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A Common Sleeping Pill May Reduce Buildup of Alzheimer’s Proteins, Study Reveals

There’s still so much we don’t know about Alzheimer’s disease, but the link between poor sleep and worsening disease is one that researchers are exploring with gusto.

A study published in 2023 found that using sleeping pills to get some shut-eye could reduce the buildup of toxic clumps of proteins in fluid that washes the brain clean every night.

People who took suvorexant, a common treatment for insomnia, for two nights at a sleep clinic experienced a slight drop in amyloid-beta and tau, two proteins that pile up in Alzheimer’s disease.

Engineering a Mechanoresponsive DNA Origami Capsule for Drug Delivery to Narrowed ArteriesClick to copy article linkArticle link copied!

Omer et al. design a DNA origami box with a lid held closed by an elastic single-stranded DNA spring. The box may selectively open in blood vessels with pathological levels of shear flow, facilitating drug delivery to sites of thrombosis while minimizing off-target toxicity. It should be noted that this paper focused entirely on the box’s design and mechanical validation (via optical tweezers) and did not perform any experiments to show drug delivery. Nonetheless, this is a good start and I’m glad to see people thinking about DNA origami for therapeutic applications. [ https://pubs.acs.org/doi/10.1021/acs.nanolett.5c04066](https://pubs.acs.org/doi/10.1021/acs.nanolett.5c04066)

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Once Thought To Support Neurons, Astrocytes Turn Out To Be in Charge

Misha Ahrens’ team at Janelia Research Campus placed zebra fish in virtual reality where swimming produced no progress. Normally, fish give up after ~20 seconds. The researchers found astrocytes were “counting” swim attempts via accumulating calcium. When calcium reached a threshold, astrocytes released adenosine to suppress swimming circuits. When researchers disabled astrocytes with a laser, the fish never stopped swimming; when they artificially activated astrocytes, the fish stopped immediately. This showed astrocytes actively mediate the transition from hope to hopelessness.

Marc Freeman’s lab showed norepinephrine doesn’t just activate astrocytes—it changes their “hearing.” At low norepinephrine (low arousal), astrocytes ignore synaptic activity. At high norepinephrine (high arousal), astrocytes suddenly “listen” to every synapse and modulate neuronal response accordingly. This creates a dynamic gain control system layered atop neuronal networks.

“We did expect that, in large part, the effect of norepinephrine on synapses would be mediated by astrocytes,” Papouin said. “But we did not expect all of it to be!”

The finding of parallel molecular pathways in such distinct species as fruit flies, zebra fish, and mice points to “an evolutionarily conserved way in which astrocytes can profoundly affect neural circuits,” Freeman said.

The results suggest a gaping hole in previous theories of neuromodulation. “In the past, neuroscientists studied neuromodulators and knew they were important in regulating neural circuit function, but none of their thinking, none of their diagrams, none of their models had anything in them other than neurons,” Fields said. “Now we see that they missed a big part of the story.”

Insect salivary effectors disrupt PIEZO1-centric mechanoimmunity against piercing-sucking vectors

Huang et al. identify the mechanosensitive channel PIEZO1 as a plant immune hub that decodes insect-feeding-derived mechanical forces and Ca2+-activated defense responses. They characterize a self-amplifying immune circuit and identify that Bsp9, an evolutionarily conserved insect salivary effector, subverts this pathway. This work provides a framework for engineering plant disease resistance.

Signature in blood to better predict type 2 diabetes risk

The metabolites associated with type 2 diabetes were also found to be genetically linked to clinical traits and tissue types that are relevant to the disease. Furthermore, the team developed a unique signature of 44 metabolites that improved prediction of future risk of type 2 diabetes. ScienceMission sciencenewshighlights.

Diabetes, a metabolic disease, is on the rise worldwide, and over 90 percent of cases are type 2 diabetes, where the body does not effectively respond to insulin. Researchers identified metabolites (small molecules found in blood generated through metabolism associated with risk of developing type 2 diabetes in the future and revealed genetic and lifestyle factors that may influence these metabolites. They also developed a metabolomic signature that predicts future risk of type 2 diabetes beyond traditional risk factors. Their results are published in Nature Medicine.

In this study, researchers tracked 23,634 individuals with diverse ethnic backgrounds across 10 prospective cohorts with up to 26 years of follow-up. These individuals were initially free of type 2 diabetes. The team analyzed 469 metabolites in blood samples, as well as genetic, diet, and lifestyle data, to see how they relate to risk of developing type 2 diabetes. Of the metabolites examined, 235 were found to be associated with a higher or lower risk of developing type 2 diabetes, 67 of which were new discoveries.

“Interestingly, we found that diet and lifestyle factors may have a stronger influence on metabolites linked to type 2 diabetes than on metabolites not associated with the disease,” said first and co-corresponding author. “This is especially true for obesity, physical activity, and intake of certain foods and beverages such as red meat, vegetables, sugary drinks, and coffee or tea. Increasing evidence suggests that these dietary and lifestyle factors are associated with greater or lower risk of type 2 diabetes. Our study revealed that specific metabolites may act as potential mediators, linking these factors with type 2 diabetes risk.”

The world’s longest underwater high-speed train is now in progress, set to link two continents beneath the sea

On a foggy morning off the coast of Finland, the sea looks perfectly ordinary. A few fishing boats, a cargo ship on the horizon, the low hum of engines and gulls complaining overhead. Yet under that flat grey surface, survey vessels are tracing invisible lines, mapping the seabed for something that sounds like science fiction: a high‑speed train that will dive under the Baltic and emerge on another continent.

On deck, an engineer in a neon jacket points to the radar screen like someone tracing the outline of a new city. He talks about boring through rock, laying tracks where only fish and submarines have passed. His words hang in the cold air.

Soon, a train will cross here faster than most people cross a city.

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