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Introduction: Ultra-high-field magnetic resonance (MR) systems (7 T and 9.4 T) offer the ability to probe human brain metabolism with enhanced precision. Here, we present the preliminary findings from 3D MR spectroscopic imaging (MRSI) of the human brain conducted with the world's first 10.5 T whole-body MR system.
Methods: Employing a custom-built 16-channel transmit and 80-channel receive MR coil at 10.5 T, we conducted MRSI acquisitions in six healthy volunteers to map metabolic compounds in the human cerebrum in vivo. Three MRSI protocols with different matrix sizes and scan times (4.4 × 4.4 × 4.4 mm³: 10 min, 3.4 × 3.4 × 3.4 mm³: 15 min, and 2.75×2.75×2.75 mm³: 25 min) were tested. Concentric ring trajectories were utilized for time-efficient encoding of a spherical 3D k-space with ∼4 kHz spectral bandwidth. B/B shimming was performed based on respective field mapping sequences and anatomical T-weighted MRI were obtained.
Results: By combining the benefits of an ultra-high-field system with the advantages of free-induction-decay (FID-)MRSI, we present the first metabolic maps acquired at 10.5 T in the healthy human brain at both high (voxel size of 4.4³ mm³) and ultra-high (voxel size of 2.75³ mm³) isotropic spatial resolutions. Maps of 13 metabolic compounds (aspartate, choline compounds and creatine + phosphocreatine, γ-aminobutyric acid (GABA), glucose, glutamine, glutamate, glutathione, myo-inositol, scyllo-inositol, N-acetylaspartate (NAA), N-acetylaspartylglutamate (NAAG), taurine) and macromolecules were obtained individually. The spectral quality was outstanding in the parietal and occipital lobes, but lower in other brain regions such as the temporal and frontal lobes. The average total NAA (tNAA = NAA + NAAG) signal-to-noise ratio over the whole volume of interest was 12.1± 8.9 and the full width at half maximum of tNAA was 24.7± 9.6 Hz for the 2.75 × 2.75 × 2.75 mm³ resolution. The need for an increased spectral bandwidth in combination with spatio-spectral encoding imposed significant challenges on the gradient system, but the FID approach proved very robust to field inhomogeneities of ∆B = 45 ± 38 Hz (frequency offset ± spatial STD) and B = 65 ± 11° within the MRSI volume of interest.
Discussion: These preliminary findings highlight the potential of 10.5 T MRSI as a powerful imaging tool for probing cerebral metabolism. By providing unprecedented spatial and spectral resolution, this technology could offer a unique view into the metabolic intricacies of the human brain, but further technical developments will be necessary to optimize data quality and fully leverage the capabilities of 10.5 T MRSI.
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http://dx.doi.org/10.1016/j.neuroimage.2025.121015 | DOI Listing |
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International School of Microelectronics, Dongguan University of Technology, Dongguan 523808, China.
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Aix Marseille Univ, INSERM, INS, Inst Neurosci Syst, 13005 Marseille, France.
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Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey, United States of America.
Research into the mechanisms underlying neuromodulation by tES using in-vivo animal models is key to overcoming experimental limitations in humans and essential to building a detailed understanding of the in-vivo consequences of tES. Insights from such animal models are needed to develop targeted and effective therapeutic applications of non-invasive brain stimulation in humans. The sheer difference in scale and geometry between animal models and the human brain contributes to the complexity of designing and interpreting animal studies.
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Obstructive sleep apnea (OSA), one of the most common sleep disorders globally, is closely linked to brain function. Resting-state electroencephalography (EEG), due to its convenience, cost-effectiveness, and high temporal resolution, serves as a valuable tool for exploring the human brain function. This study utilized a large cohort with 968 participants who joined in 15-minute daytime resting-state EEG acquisition and overnight polysomnography (PSG) monitoring.
View Article and Find Full Text PDFJCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
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