Do-Wan Lee1, Hwon Heo2, Chul-Woong Woo3, Jae-Im Kwon3, Su Jung Ham4, Yeon Ji Chae2, Kyung Won Kim1,4, Jeong Kon Kim1, Dong-Cheol Woo2,3, and Dong-Hoon Lee5
1Department of Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea, 2Department of Convergence Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea, 3Convergence Medicine Research Center, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea, 4Asan Image Research, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea, 5Faculty of Health Sciences and Brain & Mind Centre, The University of Sydney, Sydney, Australia
Synopsis
Detecting glutamate signals in vivo
within the brain may have a diagnostic potential. Recently, with many
translational research efforts leading to clinical trials, presenting the
normal in vivo glutamate distribution in pre-clinical data to establish
a database for pre-clinical studies can be valuable. In this abstract, we
investigated glutamate signal distributions in multiple brain regions of a
healthy rat brain using GluCEST imaging. Quantified GluCEST signals showed
significant differences between white and gray matter regions. Our findings and
investigations yield a valuable database and insights for comparing glutamate
signal changes in pre-clinical brain diseases.
INTRODUCTION
Glutamate is a major excitatory neurotransmitter in
the mammalian central nervous system (CNS) and is involved in neuronal
function.1,2 Detecting in vivo glutamate signal changes in
the brain can be applied to the diagnosis and treatment plan of multiple
diseases where glutamate changes are involved. Chemical exchange saturation
transfer (CEST) MRI utilizes the reduction of the bulk water magnetization through
the exchange of saturated magnetization from exchangeable protons of solute
metabolites by applying a RF pulse, and shows enhanced sensitivity compared to
other imaging methods.3,4 Recently, as many pre-clinical studies conducted
as translational research have led to clinical trials, presenting the normal in
vivo distribution of glutamate in pre-clinical data to establish a database
for various pre-clinical studies may prove valuable. In this study, we applied
GluCEST to healthy rat brains and performed extensive quantitative and
qualitative analyses in multiple brain regions to elucidate the in vivo
distribution of glutamate. We performed a stability test between two time
points (initial measurement and 1 month after) to demonstrate the signal
stability of GluCEST measurements, and also compared 1H MRS data
from the cerebral cortex and hippocampus to that obtained with the GluCEST
signal.METHODS
CEST Imaging:
All experiments were performed using a Bruker 7-T scanner, and 11 Sprague-Dawley
rats were used. GluCEST imaging was performed using a turbo-RARE pulse sequence
with the following parameters: TR/TE=4,200/36.4 ms, RARE factor=16, and 25
frequency offsets [-6 ~ +6 ppm; 0.5 ppm increment)] using a continuous-wave RF
saturation pulse (power/time=3.6μT/1s).5,6 Reference (S0)
image was then acquired. To minimize the effects of B0 and B1
field inhomogeneity-induced artifacts in GluCEST analysis, water saturation
shift referencing Z-spectra (33 frequency offsets [-0.8 ~ +0.8 ppm; 0.05 ppm
increment; 0.05 μT RF power),7 and a B1 map using the
double flip-angle (30° and 60°) method were acquired.5 Additionally,
five randomly selected rats were scanned again after 1 month to evaluate the
signal stability of GluCEST imaging.
1H MRS:
Based on the data of the stability tests in the five selected rats, water-suppressed
1H-MRS single-voxel spectra were acquired from an ROI in the left
cerebral cortex (2.0×2.0×3.0 mm3) and hippocampus (4.5×1.0×2.5 mm3)
using spin-echo-based PRESS sequence, and VAPOR water suppression with the following
parameters: TR/TE=5,000/16.3-ms, average=128, number of data
points=2,048 and spectral width=5,000Hz.
Data Processing: Using B0 corrected data,
the GluCEST map was generated as follows: GluCEST(%) = [(Msat(-Δω) – Msat(+Δω)) / Msat(-Δω)]×100,
where Msat(±Δω) is the magnetization acquired with saturation pulse
applied at ±3.0-ppm to the water resonance. Subsequently, GluCEST contrast was
corrected at each voxel using relative B1 values.5 For quantification
of GluCEST, eight ROIs were carefully drawn in the cerebral cortex,
hippocampus, corpus callosum, and the rest of the midbrain regions of the left
and right hemispheres. Spectral fitting and quantification of 1H-MRS
data were performed with a fully blind spectral process using the LCModel with
a simulated basis set including 18 metabolites. All metabolite peaks were
fitted in the chemical shift range from 4.0 to 0.3-ppm.RESULTS AND DISCUSSION
Figure 1 shows the defined ROIs (a) and
CEST asymmetry (CESTasym) curves for left (b) and right (c)
hemispheres. All CESTasym curves in gray matter regions had higher
asymmetry values than those in the white matter regions in both hemispheres. Furthermore,
as indicated in previous studies, the broadness phenomenon in asymmetry curves
can be partially attributed to potential amine CEST effects and chemical shift
average effects due to the fast exchange rate of glutamate.8,9
Figure 2 shows the GluCEST signals (a), and averaged GluCEST signals between
both hemispheres (b). The GluCEST signals in all gray matter regions are higher
than in the white matter regions, and the difference in signals calculated from
the left and right hemispheres were not statistically significant (all p
> 0.286). In the averaged GluCEST signals, the signal in the hippocampus
(5.47±0.61%) is highest among the gray matter regions, followed by the signals
in the rest of the midbrain (4.49±1.11%) and cortex (3.59±0.41%). The GluCEST
signal in the white matter regions (-1.71±1.04%) showed statistically
significant differences when compared against all gray matter regions (all p
= 0.000). Figure 3 shows a GluCEST map of manually segmented brain regions (a)
and overall brain area (b-c) in a representative rat. Reconstructed GluCEST
maps using a modified discrete color-scale bar, (based on the average signal
for each region) show a distinct contrast in all brain regions (c). Figure 4
shows the stability results of GluCEST signals for each brain region. GluCEST
signals measured after 1 month in all brain regions were not significantly
different from those initially measured (all p > 0.263). Figure 5
shows the 1H-MRS results in the cortex and hippocampus (a) in a
representative rat and calculated glutamate concentrations (b; 7.30±0.16μmol/g for
hippocampus and 6.89±0.72μmol/g for cortex).CONCLUSIONS
We demonstrated in vivo glutamate
distribution in the healthy rat brain, with clear signal differences and
mapping results between gray and white matter regions. Investigation of GluCEST
signals in the healthy rat brain may provide important data to those
researching brain diseases, in terms of providing a primary, pre-clinical
database for in vivo glutamate distribution. This can also be a useful
background resource for further translation to clinical research with GluCEST
imaging.Acknowledgements
This work was supported by grants from the Basic
Science Research Program through the National Research Foundation of Korea
[NRF-2018R1C1B6004521 and NRF-2018R1A2B2007694], funded by the Korea Government
(MSIT).References
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