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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.

This innovation is notable for its ability to function continuously for months without frequent battery replacements.

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.”

Researchers with the Advanced Science Research Center at the CUNY Graduate Center (CUNY ASRC) have unveiled a critical mechanism that links cellular stress in the brain to the progression of Alzheimer’s disease (AD).

The study, published in the journal Neuron, highlights microglia, the brain’s primary immune cells, as central players in both the protective and harmful responses associated with the disease.

Microglia, often dubbed the brain’s first responders, are now recognized as a significant causal cell type in Alzheimer’s pathology. However, these cells play a double-edged role: some protect brain health, while others worsen neurodegeneration.

Whenever a sink overflows, the flooding is usually caused by a blockage that has built up in the drains. Similarly, as we age, our bodies are flooded by aging, or senescent cells, which have stopped dividing but, instead of dying, remain active and build up in body tissues. Recent studies have shown that getting rid of these cells might delay age-related diseases, reduce inflammation and extend lives. Despite the great potential, however, there is currently no drug that can target these cells directly and efficiently.

Now, Weizmann Institute of Science researchers suggest an alternative approach. In a new study published in Nature Cell Biology, they reveal that build up in the body by clogging up the immune system, thereby preventing their own removal.

The scientists demonstrated in mice how to unclog this blockage using immunotherapy, the new generation of treatments that is revolutionizing . These findings could pave the way for innovative treatment of age-related diseases and other chronic disorders.

Here’s one definition of science: it’s essentially an iterative process of building models with ever-greater explanatory power.

A model is just an approximation or simplification of how we think the world works. In the past, these models could be very simple, as simple in fact as a mathematical formula. But over time, they have evolved and scientists have built increasingly sophisticated simulations of the world as new data has become available.

A computer model of the Earth’s climate can show us temperatures will rise as we continue to release greenhouse gases into the atmosphere. Models can also predict how infectious disease will spread in a population, for example.