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In vivo GluCEST MRI: Reproducibility, background contribution and source of glutamate changes in the MPTP model of

Puneet Bagga1, Stephen Pickup2, Rachelle Crescenzi2

  • 1Center for Magnetic Resonance and Optical Imaging, Department of Radiology, University of Pennsylvania, Philadelphia, PA, United States. puneetb@pennmedicine.upenn.edu.

Scientific Reports
|February 15, 2018
PubMed

Insights

Glutamate Chemical Exchange Saturation Transfer (GluCEST) MRI shows reproducible results for imaging glutamate. This technique detected elevated glutamate in a Parkinson

Area of Science:

  • Neuroimaging
  • Biomarker Development
  • Neuroscience

Background:

  • Glutamate Chemical Exchange Saturation Transfer (GluCEST) MRI is an emerging technique for visualizing glutamate levels in vivo.
  • Understanding the reproducibility and sources of signal variation in GluCEST is crucial for its clinical translation.
  • Parkinson's disease models offer a platform to investigate GluCEST's utility in neurological disorders characterized by altered glutamate neurotransmission.

Purpose of the Study:

  • To assess the reproducibility of GluCEST measurements in a mouse model.
  • To investigate the sources of background signal contamination in GluCEST imaging.
  • To evaluate GluCEST as a potential imaging biomarker for neuroinflammation and gliosis in Parkinson's disease.

Main Methods:

  • Evaluated intra- and inter-animal variability of GluCEST signals in healthy mice.
  • Induced Parkinson's-like pathology using MPTP in mice and measured striatal GluCEST changes.
  • Correlated 1H Magnetic Resonance Spectroscopy (MRS) glutamate concentrations with GluCEST signals to estimate background contribution.
  • Performed immunohistochemical analysis to identify the cellular source of elevated glutamate.

Main Results:

  • Demonstrated high reproducibility of GluCEST measurements with low intra-animal (2.3 ± 1.3%) and inter-animal (3.3 ± 0.3%) coefficients of variation.
  • Observed a significant elevation in striatal GluCEST contrast in MPTP-treated mice compared to controls (26.2 ± 0.8% vs. 23.3 ± 0.8%, p ≤ 0.001).
  • Estimated background signal from non-glutamate sources to be approximately 28% of the total GluCEST signal.
  • Showed co-localization of glutamate with GFAP-positive astrocytes in the striatum, indicating reactive gliosis.

Conclusions:

  • GluCEST MRI is a reproducible technique for imaging glutamate.
  • MPTP-induced Parkinson's model shows elevated striatal glutamate detectable by GluCEST.
  • Elevated GluCEST signal in this model likely reflects MPTP-induced astroglial proliferation or reactivity, suggesting GluCEST's potential for imaging inflammation-mediated gliosis.

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