Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review

Migraines are among the most common neurological disorders, disabling nearly one in seven people worldwide, whereas glioblastoma (GBM) is the most aggressive primary brain tumour, with median survival scarcely beyond 15 months. Historically considered distinct, these conditions are increasingly link...

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Main Authors: Xiaoli Song, Qian Zhu, Jieying Zhang, Jin Yang, Xinxin Zhang, Qian Song
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1632154/full
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author Xiaoli Song
Xiaoli Song
Qian Zhu
Qian Zhu
Jieying Zhang
Jieying Zhang
Jin Yang
Jin Yang
Xinxin Zhang
Xinxin Zhang
Qian Song
Qian Song
author_facet Xiaoli Song
Xiaoli Song
Qian Zhu
Qian Zhu
Jieying Zhang
Jieying Zhang
Jin Yang
Jin Yang
Xinxin Zhang
Xinxin Zhang
Qian Song
Qian Song
author_sort Xiaoli Song
collection DOAJ
description Migraines are among the most common neurological disorders, disabling nearly one in seven people worldwide, whereas glioblastoma (GBM) is the most aggressive primary brain tumour, with median survival scarcely beyond 15 months. Historically considered distinct, these conditions are increasingly linked by trigeminal nerve-driven neurogenic inflammation. Activation of trigeminovascular afferents provokes antidromic release of calcitonin gene-related peptide (CGRP), substance P (SP), and pituitary adenylate cyclase-activating polypeptide (PACAP); beyond mediating migraine pain, these peptides remodel vasculature, immune infiltrates, and extracellular matrix to facilitate GBM invasion. Pre-clinical studies show CGRP and SP up-regulate matrix-metalloproteinases and integrins, while PACAP modulates cAMP–MAPK signalling, collectively promoting perivascular migration and temozolomide resistance. Epidemiological analyses report higher migraine antecedents in patients later diagnosed with brain tumours, and high-resolution MRI frequently localises GBM spread along trigeminal pathways, underscoring anatomical plausibility. Emerging therapeutics mirror these insights: aprepitant (an NK1-receptor antagonist) triggers GBM apoptosis, gepant-class CGRP blockers curb invasive phenotypes, and radiolabelled SP analogues deliver focal alpha-therapy. These discoveries facilitate more precise pathogenetic characterisation, reduce diagnostic uncertainty, and expedite translational drug development. This review synthesises current evidence on trigeminal neurogenic inflammation as a mechanistic conduit between migraine biology and GBM progression, mapping cellular circuits, molecular crosstalk, and translational interventions. By integrating neurobiology, oncology, and pharmacology, we aim to delineate diagnostic blind spots, spotlight drug-repurposing opportunities, and chart a roadmap toward personalised strategies that simultaneously alleviate migraine burden and restrain glioblastoma aggressiveness.
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issn 1664-3224
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publisher Frontiers Media S.A.
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spelling doaj-art-3f21c955fa0f4148bc073df769cd9f4c2025-08-20T03:50:49ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-07-011610.3389/fimmu.2025.16321541632154Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature reviewXiaoli Song0Xiaoli Song1Qian Zhu2Qian Zhu3Jieying Zhang4Jieying Zhang5Jin Yang6Jin Yang7Xinxin Zhang8Xinxin Zhang9Qian Song10Qian Song11National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaMigraines are among the most common neurological disorders, disabling nearly one in seven people worldwide, whereas glioblastoma (GBM) is the most aggressive primary brain tumour, with median survival scarcely beyond 15 months. Historically considered distinct, these conditions are increasingly linked by trigeminal nerve-driven neurogenic inflammation. Activation of trigeminovascular afferents provokes antidromic release of calcitonin gene-related peptide (CGRP), substance P (SP), and pituitary adenylate cyclase-activating polypeptide (PACAP); beyond mediating migraine pain, these peptides remodel vasculature, immune infiltrates, and extracellular matrix to facilitate GBM invasion. Pre-clinical studies show CGRP and SP up-regulate matrix-metalloproteinases and integrins, while PACAP modulates cAMP–MAPK signalling, collectively promoting perivascular migration and temozolomide resistance. Epidemiological analyses report higher migraine antecedents in patients later diagnosed with brain tumours, and high-resolution MRI frequently localises GBM spread along trigeminal pathways, underscoring anatomical plausibility. Emerging therapeutics mirror these insights: aprepitant (an NK1-receptor antagonist) triggers GBM apoptosis, gepant-class CGRP blockers curb invasive phenotypes, and radiolabelled SP analogues deliver focal alpha-therapy. These discoveries facilitate more precise pathogenetic characterisation, reduce diagnostic uncertainty, and expedite translational drug development. This review synthesises current evidence on trigeminal neurogenic inflammation as a mechanistic conduit between migraine biology and GBM progression, mapping cellular circuits, molecular crosstalk, and translational interventions. By integrating neurobiology, oncology, and pharmacology, we aim to delineate diagnostic blind spots, spotlight drug-repurposing opportunities, and chart a roadmap toward personalised strategies that simultaneously alleviate migraine burden and restrain glioblastoma aggressiveness.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1632154/fullmigraineglioblastomatrigeminal nerveneurogenic inflammationneuropeptides
spellingShingle Xiaoli Song
Xiaoli Song
Qian Zhu
Qian Zhu
Jieying Zhang
Jieying Zhang
Jin Yang
Jin Yang
Xinxin Zhang
Xinxin Zhang
Qian Song
Qian Song
Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
Frontiers in Immunology
migraine
glioblastoma
trigeminal nerve
neurogenic inflammation
neuropeptides
title Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
title_full Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
title_fullStr Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
title_full_unstemmed Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
title_short Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review
title_sort trigeminal nerve driven neurogenic inflammation linking migraine to glioblastoma invasion a literature review
topic migraine
glioblastoma
trigeminal nerve
neurogenic inflammation
neuropeptides
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1632154/full
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