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Smart Brain Implants Can Now Adapt to Optimize Parkinson’s Treatment

Although the brain is our most complex organ, the ways to treat it have historically been rather simple.

Typically, surgeons lesioned (damaged) a structure or a pathway in the hope that this would “correct the imbalance” that led to the disease. Candidate structures for lesioning were usually found by trial and error, serendipity or experiments in animals.

While performing one such surgery in 1987, French neurosurgeon Alim-Louis Benabid noticed that the electrical stimulation he performed to locate the right spot to lesion had effects similar to the lesion itself.

How marine snail venom can improve medicines

Scientists are finding clues for how to treat diabetes and hormone disorders in an unexpected place: a toxin from one of the most venomous animals on the planet.

An international research team led by University of Utah scientists has identified a component within the venom of a predatory marine cone snail, the geography cone, that mimics a human hormone called somatostatin, which regulates the levels of blood sugar and various hormones in the body. The hormone-like toxin’s specific, long-lasting effects, which help the snail hunt its prey, could also help scientists design better drugs for people with diabetes or hormone disorders, conditions that can be serious and sometimes fatal.


New research explores how one venom mimics a human hormone that regulates blood sugar, which could lead to better treatment for diabetes.

Spinal fluid biomarker offers early and accurate Parkinson’s disease diagnosis

Parkinson’s disease is a neurodegenerative disorder that is usually diagnosed in its late stage on the basis of clinical symptoms, mainly motor disorders. By this point, however, the brain is already severely and irreparably damaged. Moreover, diagnosis is difficult and often incorrect because the disease takes many forms, and symptoms overlap with other disorders.

Researchers from the PRODI Center for Protein Diagnostics at Ruhr University Bochum, Germany, and the biotech company betaSENSE have now discovered a biomarker in the that facilitates a reliable diagnosis at an early stage and can shed light on the progression of the disease and the effect of a therapy. They report their findings in the journal EMBO Molecular Medicine from April 25, 2025.

How experience shapes hippocampal place cell activity to create flexible cognitive maps

The mammalian brain is known to produce mental representations of the spatial environment, known as cognitive maps, that help humans and animals navigate their surroundings. A subpopulation of neurons in the CA1 area of the hippocampus, which are referred to as place cells (PCs), have been found to become active when animals visit specific places or locations in their environment.

The activation of these cells was previously linked to the encoding of space-and goal-related information, which was predicted to support the creation of cognitive maps. While numerous past studies explored the function of PCs and their contribution to the creation of cognitive maps, the role of experience in shaping the creation of these maps has not yet been elucidated.

Researchers at Baylor College of Medicine recently shed new light on the mechanisms through which experience could influence the encoding of information by PCs. Their findings, published in Nature Neuroscience, suggest that experiences produce an adjustment of synaptic input in the , which in turn affects the activity of PCs, enabling the production of flexible cognitive maps.

Serotonin system’s hidden complexity may reshape understanding of day-to-day decision making

Our lives are filled with binary decisions—choices between one of two alternatives. But what’s really happening inside our brains when we engage in this kind of decision making?

A University of Ottawa Faculty of Medicine-led study published in Nature Neuroscience sheds new light on these big questions, illuminating a general principle of neural processing in a mysterious region of the midbrain that is the very origin of our central serotonin (5-HT) system, a key part of the nervous system involved in a remarkable range of cognitive and behavioral functions.

“The current dominating model is that individual 5-HT neurons are acting independently from one another. While it had previously been suggested that 5-HT neurons may rather be connected with one another, it had not been directly demonstrated. That is what we did here. We also identify an intriguing processing role—or a computation—that is supported by this particular type of connectivity between 5-HT neurons,” says Dr. Jean-Claude Béïque, full professor in the Faculty’s Department of Cellular and Molecular Medicine and co-director of the uOttawa Brain and Mind Research Institute’s Centre for Neural Dynamics and Artificial Intelligence.

Rare lung immune cells act as peacekeepers against deadly COVID-19 inflammation

A rare cell type in the lungs is essential to survival from the COVID-19 virus, a new study shows.

Experiments in mice infected with the SARS-CoV-2 virus revealed that the immune cell class in question, called nerve and airway-associated interstitial macrophages, or NAMs, may keep the human immune system’s initial counterattack on the virus () from spiraling out of control to endanger patients.

Macrophages are known to be the first responders to infection, as large capable of devouring invading viruses and the cells they infect.

First in 45 Years: Scientists Discover New Subtype of Castleman Disease

The discovery broadens the known spectrum of this rare disorder, emphasizing the critical role of collaboration with patient advocates. A newly discovered subtype of Castleman disease promises to improve diagnosis and treatment for thousands of patients who have not fit neatly into existing class

Cancer cells avoid ferroptosis induced by immune cells via fatty acid binding proteins

Cancer creates an immunosuppressive environment that hampers immune responses, allowing tumors to grow and resist therapy. One way the immune system fights back is by inducing ferroptosis, a type of cell death, in tumor cells through CD8 + T cells. This involves lipid peroxidation and enzymes like lysophosphatidylcholine acyltransferase 3 (Lpcat3), which makes cells more prone to ferroptosis. However, the mechanisms by which cancer cells avoid immunotherapy-mediated ferroptosis are unclear. Our study reveals how cancer cells evade ferroptosis and anti-tumor immunity through the upregulation of fatty acid-binding protein 7 (Fabp7).

To explore how cancer cells resist immune cell-mediated ferroptosis, we used a comprehensive range of techniques. We worked with cell lines including PD1-sensitive, PD1-resistant, B16F10, and QPP7 glioblastoma cells, and conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora deletion specifically in CD8+ T cells, Cd8 cre; Rorafl mice. Methods included mass spectrometry-based lipidomics, targeted lipidomics, Oil Red O staining, Seahorse analysis, quantitative PCR, immunohistochemistry, PPARγ transcription factor assays, ChIP-seq, untargeted lipidomic analysis, ROS assay, ex vivo co-culture of CD8+ T cells with cancer cells, ATAC-seq, RNA-seq, Western blotting, co-immunoprecipitation assay, flow cytometry and Imaging Mass Cytometry.

PD1-resistant tumors upregulate Fabp7, driving protective metabolic changes that shield cells from ferroptosis and evade anti-tumor immunity. Fabp7 decreases the transcription of ferroptosis-inducing genes like Lpcat3 and increases the transcription of ferroptosis-protective genes such as Bmal1 through epigenetic reprogramming. Lipidomic profiling revealed that Fabp7 increases triglycerides and monounsaturated fatty acids (MUFAs), which impede lipid peroxidation and ROS generation. Fabp7 also improves mitochondrial function and fatty acid oxidation (FAO), enhancing cancer cell survival. Furthermore, cancer cells increase Fabp7 expression in CD8+ T cells, disrupting circadian clock gene expression and triggering apoptosis through p53 stabilization. Clinical trial data revealed that higher FABP7 expression correlates with poorer overall survival and progression-free survival in patients undergoing immunotherapy.