New research shows that specific types of brain cells become active after brain injuries and exhibit properties similar to those of neural stem cells. Astrocyte plasticity might correlate with the upregulation of the Galectin 3 protein, which may significantly contribute to discovery of additional biomarkers. The study discovered that a specific protein regulates these cells and could be a target for therapy and contribute to development of better treatments options for brain injuries. The loss of neurons, which subsequently causes impairment of brain function, is caused by the onset and progression of neurological disorders, like strokes, spinal cord injuries and neurodegenerative diseases such as Parkinson’s, Alzheimers / Dementia, ALS and MND. Effective treatment options still need to be improved. However, preclinical research has shown a promising response involving reactive astrocytes, a specific type of glial cell, which is a crucial part of the nervous system alongside neurons. Microglia and Glial cells are regarded as a safeguard for neurons, demonstrating the ability to resume cell proliferation, a mechanism essential for protecting the injury-affected brain from invasion by immune cells.^[1]

Differentiation of Mesenchymal Stem Cells to Neuroglia.

Given the importance of astrocyte proliferation, these findings are relevant for understanding how changes in cerebrospinal fluid composition (upregulation of Galectin 3 protein) support the maintenance of astrocyte plasticity in the brain. Identifying Galectin 3 protein as an inducer of astrocyte plasticity has helped discover other biomarkers that offer beneficial modulation inside the injured brain parenchyma. These regulators of astrocyte proliferation after acute injury offer great promise for the future clinical applications of these biomarkers as indicators for detecting a beneficial reaction of glial stem cell therapy or help identify the presence of other cells with stemness potential in an injured patient’s brain ^[5].

Large vestibular schwannomas (VS) often compress the brainstem and differ in their relation to the internal auditory canal (IAC); the significance of these radiographic features on postoperative outcomes remains unclear. This study quantifies the impact of brainstem compression (BSC) and position relative to the IAC on surgical outcomes in VS.

We retrospectively identified 116 patients with sporadic unilateral VS ≥ 3 centimeters (2017–2022). Neurofibromatosis 2 cases were excluded. BSC was quantified with MRI T1 post-contrast axial images as the perpendicular distance from the brainstem-cerebellum to the point of maximal compression. Anterior and posterior IAC extension were measured relative to a line bisecting the IAC from the porus to fundus. Outcomes included postoperative facial nerve (FN) function, extent of resection (EOR), and length of stay (LOS).

Greater anterior extension was associated with decreased EOR in univariate analysis (OR = 1.12, p = 0.03), but not after controlling for tumor size and age (OR = 1.09, p = 0.158). Greater BSC was associated with worse FN function at 2–3 weeks postoperatively on univariate (OR = 1.08, p = 0.036) and approached significance on multivariate analysis (OR = 1.07, p = 0.08). Posterior extension was associated with increased LOS in univariate (β = 217.57 min, p = 0.024), but not multivariate analysis. Neither anterior extension nor BSC were associated with LOS. Older age correlated with a lower rate of GTR and longer LOS in multivariate analysis (EOR: OR = 1.05, p = 0.003; LOS: β = 79.84 min, p = 0.026).

Efficient brain-wide communication requires neural activity to traverse long anatomical distances rapidly. Here we examine how propagation timing is jointly associated with spatial geometry, functional network organization, and long-range white-matter pathways and their microstructural properties. And we ask whether the same rules govern epileptiform and physiological activity. Using stereo-EEG and diffusion spectrum imaging from 47 epilepsy patients (26 males and 21 females), we quantified inter-regional propagation with two complementary delay estimators: event-based interictal epileptiform discharge (IED) traveling waves and continuous lagged-correlation delays during IED-free periods. We found that IED propagation traversing gray and white matter formed reproducible spatiotemporal motifs that deviated from randomized null models, indicating structured routing rather than random spread. Epileptiform and physiological propagation delays increased over short ranges but saturated at longer distances, indicating that geometry alone cannot account for long-range fast propagation. Beyond geometry, stronger structural connectivity and higher functional connectivity were associated with shorter delays, and intrinsic functional modules facilitated efficient communication: within-network propagation was faster than between-network propagation. Crucially, diffusion-derived quantitative anisotropy (QA) revealed a microstructural mechanism for long-range fast propagation: long-range white-matter tracts showed higher QA, and QA was positively associated with apparent propagation velocity. Together, these results identify convergent, architecture-dependent constraints on propagation timing that generalize across epileptiform and normal activity, providing a principled bridge between macroscale connectome organization and fast intracranial spatiotemporal dynamics.

Significance statement Efficient communication across long anatomical distances is fundamental for the human brain. By integrating stereo-EEG with diffusion spectrum imaging, this study shows that brain-wide information propagation is not determined by distance alone, but is critically supported by long-range white-matter pathways, their microstructural properties, and intrinsic functional network organization. We also find that both pathological epileptiform discharges and physiological spontaneous activity follow shared propagation rules, exhibiting distance saturation, structural facilitation, and preferential within-network transmission. These findings provide a microstructure-grounded account of how the human brain achieves fast, efficient large-scale communication, bridging macroscale connectome architecture with millisecond-scale neural dynamics.