New research shows that individuals with higher cognitive ability have stronger, more flexible synchronization of brain rhythms—specifically theta waves—in the midfrontal region during mentally demanding tasks.

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.
Scientists at UCLA and the University of Toronto have developed an advanced computational tool, called moPepGen, that helps identify previously invisible genetic mutations in proteins, unlocking new possibilities in cancer research and beyond.
The tool, described in Nature Biotechnology, will help understand how changes in our DNA affect proteins and ultimately contribute to cancer, neurodegenerative diseases, and other conditions. It provides a new way to create diagnostic tests and to find treatment targets previously invisible to researchers.
Proteogenomics combines the study of genomics and proteomics to provide a comprehensive molecular profile of diseases. However, a major challenge has been the inability to accurately detect variant peptides, limiting the ability to identify genetic mutations at the protein level. Existing proteomic tools often fail to capture the full diversity of protein variations.
Scientists are looking at ways to tackle Alzheimer’s and dementia from all kinds of angles, and a new study has identified the molecule hevin (or SPARCL-1) as a potential way of preventing cognitive decline.
Hevin is a protein naturally produced in the brain by cells called astrocytes. These support-worker cells look after the connections or synapses between neurons, and it’s thought that hevin plays a role in this essential work.
In this new study, researchers from the Federal University of Rio de Janeiro (UFRJ) and the University of São Paulo in Brazil boosted hevin production in the brains of both healthy mice and those with an Alzheimer’s-like disease.
You stayed up too late scrolling through your phone, answering emails or watching just one more episode. The next morning, you feel groggy and irritable. That sugary pastry or greasy breakfast sandwich suddenly looks more appealing than your usual yogurt and berries. By the afternoon, chips or candy from the break room call your name. This isn’t just about willpower. Your brain, short on rest, is nudging you toward quick, high-calorie fixes.
There is a reason why this cycle repeats itself so predictably. Research shows that insufficient sleep disrupts hunger signals, weakens self-control, impairs glucose metabolism and increases your risk of weight gain. These changes can occur rapidly, even after a single night of poor sleep, and can become more harmful over time if left unaddressed.
I am a neurologist specializing in sleep science and its impact on health.