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Gliomas are known to form synaptic connections with surrounding neurons, which results in bidirectional interactions that can induce neuronal changes. The extent to which gliomas can remodel
functional neural circuits to affect cognition remains unclear. Krishna et al. performed intracranial brain recordings in patients with glioma during language tasks, and paired these data
with tumor biopsy analysis to investigate the effect of glioblastoma–synaptic integration on cognitive function. Electrocorticography of tumor regions showed task-relevant neural activity in
cortical regions outside of typical speech areas, which indicates that the tumor-affected cortex maintains task-specific neuronal responses. However, glioblastoma-infiltrated regions showed
lower decodability of neuronal signals than unaffected regions, which is indicative of lowered cognitive function.
To assess synapse formation, the authors performed RNA sequencing on tumor samples with high and low functional connectivity (HFC and LFC, respectively), which revealed distinct gene
signatures in HFC regions where genes involved in synapse formation — such as the synaptogenic factor thrombospondin 1 (THBS1, encoding TSP1) — were elevated. Indeed, biopsy samples,
co-culture of primary patient-derived glioma cells with neurons and neuronal organoid models confirmed increased synapse stability and formation of HFC-derived glioma cells.
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