Fig. 2

Progression of corpus callosum atrophy after TBI is sufficient for MRI detection in live mice and is attenuated by Sarm1 knockout. a–c TBI induces significant CC atrophy in Sarm1 WT mice. High resolution PD-weighted images showing the coronal view at the level of the impact site at baseline (a, before surgery) and at 10 weeks (b) post-TBI/sham procedures. Quantification of volume change in CC regions under the impact site (c). d–f In Sarm1 KO mice, CC atrophy is not detected in representative high resolution PD-weighted images (d, e) or based on changes in CC volume (f). g–h Direction encoded color images of diffusion tensor imaging (DTI) from a longitudinal MRI series at baseline (BL) and again at 3 days and 10 weeks post-TBI or sham procedures. Colors represent fiber directions as red (medial–lateral), blue (anterior–posterior), and green (superior-inferior). i–k Quantification of DTI measures reveals a chronic progression of CC pathology following TBI. Fractional anisotropy (FA) significantly decreases over time following TBI (i). The acute change is driven by a decrease in axial diffusivity (AD) between baseline and 3 days (j). Sarm1 KO mice have significantly higher AD values than Sarm1 WT mice (j). The FA at 10 weeks corresponds with a delayed increase in radial diffusivity (RD) in Sarm1 KO mice (k). Arrows indicate medial CC regions. Sarm1 WT: n = 10 TBI; Sarm1 KO: n = 15 TBI. ns = not significant. Further statistical details are provided in Additional File 1: Table S2