Differentiating radiation necrosis (RN) from tumor recurrence (TR) in previously irradiated brain metastases (BM) remains a challenge. Imaging techniques lack sufficient diagnostic reliability, while therapeutic implications differ between both entities. This study aims to evaluate the diagnostic, therapeutic, and prognostic value of surgery in patients with progressive irradiated BM.

We studied patients who underwent surgical resection for progressive BM after prior irradiation. Histopathological diagnosis was classified as pure RN or TR. Clinical, radiological, surgical, and survival outcomes were analyzed.

In 73 lesions, histopathology demonstrated TR in 68.5% of lesions. Among TR, 84.0% showed mixed pathological features combining viable tumor cells and radionecrotic patterns. Patients initially treated by irradiation alone were significantly more likely to present TR, whereas surgery followed by postoperative irradiation was significantly associated with RN. Median interval between radiation and surgery was significantly longer in the RN group and breast cancer seemed related to RN. Postoperative clinical improvement occurred in 80.4% of symptomatic patients and corticosteroid discontinuation within one month occurred in 72.3% of patients, without significant difference between RN and TR. Median overall survival was longer in patients with RN (39 vs. 19 months, p = 0.025).

Individuals suffering from diverse neuropsychiatric and neurodegenerative disorders often have comparable symptoms, which may underline the implication of shared hereditary influences and the same biological processes. Lysophosphatidic acid (LPA) is a bioactive phospholipid and a crucial regulator of the development of adult neuronal systems; hence, it may play an important role in the onset of certain diseases such as Alzheimer’s, Parkinson’s disease, and schizophrenia. During development, LPA signaling regulates many cellular processes such as proliferation, survival, migration, differentiation, cytoskeleton reorganization, and DNA synthesis. So far, six lysophosphatidic acid receptors that respond to LPA have been discovered and categorized based on their homology.

The brain demands a lot of energy compared with other organs. However, it can also make do when energy supplies are scarce, flexibly processing information using what is available. How the brain resourcefully allocates this limited energy across internal states remains a key question in neuroscience.

Sleep provides a useful window into answering this question. Although sleep is associated with rest, the brain remains highly active. This is especially true during rapid eye movement (REM) sleep, the stage closely linked to dreaming and memory processing. REM sleep is sometimes called “paradoxical sleep” because the body is largely still while the brain shows wake-like activity. Researchers at Tohoku University have now uncovered another paradox within REM sleep: While energy supply to the dreaming brain appears to rise, the energy molecule used directly by neurons falls. The findings are published in Communications Biology.

“Ever felt exhausted after a vivid dream?” asks Professor Ko Matsui of Tohoku University. “Sleep may appear peaceful, but the brain is highly active—especially when dreaming. We were intrigued by this paradox and wanted to look into the scientific basis behind why dreaming is somehow tiring.”

A drug briefly reversed autism-like brain and behavior changes in adult mice, hinting that affected brain circuits may remain surprisingly adaptable.

Pediatric high-grade gliomas (pHGG) are among the most aggressive childhood brain tumors, with limited treatment options and poor prognosis. Vaccine-based immunotherapy offers a promising strategy by leveraging tumor-specific or associated antigens to stimulate durable anti-tumor immune responses with minimal toxicity.

This review outlines the scientific rationale for vaccine therapies in pHGG, detailing key targets such as glioma-associated antigens (EphA2, IL-13Rα2, survivin), driver mutation–derived neoantigens (H3.3K27M, TP53, IDH1), and viral antigens (CMV pp65). We evaluate current vaccine platforms, including peptide vaccines, dendritic cell vaccines, mRNA-based vaccines, and neoantigen-personalized approaches, highlighting early-phase clinical trial results that demonstrate safety and immunogenicity. Despite encouraging preliminary data, several challenges hinder clinical translation, including the distinct immune environment in the central nervous system, intratumoral heterogeneity, low mutational burden, immunosuppressive microenvironments, steroid use, and logistical hurdles in vaccine production and trial design. Future research must address these barriers through optimized antigen selection, combinatorial therapies, novel delivery systems, and pediatric-specific immune profiling.

With continued multidisciplinary collaboration, vaccine therapies may emerge as a meaningful addition to the therapeutic arsenal for children with pHGG.