Persistent pain often has no clear cause. However, studies show measurable differences in the structure and activity of the brains of those affected. This might explain why they experience chronic pain. “Many of our study participants were grateful that someone was taking their symptoms seriously and conducting research into them,” says neuroscientist Salome Häuselmann.
A working prototype that can see, remember and interact with the world like the human brain could one day underpin smart bionic eyes while using far less energy than today’s technologies. The invention from RMIT University combines sensing, memory and information processing within the same system, reducing the need to constantly move data between separate sensors, memory banks and processors.
While still an early-stage research demonstration, the neuromorphic vision innovation could dramatically reduce the amount of data and energy required to perform complex visual tasks.
RMIT has an international patent application filed under the Patent Cooperation Treaty (PCT) for the invention.
Depression in later life may be an early warning from the brain, appearing years before Alzheimer’s begins to affect memory and thinking
A new study in JNeurosci found that faster accumulation of tau, a protein closely tied to Alzheimer’s, was associated with worsening depressive symptoms in older adults who remained cognitively healthy. Teodora Markova of Brandeis University and her colleagues investigated whether changes in mood might track the gradual buildup of tau in the aging brain.
Tau normally helps support the internal structure of neurons. When it becomes abnormal, however, it can collect into tangles that interfere with brain function. These tangles are one of the defining biological features of Alzheimer’s disease, alongside deposits of amyloid beta.
An international team of scientists has successfully tested an innovative in vivo CAR-T therapy, JY231, capable of treating severe autoimmune diseases with a single intravenous infusion. Published in the New England Journal of Medicine, the experimental treatment uses a harmless genetically modified viral vector to deliver genetic instructions directly into a patient’s T-lymphocytes, reprogramming them to target and destroy defective B-cells that produce autoantibodies. In a clinical trial involving 16 patients with treatment-resistant conditions such as multiple sclerosis, myasthenia gravis, and myopathy, the therapy demonstrated over 99% accuracy. Within two months, patients’ bone marrow began producing healthy immune cells, and after six months of observation, participants exhibited significant clinical improvements, including the elimination of chronic fatigue and the partial restoration of cognitive and muscular functions. Researchers are now preparing for large-scale randomized trials to definitively confirm the method’s long-term safety and efficacy.
Among 16 patients with refractory neurologic autoimmune disorders, lentiviral CD19 CAR T-cell therapy was associated with manageable side effects, complete B-cell depletion, and preliminary clinical improvement across disease groups.
Neurodegeneration is a pathological condition in which nervous system or neuron losses its structure, function, or both leading to progressive neural degeneration. Growing evidence strongly suggests that reduction of plasmalogens (Pls), one of the key brain lipids, might be associated with multiple neurodegenerative diseases, including Alzheimer’s disease (AD). Plasmalogens are abundant members of ether-phospholipids. Approximately 1 in 5 phospholipids are plasmalogens in human tissue where they are particularly enriched in brain, heart and immune cells. In this study, we employed a scheme of 2-months Pls intragastric administration to aged female C57BL/6J mice, starting at the age of 16 months old. Noticeably, the aged Pls-fed mice exhibited a better cognitive performance, thicker and glossier body hair in appearance than that of aged control mice. The transmission electron microscopic (TEM) data showed that 2-months Pls supplementations surprisingly alleviate age-associated hippocampal synaptic loss and also promote synaptogenesis and synaptic vesicles formation in aged murine brain. Further RNA-sequencing, immunoblotting and immunofluorescence analyses confirmed that plasmalogens remarkably enhanced both the synaptic plasticity and neurogenesis in aged murine hippocampus. In addition, we have demonstrated that Pls treatment inhibited the age-related microglia activation and attenuated the neuroinflammation in the murine brain. These findings suggest for the first time that Pls administration might be a potential intervention strategy for halting neurodegeneration and promoting neuroregeneration.
