More than a decade ago, Dr. Matthew Hebb was treating patients with Parkinson’s disease using deep brain stimulation by implanting tiny electrodes into the brain and delivering electrical signals to control tremors. He wondered if the same basic technology could be used against brain cancer.

Hebb, a neurosurgery professor at Western University’s Schulich School of Medicine & Dentistry, took tumor samples removed during surgery back to his laboratory, implanted electrodes and stimulated the cancer cells. The tumors responded.

That unexpected observation set in motion years of research into what is now called Intratumoral Modulation Therapy, or IMT—an original approach that uses low-amplitude electric fields to disrupt the growth of glioblastoma, one of the most aggressive and difficult-to-treat brain cancers.

For decades, neuroscientists have been trying to determine whether different neuropsychiatric conditions are linked to specific variations in brain structure and neural connections. While past studies identified possible signatures of various conditions, most findings have been inconsistent and do not conclusively delineate brain structural patterns associated with specific mental health disorders.

Researchers at Monash University in Australia and other institutions analyzed thousands of brain scans collected in earlier studies to better understand the reasons for these observed inconsistencies. Their findings, published in Nature Neuroscience, suggest that many widely used experimental designs and tools might fail to reliably capture the subtle differences in brain structure linked with distinct psychiatric disorders.

“Mental illnesses account for one-third of the world’s leading causes of disability and affect nearly half the adult population,” Trang Cao, first author of the paper, told Medical Xpress.

Gliomas are malignant brain tumors that originate from glial cells, which do not produce electrical impulses like neurons but instead support neurons by maintaining their structure and function. They are the most common form of brain cancer in adults and hijack normal neuronal signaling, especially the protein neuroligin-3 (NLGN3), released by active nerve cells, to fuel their own growth and spread into healthy brain tissue. Researchers wanted to uncover how NLGN3 interacts with glioma cells and healthy OPCs, and the role it normally plays in healthy brain cells.

The researchers isolated the outer membranes of brain cancer cells from pediatric and adult patients, extracted their proteins and passed them through a laboratory column containing purified NLGN3 to see which proteins stuck to it.

They discovered that NLGN3 binds directly to a cell-surface receptor protein called CSPG4 (also known as NG2) on both brain cancer cells and healthy oligodendrocyte precursor cells (OPCs), which eventually develop into oligodendrocytes that produce the fatty myelin sheath insulating nerve fibers.

In the race for new ways to treat Alzheimer’s and other devastating neurologic diseases, the protein tau has become a tantalizing target for drug developers. A new study lends support to those efforts by describing a previously unknown role that tau plays in neurodegeneration — and suggesting a novel way researchers might block the protein’s activity.

A team led by Stanford scientists found that tau can gum up the works of a cell’s mitochondria, its energy-producing powerhouse. The protein sends electrons flowing in the opposite direction of their usual microscopic relay race, a reversal that generates reactive oxygen species, cellular stress, and inflammation. Scientists found that blocking this phenomenon, known as reverse electron transport, reversed many of the harmful effects and improved learning and memory in flies and mice.

Whether the same will hold true in people is for now unclear, though an analysis of human cells grown in the lab and patient brain tissue suggests blocking the retrograde flow of electrons could make neurons healthier. Two of the study’s authors have started a biotech startup to put this idea to the test.

Most neuroscience research still runs on mice, even though much of what applies to mice does not hold up in humans. Marmosets have emerged as a bridge between species. However, comparing the brains of mice and marmosets runs into a chicken-and-egg problem. Scientists need to know which part of one brain matches the respective region of the other, but almost every brain map draws those areas differently.

For a new study published in Communications Biology, Cold Spring Harbor Laboratory Professor Partha Mitra and colleagues built the first cross-species map to systematically link mouse and marmoset brain regions.

“It’s the kind of problem that nobody wants to address, because it’s hard,” Mitra says. Comparing genomes across species is relatively straightforward. DNA aligns letter by letter. But brain circuits vary even within one species. Compounding the problem, research teams have built different brain atlases that divide the same mouse brain differently.