{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T12:06:13Z","timestamp":1788955573189,"version":"build-2803163510"},"reference-count":227,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neural Circuits"],"abstract":"<jats:p>Glioblastoma (GBM), a high-grade glioma, is the most common primary brain tumor in adults, with a dismal prognosis and a very high recurrence rate. Major challenges to effective treatment arise from the tumor\u2019s locally aggressive, diffusely infiltrative nature and extensive intratumoral heterogeneity. Recent advances in cancer neuroscience have uncovered bidirectional neuron-glioma interactions including the formation of functional neuron-glioma synapses (NGS). Neuronal activity drives tumor growth and its synaptic integration into neural circuits; tumor-induced circuit remodeling reciprocally influences neural activity. In parallel, emerging evidence implicates the immunological synapse- a dynamic interface between T cells and antigen-presenting cells analogous to its neural counterpart- as a key driver of GBM pathogenesis and progression. The tumor microenvironment (TME) in GBM is characterized by local immunosuppression, immune evasion, and resistance to immunotherapy. Notably, neural and immune synapses share fundamental architectural and functional principles\u2013spatial confinement of signaling, receptor clustering and adhesion-mediated stabilization, directional information transfer, and use-dependent plasticity\u2013and an expanding catalog of molecular hubs operates across both interfaces. In this context, glioblastoma can be reconceptualized as a disease of coupled neural and immune synaptic networks cooperating to drive tumor progression. Therapeutic strategies targeting these hubs may offer advantages over current approaches by simultaneously disrupting tumor-promoting neuronal input and enhancing antitumor immunity, providing a \u201cdouble hit\u201d with the potential to dismantle the network architecture sustaining tumor growth and resilience.<\/jats:p>","DOI":"10.3389\/fncir.2026.1919817","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T11:06:35Z","timestamp":1788951995000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities"],"prefix":"10.3389","volume":"20","author":[{"given":"Ashwin","family":"Jainarayanan","sequence":"first","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford Medicine, Stanford University","place":["Stanford, CA, United States"]},{"name":"Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford","place":["Oxford, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aishwarya","family":"Vedula","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics, University of Oxford","place":["Oxford, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neeraj","family":"Soni","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Yale School of Medicine, Yale University","place":["New Haven, CT, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,9]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"124","DOI":"10.1227\/neu.0000000000001753","article-title":"Association of neurological impairment on the relative benefit of maximal extent of resection in chemoradiation-treated newly diagnosed isocitrate dehydrogenase wild-type glioblastoma.","volume":"90","author":"Aabedi","year":"2022","journal-title":"Neurosurgery"},{"key":"B2","doi-asserted-by":"publisher","first-page":"737","DOI":"10.1038\/nrn1749","article-title":"Late-phase long-term potentiation: Getting to the nucleus.","volume":"6","author":"Adams","year":"2005","journal-title":"Nat. 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