The most important problem in medicine, and the case for acting now.
A new study from UC San Francisco shows how certain cells in the brain may cause aneurysms to weaken and rupture. It helps explain why some aneurysms burst while others do not and could lead to new ways of predicting and possibly preventing strokes.
Brain aneurysms are bulges in blood vessels that can go unnoticed for years. If they rupture, they can cause a severe and often deadly type of stroke. About one in 50 Americans has a brain aneurysm, but doctors still struggle to predict which ones are most dangerous.
The new study helps to unpack the biology behind these events by mapping the cells in artery walls and the interactions that weaken them.
A new approach for identifying signs of hidden awareness in people who cannot speak or move after severe brain injury has been demonstrated by researchers at the University of Bath in the U.K.
The system detects patterns of brain activity through a wearable headset using an advanced application of brain-computer interface (BCI) technology.
Across multiple experimental sessions, the researchers uncovered signs of consciousness that were previously undetected in unresponsive patients.
Research by the Barcelona Institute for Biomedical Research (IIBB), part of the Spanish National Research Council (CSIC), and the Institut de Recerca Sant Pau (IR Sant Pau) provides some of the first evidence that psychological therapies act as biological stimuli that induce molecular responses measurable through blood biomarkers.
The preliminary study, involving 22 patients with major depressive disorder at Hospital de Sant Pau, reveals that psychotherapy sessions trigger changes in microRNAs—molecules that regulate gene expression in cells—associated with significant improvements in the participants’ cognitive status. The results, published in Scientific Reports, represent an advance toward monitoring patients’ responses to pharmacological treatments and nonpharmacological therapeutic interventions.
The study, led by Dr. Maria J. Portella (IR Sant Pau) and Dr. Analia Bortolozzi (IIBB-CSIC), with Lluís Miquel-Rio (IIBB-CSIC) and Dr. Muriel Vicent-Gil (Hospital de Sant Pau) as first authors, focused on major depressive disorder (MDD). This condition is characterized not only by its effects on mood but also by a broad spectrum of cognitive impairments, including difficulties with attention, memory, processing speed and executive function. These symptoms frequently persist despite treatment and severely affect patients’ quality of life.
Studies of genetics conducted in yeast cells, human neurons, mice or other model systems often reveal networks of genes that could contribute to complex diseases, such as breast cancer, type 2 diabetes and Parkinson’s disease. But those findings don’t always translate to human biology. Human genetics offers a path to determining which genes among those networks are most relevant to human disease.
Researchers at Harvard Medical School have developed a new statistical framework to link networks identified in models with human genetic data. This could make it faster and easier for researchers to identify which groups of genes are most likely to contribute to a particular human disease, uncover rare disease-causing mutations and zero in on promising therapeutic targets.
The work was published in Cell Genomics.
Now, a new study conducted by researchers at Newcastle University and Technische Universität Dresden has used a new lithium MRI technique to reveal that brain lithium levels closely track blood concentrations throughout the day.
Understanding lithium tracking gaps in bipolar disorder
Bipolar disorder affects ~40 million people globally. The mental health condition is characterized by severe shifts in mood, energy, and activity levels. Patients navigate intense emotional states that alternate between mania and deep depression.
Researchers report encouraging early results from a first-in-human clinical trial led by Children’s National Hospital using a new T-cell immunotherapy for children and young adults with some of the deadliest brain tumors, including diffuse intrinsic pontine glioma (DIPG) and relapsed central nervous system (CNS) tumors. These findings, published in Nature Medicine, are particularly significant given the challenges of treating pediatric brain tumors, which remain the leading cause of cancer-related deaths in children. Immunotherapies have been shown to work in blood cancers but rarely succeed in solid tumors, especially brain tumors.
“This study represents an important step toward developing safer and more effective T-cell therapies for children with devastating brain cancers,” said Catherine Bollard, MBChB, MD, senior vice president and chief research officer at Children’s National, and co-senior author of the study. “Even in this early-stage trial focused on safety, we were encouraged to see lasting clinical benefit in several patients who otherwise had very few options.”
Mouse brain activity was used to recreate 10-second videos, offering a new way to study how vision is represented in the brain.
A compelling longitudinal study of over 350 older adults with early beta-amyloid accumulation reveals that the genetic risk for Alzheimer’s disease is not strictly deterministic, but is profoundly modulated by sleep quality through the AQP4 gene—a critical regulator of the brain’s glymphatic waste-clearance system. By cross-referencing specific AQP4 variants with multi-year MRI and PET imaging alongside cognitive assessments, researchers demonstrated that poor sleep parameters, such as shorter duration and delayed onset, significantly accelerate neurodegenerative markers like gray matter loss and ventricle expansion in carriers of specific risk alleles. Paradoxically, however, carriers of certain rare variants exhibited slower cognitive decline even in the presence of sleep disturbances. Ultimately, these findings illuminate a complex gene-environment interplay, proving that identical genetic predispositions can either expedite or buffer against brain atrophy depending on sleep architecture, thereby highlighting the critical necessity of personalized, sleep-targeted lifestyle interventions as a highly actionable strategy for Alzheimer’s prevention.
Scientists have discovered an important link between sleep, genetics, and Alzheimer’s disease. New findings suggest that getting poor sleep can accelerate brain shrinkage and memory loss in older adults carrying specific genetic variants.