Myelin Quantification Using Ultrashort Echo Time Magnetization Transfer Ratio in a Mouse Model of Traumatic Brain Injury

利用超短回波时间磁化转移比率对创伤性脑损伤小鼠模型中的髓鞘进行定量分析

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Abstract

BACKGROUND AND PURPOSE: This study aims to assess the potential of ultrashort echo time imaging-based magnetization transfer ratio (UTE-MTR) in detecting demyelination in mice with mild traumatic brain injury (mTBI) caused by an open-field low-intensity blast (LIB) injury model. METHODS: This study included 30 male C57BL/6 mice, approximately 8 weeks old, sourced from Jackson Laboratories in Bar Harbor, ME, and conducted under institutional guidelines. The mice were divided into the mTBI group (n = 15) and the sham control group (n = 15). All animal experiments followed the approved protocols for the Care and Use of Laboratory Animals and Animal Research. The mTBI group underwent the open-field LIB injury. Behavioral tests were conducted to assess motor activity and anxiety-like responses. UTE-MT imaging was performed using a 3 Tesla Bruker system to measure UTE-MTR from two UTE-MT datasets with saturation powers of 1500° and 500°, and two frequency offsets of 2 and 50 kHz, respectively. Luxol fast blue (LFB) staining was performed to evaluate myelin content. The mean UTE-MTR values for regions of interest centered at the medial section of the corpus callosum were computed. The behavioral tests, LFB myelin staining, and UTE-MTR values were compared between the two groups using the independent t-test. p values <0.05 were considered significant. RESULTS: The mTBI mice demonstrated decreased motor activity and increased anxiety-like response over sham controls. The mTBI mice also showed significantly lower UTE-MTR values (0.399±0.007 vs. 0.393±0.005; p<0.05) and reduced LFB myelin staining (0.848±0.324 vs. 1.145±0.260; p = 0.048) over sham controls. CONCLUSION: The significantly lower UTE-MTR values in the corpus callosum of mTBI mice are consistent with reduced LFB myelin staining, indicating that UTE-MTR can detect myelin loss and associated alterations in motor and anxiety domains post-LIB exposure.

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