Purpose <p>To determine whether measured longitudinal relaxation time (T<sub>1</sub>) differences explain glutamate-weighted CEST (GluCEST) group differences across four rat disease models associated with glutamatergic alterations.</p> Methods <p>GluCEST imaging and quantitative T<sub>1</sub> mapping were performed at 7T in four rat models (insomnia, depression, demyelination, and sepsis). Group differences were assessed using Welch’s t-test and standardized effect sizes. The influence of T<sub>1</sub> on GluCEST was examined using disease-specific and pooled analyses of covariance (ANCOVA), as well as correlation analyses.</p> Results <p>Across all models, T<sub>1</sub> values did not significantly differ between control and disease groups (all p ≥ 0.53), whereas GluCEST showed significant group differences in each condition (all p &lt; 0.01) with large effect sizes (Cohen’s d = 1.75–7.02). In ANCOVA models, group effects remained significant after adjustment for T<sub>1</sub>, and T<sub>1</sub> was not a significant predictor of GluCEST in disease-specific or pooled analyses. No consistent correlation between T<sub>1</sub> and GluCEST was observed.</p> Conclusions <p>Under the present experimental conditions, between-group T<sub>1</sub> differences were limited and did not significantly explain GluCEST group separation across the four rat models examined. These findings suggest that the T<sub>1</sub> contribution to GluCEST group comparisons should be interpreted in relation to the biological model, the magnitude of between-group T<sub>1</sub> differences, and the acquisition conditions.</p>

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Limited Contribution of T1 Relaxation to GluCEST MRI Signal Differences Across Four Rat Models with Distinct Pathophysiological Features

  • Donghoon Lee,
  • Hind Binjaffar,
  • Yeon Ji Chae,
  • Chul-Woong Woo,
  • Jung-Hyun Choi,
  • Dong-Cheol Woo,
  • Hyunju Ryu,
  • Do-Wan Lee

摘要

Purpose

To determine whether measured longitudinal relaxation time (T1) differences explain glutamate-weighted CEST (GluCEST) group differences across four rat disease models associated with glutamatergic alterations.

Methods

GluCEST imaging and quantitative T1 mapping were performed at 7T in four rat models (insomnia, depression, demyelination, and sepsis). Group differences were assessed using Welch’s t-test and standardized effect sizes. The influence of T1 on GluCEST was examined using disease-specific and pooled analyses of covariance (ANCOVA), as well as correlation analyses.

Results

Across all models, T1 values did not significantly differ between control and disease groups (all p ≥ 0.53), whereas GluCEST showed significant group differences in each condition (all p < 0.01) with large effect sizes (Cohen’s d = 1.75–7.02). In ANCOVA models, group effects remained significant after adjustment for T1, and T1 was not a significant predictor of GluCEST in disease-specific or pooled analyses. No consistent correlation between T1 and GluCEST was observed.

Conclusions

Under the present experimental conditions, between-group T1 differences were limited and did not significantly explain GluCEST group separation across the four rat models examined. These findings suggest that the T1 contribution to GluCEST group comparisons should be interpreted in relation to the biological model, the magnitude of between-group T1 differences, and the acquisition conditions.