Elior Drori1, Shir Filo1, and Aviv Mezer1
1The Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
Synopsis
The striatum is a heterogeneous brain structure with
microstructural gradients along its main axes. Changes in its organization are
associated with normal aging and disease. Yet the spatial variability in the
human striatum is not well characterized and is mostly limited to postmortem studies.
We propose a robust non-invasive method for detection and quantification of
microstructural gradients along axes of the striatum in individuals in vivo, using qMRI.
We show distinct profiles of spatial and aging-related changes in the striatum,
associated with different biophysical sources such as tissue density and iron
content, estimated in
vivo.
Introduction
The dorsal striatum, composed of the caudate
nucleus and the putamen, is involved in motor control and goal-directed
behavior1. It is characterized by spatial heterogeneity in
neurochemical environments and connectivity, showing gradients along its main
axes2,3. Changes in the striatal microstructure are associated with basal ganglia disease (e.g. Parkinson’s disease) and aging-related declines in motor and cognition4,5. Therefore, non-invasive quantification of the gradual
changes that characterize the human striatal tissue has scientific and clinical
importance. Quantitative
MRI (qMRI) methods are sensitive to the micro-environment of the tissue, allowing for “in
vivo histology” of the human brain6. We have recently developed a non-invasive tool
for quantifying
structural heterogeneity along axes of the human striatum of individuals, using qMRI7. Here, we use this method to detect spatially
dependent and aging-related microstructural changes, and give evidence for the
robustness of our method across datasets. Furthermore, we explore different
biophysical sources of the spatial and aging-related variation, demonstrating
different effects of iron content and tissue density, in vivo.Methods
MRI acquisition – 3T MRI scans were performed on 20 young adults (aged 27 ± 2 years, 10 females)
and 18 older adults (aged 67 ± 6 years, 5 females)8. Data for quantitative R1, R2* and the macromolecular tissue volume (MTV)
mapping were acquired using siemens FLASH sequence, with SEIR data for B1+ bias correction9. R1 and MTV maps were computed using
mrQ9 and R2* fitting was done using MPM10.
Dataset for replication – We analyzed 3T
quantitative R1 data of 20 young adults
and 18 older adults, matched in age and sex to our own data. This data was collected in
Stanford University11,12.
Spatial change analysis – We have developed a tool for quantification of
microstructural variations along the main axes of subcortical structures, using
qMRI. For each individual structure, we compute the main orthogonal axes using
SVD on the 3D coordinates and measure the median qMRI parameter in segments along
each axis.
Statistical analysis – We used linear
mixed-effect models (MATLAB’s fitlme) for each structure and axis. We modelled subjects’
ID as a random effect and included sex as a covariate. Main and interaction
effects were modelled for age group, hemisphere, and position along the axis.
We used FDR to control for multiple comparisons, with alpha set to 0.05.Results
We found R1 gradients along axes of the putamen and
caudate that were robust across subjects and two independent datasets (Fig. 1,2).
These gradients showed laterality and aging-related changes that were
replicated in both datasets. Linear mixed-design models (covaried for sex) showed spatial effects along the
anterior-posterior (AP), ventral-dorsal (VD) and medial-lateral (ML) axes of
the putamen, and along the AP and ML axes of the caudate. In addition, in the
caudate it showed a three-way interaction effect of age group,
hemisphere, and position along the AP axis (pFDR corrected
< 0.001), thus showing an aging-related increase in
the interhemispheric microstructural asymmetry of the caudate (Fig. 1).
To investigate
the biophysical sources of spatial changes in the aging striatum, we examined
the spatial variability of several qMRI parameters, associated with myelin and
lipid content (R1), the non-water content of the tissue (MTV) and the iron
concentration (R2*). We found distinct profiles of spatial change in the
striatum for each of these parameters, as well as distinct associated
aging-related changes (Fig. 3). In order to compare the different profiles of
change, we normalized the R1, MTV and R2* gradients to their corresponding
white-matter median values and used each of them as the response variable in
mixed effect models. In many cases, changes in R1 were accompanied by similar
effects in MTV (Fig 4), suggesting that much of the observed variability
revealed by R1 is associated with tissue density. However, along the AP axes of
the caudate and putamen, R1 showed some hemispheric effects that were not
revealed by MTV, implying additional sensitivities of R1. In contrast, R2* generally
demonstrated a different pattern. Although R2* and R1 showed some overlaps, R2*
mostly showed main effects of age group, in addition to other spatial effects
that were not always similar to those observed in R1 or MTV (Fig 5).Conclusions
Our findings suggest that different parameters of qMRI
reveal distinct biological sources involved in the spatial heterogeneity of the
striatal tissue in vivo.
Moreover, aging-related changes involving these sources manifest differently in
the striatum. While R1 changes are mostly associated with variation in tissue
density, as uncovered by MTV, it reflects additional sources of variation,
mainly along the AP axes of the caudate and putamen. In contrast, changes in
iron concentration, estimated by R2*, show different patterns of spatial and aging-related
changes. This may suggest that changes in water content and iron accumulation
constitute distinct aging mechanisms. Further work will use postmortem validation
of this in vivo
biophysical analysis to strengthen our findings. In addition to its application
to the study of normal aging, our method may prove useful for quantification of
abnormal changes in basal ganglia disease such as Parkinson’s diseaseAcknowledgements
No acknowledgement found.References
-
Kravitz, A. V.
& Kreitzer, A. C. Striatal mechanisms underlying movement, reinforcement,
and punishment. Physiology vol. 27 167–177 (2012).
- Graybiel, A.
M. & Ragsdale, C. W. Histochemically distinct compartments in the striatum
of human, monkeys, and cat demonstrated by acetylthiocholinesterase staining. Proc.
Natl. Acad. Sci. 75, 5723–5726 (1978).
- Haber, S. N.
Corticostriatal circuitry. Dialogues Clin. Neurosci. 18, 7–21
(2016).
- Crittenden, J.
R. & Graybiel, A. M. Basal ganglia disorders associated with imbalances in
the striatal striosome and matrix compartments. Frontiers in Neuroanatomy
vol. 5 59 (2011).
- Umegaki, H.,
Roth, G. S. & Ingram, D. K. Aging of the striatum: Mechanisms and
interventions. Age vol. 30 251–261 (2008).
- Weiskopf, N.,
Mohammadi, S., Lutti, A. & Callaghan, M. F. Advances in MRI-based
computational neuroanatomy: From morphometry to in-vivo histology. Current
Opinion in Neurology vol. 28 313–322 (2015).
- Drori, E.,
Filo, S. & Mezer, A. Measuring Biological Gradients along the Human Dorsal
Striatum in vivo using Quantitative MRI. in ISMRM Annual Meeting (2020).
- Filo, S. et
al. Disentangling molecular alterations from water-content changes in the
aging human brain using quantitative MRI. Nat. Commun. 10,
(2019).
- Mezer, A. et
al. Quantifying the local tissue volume and composition in individual
brains with magnetic resonance imaging. Nat. Med. 19, 1667–1672
(2013).
- Weiskopf, N. et
al. Quantitative multi-parameter mapping of R1, PD*, MT, and R2* at 3T: a
multi-center validation. Front. Neurosci. 7, (2013).
- Yeatman, J.,
Wandell, B. & Mezer, A. Lifespan maturation and degeneration of human brain
white matter. Nat. Commun. 5, (2014).
- Sacchet, M.
& Gotlib, I. Myelination of the brain in major depressive disorder: an in
vivo quantitative magnetic resonance imaging study. Sci. Rep. 7,
(2017).