A new study reveals that mitochondrial dysfunction plays a central role in the loss of Purkinje neurons in the cerebellum, contributing to motor impairments in people with multiple sclerosis (MS).

The brain is constantly mapping the external world like a GPS, even when we don’t know about it. This activity comes in the form of tiny electrical signals sent between neurons—specialized cells that communicate with one another to help us think, move, remember and feel. These signals often follow rhythmic patterns known as brain waves, such as slower theta waves and faster gamma waves, which help organize how the brain processes information.

Understanding how individual neurons respond to these rhythms is key to unlocking how the brain functions related to navigation in real time—and how it may be affected in disease.

A new study by Florida Atlantic University and collaborators from Erasmus Medical Center, Rotterdam, Netherlands, and the University of Amsterdam, Netherlands, has uncovered a surprising ability of brain cells in the hippocampus to process and encode and respond to information from multiple brain rhythms at once.

Huntington’s disease has long defied attempts to rescue suffering neurons. A new study in Cell Reports shows that transplanting healthy human glial progenitor cells into the brains of adult animal models of the disease not only slowed motor and cognitive decline but also extended lifespan. These findings shift our understanding of Huntington’s pathology and open a potential path to cell-based therapies in adults already showing symptoms.

“Glia are essential caretakers of neurons,” said Steve Goldman, MD, Ph.D., co-director of the University of Rochester Center for Translational Neuromedicine and lead author of the study.

“The restoration of healthy glial support—even after symptoms begin—could reset neuronal gene expression, stabilize synaptic function, and meaningfully delay disease progression. This study shifts the perspective on Huntington’s from a neuron-centric view to one that shows a critical role for glial pathology in driving synaptic dysfunction. It also tells us that the adult brain still has the capacity for repair when you target the right cells.”

Researchers at Karolinska Institutet and Lund University in Sweden have identified a new treatment strategy for neuroblastoma, an aggressive form of childhood cancer. By combining two antioxidant enzyme inhibitors, they have converted cancer cells in mice into healthy nerve cells.

The study, “Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment,” is published in the journal Proceedings of the National Academy of Sciences.

Neuroblastoma is a type of childhood cancer that affects the nervous system and is the leading cause of cancer-related death in young children. Some patients have a good prognosis, but those with metastatic tumors often cannot be cured despite modern combinations of surgery, radiation, chemotherapy and immunotherapy.