To explore the spatial heterogeneity of human glioma vasculature, we established a tissue clearing framework that enables comprehensive and precise three-dimensional visualisation of the vasculature and cells within 500-μm-thick glioma tissue. Subsequently, we devised a deep learning–based algorithm for accurate and automated segmentation and quantification of glioma vasculature, demonstrating superior performance compared to Imaris and facilitating robust analysis of vascular morphology. The integration of tissue clearing and deep learning has enabled detailed dissection of three-dimensional vascular morphological differences across glioma grades, potentially providing new insights into pathological classification, therapeutic intervention and prognostic evaluation.

The RT-QuIC assay showed high sensitivity and specificity in detecting prion seeding activity in archival FFPE brain tissues, comparable to results obtained from frozen samples. Notably, prion activity remained detectable in FFPE tissues even after long-term storage. This highlights the potential of using FFPE samples to support retrospective studies and streamline sample handling and transportation. Created in BioRender. https://BioRender.com/ft1oayi.

Caribbean atypical Parkinsonism (CAP) is believed to be associated with the consumption of Annonaceae plant products containing the mitochondrial toxin, annonacin. The analysis of brain samples from CAP patients revealed a co-pathology involving tau and α-synuclein (αS) in the majority of cases. Tau and αS aggregates sometimes co-localised in the same brain regions or cells. Biophysical assays demonstrated that annonacin can promote αS aggregation and that newly formed αS fibrils can cross-seed tau aggregation. Pro-aggregation effects of annonacin may represent a new pathogenic mechanism contributing to CAP.

Direct intracerebral inoculation of Enterovirus A71 (EV-A71) in a murine model resulted in restricted local spread within the brain. The primary pathway for neuroinvasion appears to involve viral leakage into the bloodstream, robust infection of peripheral muscle, and subsequent retrograde axonal transport from the muscle back into the central nervous system (CNS). This circuitous route targets motor neurons and is independent of mSCARB2 receptor distribution, highlighting a key mechanism of EV-A71 neuropathogenesis.