called nociceptive fibers were thought to be the main starting points for this kind of pain.