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<p>Stereotactic radiosurgery (SRS) is a procedure that delivers high-dose single fraction, targeted radiation to treat brain pathologies. Brain radiation necrosis is a significant side effect of SRS, resulting in severe clinical sequelae such as seizure, hemorrhage, stroke, and neurological deficit. While focused radiation causes DNA damage and cell death, radiation necrosis is mostly mediated by vascular injury. Yet the effects of SRS on the neurovascular unit (NVU) cells—microglia, astrocytes, and endothelial cells—remain poorly understood. This study establishes a mouse SRS model using 15 to 60&#xa0;Gy to characterize NVU stress, providing histological and transcriptomic profiles of radiation-induced damage. Our findings demonstrate blood-brain-barrier (BBB) disruption, inflammatory cell infiltration, and microvascular pathology. Spatial transcriptomics identified differentially expressed genes and cell-cell communication across NVU components, revealing a coordinated stress response involving immune modulation, barrier integrity, and tissue remodeling pathways. This model provides a mechanistic framework for developing strategies to mitigate BBB and NVU stress.</p>

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A mouse model of stereotactic radiosurgery-induced neuroinflammation and blood-brain barrier compromise

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年9月24日

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  • Roberto J. Alcazar-Felix,
  • Lin Cheng,
  • Abhinav Srinath,
  • Akash Bindal,
  • David Tieri,
  • Diana Vera-Cruz,
  • Madison Yuan,
  • Sammy Allaw,
  • Nitha Aima Muntu,
  • Dominic Montas,
  • András Piffkó,
  • Erik Pearson,
  • Bader Ali,
  • Peter Pytel,
  • Issam A. Awad,
  • Sean P. Polster

摘要

Stereotactic radiosurgery (SRS) is a procedure that delivers high-dose single fraction, targeted radiation to treat brain pathologies. Brain radiation necrosis is a significant side effect of SRS, resulting in severe clinical sequelae such as seizure, hemorrhage, stroke, and neurological deficit. While focused radiation causes DNA damage and cell death, radiation necrosis is mostly mediated by vascular injury. Yet the effects of SRS on the neurovascular unit (NVU) cells—microglia, astrocytes, and endothelial cells—remain poorly understood. This study establishes a mouse SRS model using 15 to 60 Gy to characterize NVU stress, providing histological and transcriptomic profiles of radiation-induced damage. Our findings demonstrate blood-brain-barrier (BBB) disruption, inflammatory cell infiltration, and microvascular pathology. Spatial transcriptomics identified differentially expressed genes and cell-cell communication across NVU components, revealing a coordinated stress response involving immune modulation, barrier integrity, and tissue remodeling pathways. This model provides a mechanistic framework for developing strategies to mitigate BBB and NVU stress.