Lifeboat Foundation

The lethargy that many Alzheimer’s patients experience is caused not by a lack of sleep, but rather by the degeneration of a type of neuron that keeps us awake, according to a study that also confirms the tau protein is behind that neurodegeneration.

The study’s findings contradict the common notion that Alzheimer’s patients sleep during the day to make up for a bad night of sleep and point toward potential therapies to help these patients feel more awake.

The data came from study participants who were patients at UC San Francisco’s Memory and Aging Center and volunteered to have their sleep monitored with electroencephalogram (EEG) and donate their brains after they died.

Continuously evolved double-stranded DNA deaminases increase the efficiency and targeting scope of all-protein base editors.

To effectively interact with humans in crowded social settings, such as malls, hospitals, and other public spaces, robots should be able to actively participate in both group and one-to-one interactions. Most existing robots, however, have been found to perform much better when communicating with individual users than with groups of conversing humans.

Hooman Hedayati and Daniel Szafir, two researchers at University of North Carolina at Chapel Hill, have recently developed a new data-driven technique that could improve how robots communicate with groups of humans. This method, presented in a paper presented at the 2022 ACM/IEEE International Conference on Human-Robot Interaction (HRI ‘22), allows robots to predict the positions of humans in conversational groups, so that they do not mistakenly ignore a person when their sensors are fully or partly obstructed.

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A new tool speeds up development of vaccines and other pharmaceutical products by more than 1 million times while minimizing costs.

In search of pharmaceutical agents such as new vaccines, industry will routinely scan thousands of related candidate molecules. A novel technique allows this to take place on the nano scale, minimizing use of materials and energy. The work is published in the journal Nature Chemistry.

More than 40,000 molecules can be synthesized and analyzed within an area smaller than a pinhead. The method, developed through a highly interdisciplinary research effort in Denmark, promises to drastically reduce the amounts of material, energy, and economic cost for pharmaceutical companies.

Remember He Jiankui, the Chinese scientist who shocked the world when it emerged in late 2018 that he had used CRISPR to tinker with the genetic code of IVF embryos, leading to the birth of twins who are likely the world’s first genetically modified humans?

The news led to a broad outcry among scientists, ethicists and regulators, not the least because experts in the field later found the experiment to be tainted by “egregious scientific and ethical lapses.”

Long story shot, China ended up imprisoning He, who also lost his research position at the Southern University of Science and Technology in China — but now MIT Technology Review, which first broke the news of the experiment back in 2018, reports that he’s out of prison and even answered his cell phone for a brief call.

Revolutionary tool will meet future pandemics with accelerated response.

A new tool speeds up development of vaccines and other pharmaceutical products by more than one million times while minimizing costs.

In search of pharmaceutical agents such as new vaccines, industry will routinely scan thousands of related candidate molecules. A novel technique allows this to take place on the nano scale, minimizing use of materials and energy. The work is published in the prestigious journal Nature Chemistry.

Scientists at The University of Texas at Austin have redesigned a key component of a widely used CRISPR-based gene-editing tool, called Cas9, to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version, making it potentially much safer.

Other labs have redesigned Cas9 to reduce off-target interactions, but so far, all these versions improve accuracy by sacrificing speed. SuperFi-Cas9, as this new version has been dubbed, is 4,000 times less likely to cut off-target sites but just as fast as naturally occurring Cas9. Bravo says you can think of the different lab-generated versions of Cas9 as different models of self-driving cars. Most models are really safe, but they have a top speed of 10 miles per hour.

“They’re safer than the naturally occurring Cas9, but it comes at a big cost: They’re going extremely slowly,” said Bravo. “SuperFi-Cas9 is like a self-driving car that has been engineered to be extremely safe, but it can still go at full speed.”

Macrophages travel through our arteries, gobbling fat the way Pac-man gobbled ghosts. But fat-filled macrophages can narrow blood vessels and cause heart disease. Now, UConn Health researchers describe in Nature Cardiovascular Research how deleting a protein could prevent this and potentially prevent heart attacks and strokes in humans.

Macrophages are large white blood cells that cruise through our body as a kind of clean-up crew, clearing hazardous debris. But in people with atherosclerosis—fatty deposits and inflammation in their blood vessels— macrophages can cause trouble. They eat excess fat inside artery walls, but that fat causes them to become foamy. And foamy macrophages tend to encourage inflammation in the arteries and sometimes bust apart plaques, freeing clots that can cause heart attack, stroke, or embolisms elsewhere in the body.

Changing how macrophages express a certain protein could prevent that kind of bad behavior, reports a team of researchers from UConn Health. They found that the protein, called TRPM2, is activated by inflammation. It signals macrophages to start eating fat. Since inflammation of the blood vessels is one of the primary causes of atherosclerosis, TRPM2 gets activated quite a bit. All that TRPM2 activation pushes macrophage activity, which leads to more foamy macrophages and potentially more inflamed arteries. The way that TRPM2 activated macrophage activity was surprising, says Lixia Yue, a UConn School of Medicine cell biologist.

Some diabetes therapies work by ramping up the body’s secretion of insulin to counteract high blood sugar levels. | Preserving insulin-producing pancreatic beta cells—rather than exhausting them—might be a better strategy in the treatment of diabetes. Following that thinking, scientists at the Karolinska Institute found a cancer drug by Seagen holds promise for the metabolic disease.