Mustapha Bouhrara1, Joseph E. Alisch1, Nikkita Khattar1, Abinand C. Rejimon1, Luis E. Cortina1, and Richard G. Spencer1
1NIA, NIH, Baltimore, MD, United States
Synopsis
Little is
known about the relationship between white matter (WM) perfusion and
microstructure across cognitively normal or impaired subjects. WM maintenance
through oligodendrocyte metabolism is an energy-intensive process, so that
myelin homeostasis is particularly sensitive to hypoxia, ischemia, or hypoperfusion.
In addition to substrate delivery, adequate cerebral blood flow (CBF) is
crucial for removal of metabolic byproducts. We investigated associations
between CBF deficits and myelin loss in multiple brain regions in a cohort of cognitively
unimpaired participants across a wide age range. We show significant correlations
between CBF deficits and myelin loss in critical brain structures.
PURPOSE
To investigate the potential association
between CBF deficits and myelin loss in a cohort of cognitively unimpaired
subjects across a wide age range. Our goals are to characterize regional
associations between CBF decline, measured using the pseudo-continuous arterial
spin labeling (pCASL) technique (1), and myelin content, measured using the BMC-mcDESPOT myelin water
fraction (MWF) imaging technique (2-6)
and longitudinal relaxation rate, R1, (7), in normal aging. These relationships provide further insights
into the effect of normal aging and CBF deficits on myelin integrity.METHODS
Subjects and MRI
The study cohort consisted of 74 cognitively
unimpaired participants (49.2±19.3 years, age range 22-88 years) consisted of 30
women (48.6±19.8 years) and 44 men (49.6±19.2 years). Age was not statistically
different between men and women. The BMC-mcDESPOT and ASL protocols were as
follow:
- BMC-mcDESPOT for MWF mapping and R1: ten 3D spoiled-gradient-recalled-echo (SPGR)
images were acquired with flip angles (FAs) of [2 4 6 8 10 12 14 16 18 20]°,
echo time of (TE) 1.37ms and repetition time (TR) of 5ms, and ten 3D balanced
steady-state free-precession images were acquired with FAs of [2 7 11 16 24 32
40 60]°, TE of 2.8ms, TR of 5.8ms, and radiofrequency excitation pulse phase
increments of 0o or 180o to account for off-resonance
effects (8). All images were acquired
with a voxel size of 1.6mm × 1.6mm × 1.6mm. The DAM was used to correct for B1
inhomogeneity (9). The DAM protocol consists
of two fast spin-echo images acquired with FAs of 45° and 90°, TE of 102ms, TR
of 3s, and acquisition voxel size of 2.6mm × 2.6mm × 4mm. All images were obtained
with a field-of-view (FoV) of 240mm × 208mm × 150mm and reconstructed on the
scanner to a voxel size of 1mm× 1mm × 1mm.
- pCASL for CBF mapping (1): control, labeled, and
proton density (PD) images were acquired with incorporation of background
suppression, FoV of 220mm x 210mm x 120mm, and spatial resolution of 2.5mmx2.5mmx5mm,
and reconstruction to 1mmx1mmx1mm. Other experimental parameters were: TE of 15ms,
TR of 7.5s, labeling duration of 1.8s, post-labeling duration of 2s, and 30
signal averages.
Image processing and statistical analysisFor each participant, a whole-brain
MWF map was generated from the SPGR, bSSFP, and DAM datasets using BMC-mcDESPOT
(4-6), a
R1 map
was generated from the SPGR and DAM datasets (7), and a CBF map was
generated from the pCASL dataset using the NESMA analysis to improve accuracy
and precision in CBF determination (10). Further, using the FSL
software (11), the averaged SPGR image
over FAs was nonlinearly registered to the MNI space and the computed
transformation matrix was then applied to the corresponding MWF and
R1 maps. Similarly, the PD image was nonlinearly registered to the MNI space and
the computed transformation matrix was then applied to the corresponding CBF map.
FAST segmentation was also performed to generate WM and cortical GM masks (11). Six regions of interest (ROIs) were defined
from the MNI structural atlas corresponding to the whole brain, and the
frontal, parietal, temporal and occipital lobes, and cerebellum. Within each
ROI, the mean MWF,
R1, and CBF values were calculated.
Analysis was restricted to WM ROIs for MWF and to cortical GM or WM for CBF; this
is due to the small amount of myelin in GM imposing a well-recognized challenge
for accurate MWF determination. Finally, for each ROI, the effect of CBF on MWF
or
R1 was investigated using multiple linear regression with
the mean MWF or
R1 value as the dependent variable and the
mean CBF value, sex, age, and age
2 (12, 13) as the independent
variables.
RESULTS & DISCUSSION
Figure 1 shows the regressions of
MWF with CBF indicating a statistically significant positive correlation in most
WM and GM brain regions studied. This indicates that decreased CBF corresponds
to decreased MWF. These results agree with, and are complementary to, previous
DTI-based investigations showing an association between reduced brain perfusion,
and increased white matter lesion burden and decreased anisotropy of water
diffusion. However, DTI-outcomes, including fractional anisotropy, while sensitive
to microstructural changes, are not specific, so that potential microstructural
correlates of the decline in CBF in these studies include not only myelin loss,
but also axonal damage, or other forms of neurodegeneration. Our highlights the
specific implication of CBF deficits for myelin loss. Indeed, this relationship
between perfusion and myelination provides insights into the processes
underlying demyelination and its potential role in neurodegenerative diseases,
especially given the vulnerability of oligodendrocyte metabolism to local blood
flow. These
results indicate that interventions related to CBF may represent a novel
therapeutic target in dementia.
Figure 2 indicates the
statistically significant decrease in R1 with CBF. This further supports our main hypothesis of a
potential association between myelin breakdown with CBF decline (Fig. 1, CBF vs.
MWF). Indeed, while not specific to myelin content, R1 is
very sensitive to changes in lipid content (14), with lipid being the main constituent of myelin.CONCLUSIONS
In this
first study examining the association between CBF deficits and myelin integrity,
we showed that myelin content declines with CBF across a wide age range of
cognitively normal subjects.Acknowledgements
This work was supported by the Intramural Research Program of the National Institute on Aging of the National Institutes of Health.
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