Synopsis
Altered
lipid and protein contents have been detected with MR spectroscopy in acute
multiple sclerosis lesions and speculated to reflect de- and remyelination
processes. To date, however, neither the metabolites involved nor their
pathological relevance have been satisfactorily described. Hofmann et al.
introduced an elegant concept for the separation of biochemicals of varying
metabolic weight based on differences in T1 relaxation behavior (MRM 46, 2001).
Here, we describe T1-encoded MR spectroscopy at 7 Tesla, the extraction of
individual, spectroscopically overlapping lipid/protein signals by
two-dimensional processing and initial applications to the study of the pathological processes associated
to multiple sclerosis tissue injury and repair.Introduction
Multiple sclerosis (MS) is a chronic disorder
of the central nervous system that leads to demyelination and
neurodegeneration. Magnetic resonance spectroscopy (MRS) allows the assessment
of the pathological changes and brain damage from the earliest stage of the disease
1-4. Altered lipid and protein contents have been detected with MRS in
acute MS lesions and speculated to reflect de- and remyelination
processes
5-9. Lipids/proteins
have been characterized in detail with MRS in the healthy human brain
10 and assigned based
on measurements in rat brain extracts
11. In MS, however, neither the particular
lipids/proteins involved nor their pathological relevance have been
satisfactorily described, at least in part due to methodological obstacles to
quantify them
in vivo. The purpose of this study was the establishment of dedicated lipid/protein MRS as a tool for clinical MS research.
Methods
Signals from
lipids/proteins, so-called macromolecules (MM, 10-100 kD), overlap with
signals from low molecular weight (LMW) neurochemicals including NAA, choline,
or glutamate in
1H MRS of the
in vivo human brain
(Fig. 1E, gray) which fundamentally limits reliable lipid/protein quantification. Commonly used approaches to disentangle the MM baseline from
the LMW signals rely on inversion-recovery preparation to "null" the
LMW contribution. These techniques, however, are limited by the
substance-specific spread of T1 relaxation times of both MM and LMW
metabolites. Hofmann et al. introduced an elegant way to encode metabolite T1’s
with an array of saturation-recovery prepared MRS acquisitions
12. This technique
employs the systematically shorter and longer T1 times of
MMs compared to LMW substances, respectively, to separate both groups based on
a T1 threshold. Their work was primarily aimed at improving the
quantification of LMW metabolites. Here, the quantification of the
lipid/protein profile, i.e. the MM baseline, was the primary goal.
Lipid/protein concentrations and composition are thought to reflect processes
involved in MS tissue injury and repair. The level of lipid elevation is
hypothesized to correlate with the active inflammation process, e.g. in new
plaques, based on the macrophage lipid signal similar to stroke tissue
13,14. T1-decomposition was employed with optimized 7 Tesla
technology for gains in sensitivity and spectral dispersion. Non-selective
saturation was followed by short echo-time STEAM
15 (TE 10 ms) for an array of logarithmically scaled recovery delays ranging
from 0.2 to 10/14 sec. Third order B
0 shimming and an 8-channel RF
phased-array coil were used to achieve optimized B
0 homogeneity and B
1
sensitivity, respectively
16. In addition, two-dimensional processing
(similar to 2D NMR) was applied to disentangle not only the MM baseline from
LMW neurochemicals, but also individual, spectroscopically overlapping lipid/protein signals.
Results
T1-encoded MRS at 7 Tesla obtained from the healthy human brain allowed the separation
of the short-T1 MM baseline from LMW metabolites, in line with Hofmann et al. (Fig. 1). The lipid/protein
signals are consistent with the MM
resonances reported by Behar et al.10, including the superposition
of long-T1 glutamate and short-T1 'M6' macromolecule signals at 2.3 ppm. The integration of T1-frequency regions (as opposed to T1
thresholding) furthermore allowed the separation of individual lipid/protein
signal components, which is a requirement for their independent quantification (Fig. 2). While the measurement of lipids/proteins was the primary goal, the complementary quantification of 10+ additional
substances including glutamate and established biomarkers of MS1-4 is crucial for the comprehensive study of MS pathological processes.
A clinical research study to validate the method as a tool for diagnostics and monitoring is currently under way that includes a
cross-sectional comparison of the lipid/protein profile in MS lesions and of
contra-lateral, normal appearing control areas in the same patient and in healthy
controls (Figs. 3/4, >10 subjects completed).
Discussion / Outlook
T1-decomposed MRS with improved sensitivity and spectral dispersion at 7 Tesla is presented for the quantification
of lipids/proteins associated with MS pathology. An increase of the combined valine+leucine+isoleucine
signals from proteins around 0.9 ppm and threonine+alanine signals around 1.3 ppm
in lesions in MS subjects compared to healthy controls has been described previously6. Once fully validated, the method is
expected to promote the assignment of specific spectral components to specific
protein/lipid changes characteristic of different stages of the pathological
process and to thereby shed light on the role of individual compounds in MS
tissue and repair processes. We note that such in
vivo direct knowledge of the de- and remyelination processes is not
accessible otherwise. T1-encoded MRS at 7 Tesla is expected to allow 1) the assessment of the pathobiochemistry of lipids/proteins in MS lesions, 2) the development of sensitive
lipid/protein-based MRS biomarkers and 3) the correlation of clinical prognosis to
injury severity and potential for repair, e.g. remyelination, in future
studies.
Acknowledgements
Research Participants:
We are very grateful to the MS patients and healthy controls who participated in this research.
Clinical Support:
We are very grateful for the continuous support from the neurologists and staff of the Yale Multiple Sclerosis Center
Grant Support:
1)
National Multiple Sclerosis Society (Research Grant RG-4319, Pilot Grant PP-3356)
2)
Nancy Davis Foundation (Pilot Grant, ”Race-to-Erase”)
3)
Yale Center for Clinical Investigation (CTSA Scholar Award, UL1 TR 000142)
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