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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Genetic inactivation of SARM1 axon degeneration pathway improves outcome trajectory after experimental traumatic brain injury based on pathological, radiological, and functional measures

Fig. 3

Sarm1 knockout reduces corpus callosum atrophy, myelin loss, and axon damage at 10 weeks post-TBI. ad Representative images from CC coronal sections of Sarm1 WT and Sarm1 KO mice after sham or TBI procedures. Myelin is detected with immunolabeling for MOG (red). DAPI nuclear stain is shown in blue. Insets show axonal swellings with β-APP immunoreactivity (examples indicated by arrows). CC borders are indicated by dashed lines. e Sarm1 knockout attenuates CC atrophy, which is quantified based on the CC width. f TBI results in significant myelin loss as detected by reduced MOG immunoreactivity. Myelin loss after TBI is significantly reduced in Sarm1 KO mice compared to Sarm1 WT mice. g Axon damage in TBI mice was significantly reduced in Sarm1 KO mice compared to Sarm1 WT mice. MOG quantification included Sarm1 WT: n = 7 sham, n = 11 TBI; Sarm1 KO: n = 6 sham, n = 11 TBI. β-APP quantification included Sarm1 WT: n = 6 TBI; Sarm1 KO: n = 9 TBI. ns = not significant. Further statistical details are provided in Additional File 1: Table S3. Scale bars ad = 100 µm, insets b, d = 25 µm

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