Abstract #0659

Sex chromosomes and sex hormones differentially mitigate radiation-induced neuroanatomic deficits in Ccl2 knockout mice.

Jonas Yeung^1,2, Taylor De Young¹, Shoshana Spring¹, Qi Xiao³, Jason Lerch⁴, Mark Palmert⁵, and Brian J. Nieman^1,2,6

¹Translational Medicine, The Hospital for Sick Children, Toronto, ON, Canada, ²Medical Biophysics, University of Toronto, Toronto, ON, Canada, ³The Hospital for Sick Children, Toronto, ON, Canada, ⁴Wellcome Centre for Integrative Neuroimaging, University of Oxford, Oxford, United Kingdom, ⁵Department of Paediatrics, The Hospital for Sick Children, Toronto, ON, Canada, ⁶Ontario Institute for Cancer Research, Toronto, ON, Canada

Synopsis

Keywords: Neuroinflammation, Preclinical, mouse, structural, radiation, Ccl2Females tend to exhibit worse cognitive outcomes than males after pediatric cranial radiation therapy (CRT). Previous literature suggest that these sex differences may be driven by neuroinflammatory responses that involve CCL2. The objective of this study was to determine whether protection from Ccl2 knockout is mediated by sex hormones or sex chromosomes. We employ MRI on a CRT mouse model with mixed sex hormone and chromosome complements (i.e., four core genotypes model) to determine neuroanatomical changes. We found that both male chromosome and male sex hormones separately benefit regions of the brain in CCL2 deficient mice after CRT.

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