Koji Kamagata1, Kouhei Tsuruta2, Taku Hatano3, Keigo Shimoji4, Masaaki Hori1, Ayami Okuzumi3, Misaki Nakazawa2, Syo Murata2, Ryo Ueda2, and Shigeki Aoki1
1Department of Radiology, Juntendo University, Tokyo, Japan, 2Department of Radiological Sciences, Tokyo Metropolitan University, Tokyo, Japan, 3Department of Neurology, Juntendo University, Tokyo, Japan, 4Department of Diagnostic Radiology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan
Synopsis
In this study, neurite-orientation
dispersion and density imaging were used to estimate structural changes of
neurites in the gray matter of the brain, which is the earliest pathological
change in patients with PD. The results showed a significant decrease in the intracellular
volume fraction in the right amygdala and right putamen in PD, suggesting a
decrease in neurite density that may reflect actual pathological change. Given
that NODDI could detect pathological changes at the earliest stages in PD, it
may be useful for early diagnosis.PURPOSE
Abnormal accumulation of Lewy-related pathology
in the nervous system has been reported as a key part of the pathological
changes in Parkinson’s disease (PD) [1]. The
earliest degenerative changes, called Lewy neurites, aggregate at the neurites
and are related to neurite loss or structural change [2]. In
recent years, multishell diffusion-weighted MRI (dMRI) and neurite-orientation
dispersion and density imaging (NODDI) models have allowed researchers to
estimate neurite structure and density in the gray matter [3, 4]. The
purpose of this study is to use NODDI to quantitatively evaluate neurite
degeneration in the gray matter in PD.
METHODS
Multishell dMRI was performed using 3T MRI
(Achieva, Philips) on 11 patients with PD and 13 healthy controls matched for
age and sex. Multishell dMRI data were acquired with a spin-echo EPI sequence along 32 isotropic
diffusion gradient directions. For each direction, Multishell
dMRI were acquired with three values of b (0, 1,000, and 2,000
s/mm2). The sequence parameterswere as follows: image orientation, axial; repetition time
(TR), 7,041 ms; echo time (TE), 70 ms; diffusion gradient pulse duration (δ), 13.3 ms; diffusion
gradient separation (Δ), 45.3 ms;
number of excitations (NEX), 1; field of view, 240 mm; matrix, 80×80;
slice thickness, 3 mm; number of slices, 50; and imaging time, 6 min 26 s. The
intracellular volume fraction (Vic) and orientation dispersion index (OD) were
calculated using the NODDI toolbox and the gray matter on the Vic, OD, FA, and
MD maps was analyzed by using gray matter-based spatial statistics (GBSS). Region-of-interest
(ROI) analysis was added using an ROI template taken from the Harvard-Oxford
subcortical and cortical structural atlas.
RESULTS
The GBSS results showed a significant
decrease in Vic in the right amygdala and right posterior putamen, right hippocampus, right
parahippocampal gyrus, right frontal orbital cortex, right temporal pole in the PD group compared with the healthy controls (uncorrected p <
0.0005). No significant change was observed in OD, FA, or MD. ROI analysis also
showed a significant decrease in Vic in the right amygdala (p = 0.0017), in the right parahippocampal gyrus
(p = 0.0034), but no significant change was observed in
the any other area.
DISCUSSION
The amygdala, parahippocampal
gyrus is
a region where Lewy pathology occurs at the early stages of PD, with Lewy
neurite aggregation at the neurites and Lewy body deposits in the cell bodies, accompanied
by neuronal loss and degeneration of neurite structures [3]. Because Vic reflects
neurite density, the decrease in Vic in the amygdala may indicate a decrease in
neurite density in the amygdala of PD patients.
CONCLUSION
The amygdala, parahippocampal
gyrus is
a region where Lewy pathology occurs at the early stages of PD, with Lewy
neurite aggregation at the neurites and Lewy body deposits in the cell bodies, accompanied
by neuronal loss and degeneration of neurite structures [3]. Because Vic reflects
neurite density, the decrease in Vic in the amygdala may indicate a decrease in
neurite density in the amygdala of PD patients.
Acknowledgements
This study has received funding by a Grant-in-Aid for Scientific Research on Innovative Areas (ComprehensiveBrain Science Network) from the Ministry of Education, Culture,Sports, Science, and Technology (MEXT) of Japan and by MEXT/JSPSKAKENHI Grant Number 24591787.References
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