Researchers have built a tiny, lightweight microscope that captures neuron activity with unprecedented speed that can be used in freely moving animals. The new tool could give scientists a more complete view of how brain cells process information during natural behavior.

The microscope is designed to image genetically encoded voltage indicators —fluorescent dyes that rapidly change brightness when a neuron fires—through a small window in the skull while the animal is awake.

“Unlike most miniature microscopes that track slower calcium signals, ours captures electrical spikes at hundreds of frames per second,” said Emily Gibson from the University of Colorado Anschutz Medical Campus. “This makes it possible to capture the moment a neuron fires as well as the quieter signals that build up inside neurons before firing.”

New research published in the journal eNeuro examined whether eliminating a protein that is elevated in the brains of those with Alzheimer’s could prevent or reduce damage and behavioral symptoms in a mouse model of Alzheimer’s disease.

“Previous work from our research team and others found evidence that a specific protein named Centaurin-α1 is involved in the progression of Alzheimer’s damage within neurons,” explained lead author of the study, Dr. Erzsebet Szatmari. “To confirm the role of this protein and see if it might be a good therapeutic target, we tested whether genetically removing it would prevent or slow disease progression in a mouse model of the disease.”

The scientists used a well-characterized model of Alzheimer’s disease in mice. The disease model (called J20) contains two genetic mutations associated with rare familial variants of Alzheimer’s disease. These animals develop changes in brain tissue and behavioral deficits characteristic of many symptoms seen in human Alzheimer’s disease, including neuroinflammation, accumulation of neuronal plaques, synapse loss, and impairments in spatial memory and learning.

A new study shows that children born preterm who are later diagnosed with autism often present with more extensive support needs and a higher number of co-occurring conditions than autistic children born at full term. Surprisingly, however, the researchers found no differences in genetic variants across the genome, nor in specific genes already linked to autism, between the groups—a result that contradicted their initial hypothesis.

The study was conducted at KIND (Center of Neurodevelopmental Disorders at Karolinska Institutet) and published in October 2025 in the journal Genome Medicine.

“We did not observe any genetic differences between preterm and full-term autistic children, which was unexpected. We initially thought that preterm children might show fewer of the genetic factors associated with autism, as their early birth can be viewed as an environmental factor,” says Yali Zhang, doctoral student at Tammimies research group at KIND and first author of the study.