Plasmalogens (Pls) are a special type of vinyl ether-bonded phospholipids actively participating in structure and function of biological membranes. Approximately 20% of phospholipids are plasmalogens in human tissue, where they are particularly rich in the brain, heart, and immune cells (Lessig and Fuchs 2009; Braverman and Moser 2012). In brain, ethanolamine plasmalogens (PlsEtns) constitute approximately 60 and 80% of the total ethanolamine phospholipids in gray and white matter, respectively (Macala et al., 1983). Pls are also concentrated in specialized membranes, such as sarcolemma, myelin, and synaptic vesicles (Post et al., 1988; Takamori et al., 2006; Poitelon et al., 2020). Reduced levels of PlsEtns have been found to be associated with aging (Pradas et al., 2019) and several neurodegenerative diseases, including Alzheimer’s disease (AD) (Guan et al., 1999; Han et al., 2001; Goodenowe et al., 2007; Wood 2010; Wood et al., 2015; Yamashita et al.
Recurrent high‑grade glioma (HGG)—including glioblastoma—remains lethal, with median survival of approximately 6–10 months after first progression, although patients with IDH mutant tumors often have better survival. Recent ASCO/SNO data and expanding trial data are reshaping available treatment strategies.
We review evidence for alkylators and anti‑angiogenic therapy; summarize targeted options for rare, actionable alterations; review immuno‑oncology combinations and cellular therapies; highlight DNA damage response (DDR)/radiosensitization strategies and discuss advances in blood–brain barrier modulation and locoregional delivery. We propose a patient‑centered algorithm that prioritizes trial enrollment, biomarker‑guided approaches, steroid stewardship, and quality of life.
Lomustine, temozolomide rechallenge, and bevacizumab remain commonly used but provide modest benefit. Targeted agents show meaningful activity only in select subsets (BRAF V600E, NTRK). DDR-directed agents such as ATM/ATR inhibitors show early promise. Immunotherapy advances center on rationale combinations, oncolytic viruses, and locoregionally delivered CAR-T/TCR platforms. Blood-Brain-Barrier (BBB) modulation strategies and adaptive trials are broadening access to innovative therapies. The 2025 landscape features meaningful, if incremental, options—alongside the first ever FDA‑approved therapy for H3K27M‑mutant diffuse midline glioma at relapse—and a pipeline of rational combinatorial approaches poised to refine outcomes for selected patients. This article concentrates on medical options and intentionally omits extended discussions of surgery and radiation beyond their integration with systemic therapies at recurrence.
Sometimes, even a single experience can be highly impactful, prompting humans and other animals to change their behavior or influencing their future choices. The formation of influential memories from a single, brief experience is also known as one-shot learning.
Researchers at Collège de France (CNRS/INSERM/Université PSL), Inria, Université Claude Bernard Lyon 1 and Brandeis University recently conducted a study investigating the neural underpinnings of one-shot learning in mice.
Their findings, published in Nature Neuroscience, suggest that one-shot learning is partly supported by endocannabinoid-mediated long-term potentiation (eCB-LTP), a lasting strengthening of communication at synapses, the junctions through which neurons exchange signals.
University of California, Davis, researchers have stripped down LSD to the base features responsible for its hallucinogenic and therapeutic effects.
In a study published in Proceedings of the National Academy of Sciences, the researchers whittled away at LSD’s core multiring structure and synthesized new, simplified versions to probe its functionality. The researchers developed several compounds with reduced hallucinogenic and cardiotoxic effects while identifying one compound that produced antipsychotic-like effects.
“By systematically deconstructing LSD, we have identified simplified cores that are better starting points for medicinal chemistry efforts,” said study corresponding author David E. Olson, director of the Institute for Psychedelics and Neurotherapeutics and a professor of chemistry and biochemistry and molecular medicine at UC Davis.
Practice may teach the brain a new movement, but what happens immediately afterward could determine whether that skill lasts.
Scientists have long known that repetition alone does not guarantee learning. A newly practiced movement must be stabilized through memory consolidation, a process that continues after training ends. New research in mice suggests that signals arriving from the body can help create the conditions needed for that transformation.
Researchers at Tohoku University who specialize in super-network brain physiology found that stimulating the vagus nerve after training produced stronger motor learning over the following days. The results reveal a potentially important role for communication between the internal organs and the brain in shaping long-term learning.