Tiny, ant-inspired magnetic microbots are capable of scaling obstacles, transporting heavy loads, and redefining medical technology.
The standard medication levodopa does not always work against tremors in Parkinson’s disease, especially in stressful situations. Propranolol, however, does work during stress, providing insight into the role of the stress system in tremors. MRI scans reveal that propranolol directly inhibits activity in the brain circuit that controls tremors. Doctors may consider this medication when levodopa is ineffective.
People with Parkinson’s disease report that tremors worsen during stressful situations. “Tremors act as a sort of barometer for stress; you see this in all people with Parkinson’s,” says neurologist Rick Helmich from Radboud university medical center.
The commonly used drug levodopa usually helps with tremors, but it tends to be less effective during stress, when tremors are often at their worst. Helmich and his team wanted to investigate whether a medication targeting the stress system could help and how this effect of stress on tremors works in the brain. The work is published in the journal Annals of Neurology.
In a discovery that could redefine how we understand cellular resilience and adaptability, scientists at Scripps Research have unlocked the secret interactions between a primordial inorganic polymer of phosphate known as polyphosphate (polyP), and two basic building blocks of life: DNA and the element magnesium. These components formed clusters of tiny liquid droplets–also known as condensates–with flexible and adaptable structures.
PolyP and magnesium are involved in many biological processes. Thus, the findings could lead to new methods for tuning cellular responses, which could have impactful applications in translational medicine.
The ensuing study, published in Nature Communications on October 26, 2024, reveals a delicate “Goldilocks” zone—a specific magnesium concentration range—where DNA wraps around polyP-magnesium ion condensates. Similar to a thin eggshell covering a liquid-like interior, this seemingly simple structure may help cells organize and protect their genetic material.
Researchers from Helmholtz Munich and Ludwig-Maximilians-Universität (LMU) have identified a mechanism that may explain the neurological symptoms of long COVID.
The study shows that the SARS-CoV-2 spike protein remains in the brain’s protective layers, the meninges, and the skull’s bone marrow for up to four years after infection. This persistent presence of the spike protein could trigger chronic inflammation in affected individuals and increase the risk of neurodegenerative diseases.
The team, led by Prof. Ali Ertürk, Director at the Institute for Intelligent Biotechnologies at Helmholtz Munich, also found that mRNA COVID-19 vaccines significantly reduce the accumulation of the spike protein in the brain. However, the persistence of spike protein after infection in the skull and meninges offers a target for new therapeutic strategies.
But when, where and how that could come to pass is hard to predict — in part, some researchers say, because of guardrails the federal government has placed around gain-of-function research.
The term describes experiments that seek to understand a virus’ potential to adapt to new hosts, spread more easily, survive longer in the environment and cause those infected to become sicker. Though many scientists view the approach as a critical tool for conducting biological research, other experts have long complained that it’s unacceptably risky — a reputation exacerbated by persistent speculation that the virus responsible for the COVID-19 pandemic was created in gain-of-function experiments in a laboratory in Wuhan, China.
Energy-efficient AI module for wearables, medical devices, and activity recognition.
Ambient Scientific has unveiled its new AI module, the Sparsh board, which operates on a coin cell battery, making it suitable for a wide array of on-device AI applications.
The module aims to offer solutions for tasks such as human activity recognition, voice control, and acoustic event detection.
Continue reading “AI module capable of months-long operation on coin cell battery unveiled” »
Objective To analyze mortality attributed to Alzheimer’s disease among taxi drivers and ambulance drivers, occupations that demand frequent spatial and navigational processing, compared with other occupations.
Design Population based cross-sectional study.
Setting Use of death certificates from the National Vital Statistics System in the United States, which were linked to occupation, 1 January 2020–31 December 2022.
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Sometimes pain is a necessary warning signal; for example, if we touch something very hot and it burns, we know to move our hand away. But chronic pain can destroy a person’s quality of life, and it can be extremely challenging to get relief. Some researchers have been searching for ways to deactivate pain receptors, so the body no longer feels the neural signals of chronic pain. Using mouse models of acute inflammatory pain, scientists have shown that it is possible to deactivate pain receptors with genetic engineering tools. The work has been reported in Cell.
“What we have developed is potentially a gene therapy approach for chronic pain,” said senior study author Bryan L. Roth, MD, PhD, a distinguished professor at the University of North Carolina (UNC) School of Medicine, among other appointments. “The idea is that we could deliver this chemogenetic tool through a virus to the neurons that sense the pain. Then, you could just take an inert pill and turn those neurons off, and the pain will literally disappear.”
What causes autism? It isn’t vaccines, studies show. Here are some possibilities that researchers are exploring.
There is no one factor that causes autism — or explains its growing prevalence. Researchers are seeking explanations for the surge. Here are some possibilities.
