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Quantifying Cognitive Decrements Caused by Cranial Radiotherapy
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C5aR1 Inhibition Alleviates Cranial Radiation-Induced Cognitive Decline.

Robert P Krattli1, An H Do1, Sanad M El-Khatib1

  • 1Department of Anatomy & Neurobiology, University of California Irvine, Irvine, California.

Cancer Research
|October 14, 2025
PubMed
Summary
This summary is machine-generated.

Radiation therapy for brain cancer causes cognitive decline. Inhibiting the C5a-C5aR1 signaling pathway protected against this decline and improved memory in mouse models, offering a potential treatment for brain cancer survivors.

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Area of Science:

  • Neuroscience
  • Immunology
  • Oncology

Background:

  • Cranial radiotherapy (RT) for brain cancers causes irreversible cognitive decline (RICD).
  • RICD is a significant problem for brain cancer survivors, linked to neuroinflammation, gliosis, and synaptic loss.
  • Current treatments for RICD are lacking.

Purpose of the Study:

  • To investigate the neuroprotective potential of inhibiting the complement C5a-C5aR1 signaling axis against radiation-induced cognitive decline (RICD).
  • To evaluate the efficacy of C5aR1 blockade in both healthy and brain cancer mouse models.

Main Methods:

  • Utilized intact and brain cancer-bearing mouse models.
  • Employed genetic knockout (C5ar1 knockout mice) and pharmacologic inhibition (PMX205) of C5aR1 signaling.
  • Assessed neurocognitive function using object recognition memory and memory consolidation tasks.
  • Analyzed brain tissue for markers of microglial activation, astrogliosis, and synaptic loss.

Main Results:

  • Inhibition of C5aR1 signaling, via genetic or pharmacologic means, reversed RICD and improved cognitive function in mice.
  • C5aR1 blockade reduced neuroinflammation, astrogliosis, and synaptic loss in the irradiated brain.
  • In glioblastoma models, C5aR1 inhibition protected against RICD without compromising RT's anti-tumor efficacy.

Conclusions:

  • The C5a-C5aR1 signaling axis plays a critical role in mediating radiation-induced cognitive decline.
  • Inhibiting C5aR1 signaling is a neuroprotective strategy against RICD.
  • C5aR1 blockade represents a translationally feasible therapeutic approach for brain cancer patients experiencing cognitive dysfunction post-RT.