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Introduction/Purpose Recurrent, multiply-operated, and surgically inaccessible meningiomas remain a significant unmet need; systemic therapies offer limited efficacy and repeat irradiation carries cumulative toxicity. Neurointerventionalists already catheterize tumor-dominant dural pedicles for preoperative devascularization, yet the therapeutic potential of this access has not been fully exploited. Transarterial radioembolization (TARE) with yttrium-90 (90Y) microspheres is an established locoregional brachytherapy platform in hepatic oncology with mature mapping, dosimetry, and post therapy imaging workflows. We hypothesized that meningiomas’ discrete, compartmentalized dural blood supply could be leveraged to deliver targeted short-range beta radiation via intra-arterial 90Y microspheres, combining low-dose-rate brachytherapy with flow disruptive effects.Materials and Methods We performed a systematic search of PubMed and ClinicalTrials.gov for literature directly addressing intracranial TARE planning or delivery, supplemented by a scoping synthesis of adjacent literatures including meningioma embolization biology, peptide receptor radionuclide therapy (PRRT), hepatic TARE dosimetry and device comparisons, vascular anatomy, hypoxia mediated radioresistance, and neurotoxicity.Results Five studies and one registered clinical trial directly addressed intracranial TARE or planning; 53 additional studies informed translational synthesis. Key findings include: (1) superselective 99mTc-MAA particle simulation is feasible in meningiomas, with 9/11 tumors in one series demonstrating lung shunt fractions <5%, confirming favorable particle containment; (2) systemic 90Y-PRRT achieves disease stabilization in approximately two-thirds of refractory meningiomas, and direct intra-arterial delivery should yield substantially higher tumoral absorbed doses; (3) canine proof of concept demonstrated intracranial 90Y delivery achieving tumoral doses of 45-77 Gy without permanent neurologic deficit; (4) glass and resin microsphere platforms differ critically in particle number and embolic burden, directly influencing the balance between brachytherapy and ischemic effects in confined intracranial vascular beds; (5) bland embolization literature demonstrates durable tumor shrinkage and symptom improvement in select meningiomas, supporting ischemic susceptibility as a therapeutic mechanism. Integrating these findings, we propose a hypothesis-generating dual-hit framework: flow disruption producing acute ischemic stress coupled with temporally sustained low-dose-rate beta brachytherapy that suppresses HIF-1α mediated vascular recovery, and present a pragmatic six-phase neurointerventional workflow (figure1) spanning patient selection through post-therapy dosimetric verification.Conclusion TARE represents a biologically rational, testable endovascular strategy for meningiomas that repurposes existing catheter-based access and established radioembolization infrastructure for an intracranial indication. The proposed dual-hit framework and six-phase decision-tree workflow provide an actionable roadmap for designing early-phase clinical trials with prospective dosimetry-to-toxicity validation. This approach may offer a new therapeutic option for patients with progressive or recurrent meningiomas who have exhausted conventional surgery and radiation.Disclosures A. Brake: None. K. John: None. S. Jain: None. G. Green: None. R. Salem: None. A. Sarwar: None. S. Laroia: None. M. Zanaty: None.Abstract O-032 Figure 1Proposed workflow for 90Y TARE for meningioma