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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 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.

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.

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.

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.

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.

Editor’s note: This story has been updated to clarify the type of trees affected by Phanerochaete velutina.

A species of wood-eating fungus didn’t need a brain to pass a cognitive test with flying colors, and researchers say this first-of-its-kind discovery could have broader implications for understanding consciousness and intelligence in a variety of life forms.

A team of researchers at Japan’s Tohoku University, led by Yu Fukasawa, associate professor in the Graduate School of Agricultural Science, set out to determine whether fungi could recognize shapes. Their study, published in the journal Fungal Ecology in October, found evidence that these bottom feeders possess memory and decision-making abilities despite not having a central nervous system.

Cytomegalovirus (CMV), which causes a cold-like illness, can be spread in the same way as other viruses from person to person through body fluids such as blood, saliva and urine.

But the infection is present in up to 45 per cent of Alzheimer’s cases, US scientists have claimed.

Some people exposed to the bug may develop a chronic intestinal infection, allowing it to enter the bloodstream and travel to the brain.

Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder associated with a progressive decline in memory and mental abilities, which can significantly hinder people’s ability to complete daily tasks. Past studies found that patients diagnosed with AD, as well as some other neurodegenerative disorders, exhibit an abnormal accumulation of tau protein in their neurons.

Tau protein is a microtubule-associated protein (MAP) known to stabilize the internal structure of neurons, binding to microtubules. These are microscopic tubular structures that support the transport of nutrients, proteins and other vital molecules within individual neurons or other cells.

Recent findings suggest that tau proteins interact with extracellular vesicles (EVs), small membrane-bound particles secreted by cells that carry molecules and deliver them to other cells. While the research hints at a connection between these vesicles and tau proteins in AD, the link between the two is not yet fully understood.