Naila Rahman1,2, Jake Hamilton1,2, Kathy Xu2, Arthur Brown2,3, and Corey Baron1,2
1Medical Biophysics, Western University, London, ON, Canada, 2Robarts Research Institute, London, ON, Canada, 3Anatomy and Cell Biology, Western University, London, ON, Canada
Synopsis
Keywords: Microstructure, Diffusion/other diffusion imaging techniques, Brain Maturation, Tensor-valued diffusion MRI
Motivation: Healthy rodent brain maturation research remains limited, although rodents are a predominant study model, which motivates further study to exclude confounds of developmental changes from pathophysiological interpretations.
Goal(s): Our goals were to investigate how microstructural MRI metrics change over the course of brain maturation and disentangle what changes in these metrics may indicate on a neurobiological level.
Approach: 11 mice were scanned at 9.4T between 3-8 months of age, with histology (n=4) performed at 3 and 8 months.
Results: Total diffusional kurtosis and myelin-specific metrics showed significant increases over time, paired with increased isotropic kurtosis and increased histological oligodendrocyte and astrocyte content.
Impact: This
work shows that there are ongoing microstructural changes even after mice are
considered “adults”, detectable by isotropic kurtosis. We provide new
interpretations of diffusion MRI changes during brain maturation, with evidence
of the underlying mechanisms impacting isotropic kurtosis.
Introduction
Most studies consider a steady state condition
of adulthood in rodents aged 2-3 months1. However, diffusion MRI (dMRI) and histology rodent
studies have demonstrated that myelination continues to increase past 3 months
of age1,2. As literature about healthy rodent brain
maturation remains sparse, we investigate how tensor-valued dMRI and
magnetization transfer (MT) MRI metrics evolve over the course of brain
maturation and disentangle what this may indicate on a neurobiological level. Tensor-valued
dMRI measures diffusion anisotropy independent of orientation dispersion and distinguishes
various sources of kurtosis3–5 and MT MRI provides specificity to myelin
content6.Methods
11
C57Bl/6 mice (6 males)
were scanned longitudinally at 3, 4, 5, and 8 months of age. Imaging was
performed at 9.4T with a 1T/m gradient insert using single-shot EPI with an
in-plane resolution of 0.175x0.2mm2, 0.5mm slice thickness.
Tensor-valued dMRI was implemented using a single diffusion encoding scheme
with linear and spherical tensor encodings at b=2000s/mm2 (30
directions), b=1000s/mm2 (12 directions), and 8 b=0s/mm2.
The MT protocol comprised three FLASH-3D scans, including an MTon, MToff, and
reference T1-weighted scan. The protocols and preprocessing steps are described
in detail in earlier work7–9. Mice were euthanized for histology
after the 8-month scan and another cohort of mice (not imaged) was acquired for
histology at 3 months. Immunohistochemistry was performed (n=4 for each
timepoint) using primary antibodies Olig2, GFAP, and Iba-1 to stain for glial
cells: oligodendrocytes (myelinating cells), astrocytes, and microglia,
respectively.
Metrics investigated include: mean,
axial, radial diffusivity (MD, AD, RD); fractional anisotropy (FA); total,
isotropic, anisotropic kurtosis (Ktotal, Kiso, Kaniso);
microscopic fractional anisotropy (µFA); magnetization transfer ratio and
saturation (MTR and MTsat). Ktotal (conventionally reported mean
kurtosis) is the summation of Kaniso and Kiso (related to
cell size/density heterogeneity)3.Results
Figure 1
shows representative parameter maps. For global white matter (WM), deep gray
matter (DGM), and cortex (CX), the decreases in RD agree with increases in FA (Figure
2). Ktotal shows significant increases, paired with increasing
trends of Kiso and MTsat, while Kaniso and µFA (which
show similar trends as they are monotonically related) remain stable. The
trends are similar for smaller ROIs (Figure 3). As there is a trend of
increasing Ktotal, Kiso, and MTsat, Figure 4 explores
the relationship of kurtosis metrics with MTsat over time, and between brain
regions. Figure 5 shows a marked increase in histological oligodendrocyte
content over time in both white and gray matter regions and increased astrocyte
content in the hippocampus (CA1). At 8 months of age, activated microglia (amoeboid
rather than ramified shapes) are present in the corpus callosum and cortex
(shown in white circles).Discussion
MRI Parameter Evolution
Similar
to our results, Hammelrath et al. reported that in most rodent white matter
ROIs, FA increased in agreement with increased intensity on myelin staining,
and interpreted that the drop in MD and RD with age was due to myelination1. The Ktotal increases are
comparable to previous brain maturation studies10–12, which related Ktotal
increases to myelination/dense axonal packing in white matter and dendritic
architectural modifications in gray matter. However, these interpretations
would be expected to coincide with changes in Kaniso (which is
specific to fibres while Kiso is not), which was not seen here. In
contrast, the Ktotal increases here are paired with increasing MTsat
and Kiso.
Relationship
of Kurtosis Metrics with MTsat
Figure 4 highlights a key finding in this
study, that changes in total kurtosis found over
time (in normal brain development) are driven by isotropic kurtosis, while
differences in total kurtosis found between brain regions are driven by
anisotropic kurtosis. This
indicates that while the main differences between white and gray matter regions
stem from fiber content/alignment (changing Kaniso), the main
differences over time are not related to changes in axonal content. Our results
suggest myelination of axons is not a main contributor to µFA and Kaniso.
Kiso as a marker of glial cell
content and diversification
Immunohistochemistry shows increased
oligodendrocyte and astrocyte content and microglial activation, at 8 months of
age compared to 3 months (Figure 5). Increased Kiso may
reflect the increased oligodendrocyte content, which is linked to myelin
formation, supported by increased MTsat. Kiso may also be sensitive
to microglia activation associated with development, and astrocyte cell size
and density increasing at different rates in different regions, which would
result in diversification of cell morphology13,14. It has previously been hypothesized
that increasing Kiso may reflect higher oligodendrocyte content15, and here we provide histological
support that changes in Kiso may reflect a combination of glial cell
content and diversification.Acknowledgements
The authors would like to acknowledge the funding sources: NSERC (Natural Sciences and Engineering Research Council), OGS (Ontario Graduate Scholarship), NFREF (New Frontiers in Research Fund).References
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