An Open Resource for Non-human Primate Imaging.

Non-human primate neuroimaging is a rapidly growing area of research that promises to transform and scale translational and cross-species comparative neuroscience. Unfortunately, the technological and methodological advances of the past two decades have outpaced the accrual of data, which is particularly challenging given the relatively few centers that have the necessary facilities and capabilities. The PRIMatE Data Exchange (PRIME-DE) addresses this challenge by aggregating independently acquired non-human primate magnetic resonance imaging (MRI) datasets and openly sharing them via the International Neuroimaging Data-sharing Initiative (INDI). Here, we present the rationale, design, and procedures for the PRIME-DE consortium, as well as the initial release, consisting of 25 independent data collections aggregated across 22 sites (total = 217 non-human primates). We also outline the unique pitfalls and challenges that should be considered in the analysis of non-human primate MRI datasets, including providing automated quality assessment of the contributed datasets

B₀ inhomogeneity-insensitive triple-quantum-filtered sodium imaging using a 12-step phase-cycling scheme

none3Triple-quantum-filtered (TQF) sodium MRI can be used to separate sodium NMR signals from different physiological compartments. Although three-pulse triple-quantum filtering has been demonstrated to be better suited for in vivo imaging, the absence of the refocusing pulse in the filter increases its sensitivity to magnetic field inhomogeneities. Therefore, several TQF cycles have been developed previously to correct image distortions caused by B(0) inhomogeneities. In this paper, we present a new 12-step phase-cycling TQF scheme based on three radiofrequency pulses which allows the compensation of B(0) variations both with and without ancillary B(0) map information. The method offers 40% higher signal-to-noise-ratio efficiency compared with the previously developed B(0)-correcting phase-cycling schemes.openFleysher, L; Oesingmann, N; Inglese, M.Fleysher, L; Oesingmann, N; Inglese, MARIA MATILD

Sodium MRI of multiple sclerosis

reserved4siMultiple sclerosis (MS) is the most common cause of non-traumatic disability in young adults. The mechanisms underlying neurodegeneration and disease progression are poorly understood, in part as a result of the lack of non-invasive methods to measure and monitor neurodegeneration in vivo. Sodium MRI is a topic of increasing interest in MS research as it allows the metabolic characterization of brain tissue in vivo, and integration with the structural information provided by 1H MRI, helping in the exploration of pathogenetic mechanisms and possibly offering insights into disease progression and monitoring of treatment outcomes. We present an up-to-date review of the sodium MRI application in MS organized into four main sections: (i) biological and pathogenetic role of sodium; (ii) brief overview of sodium imaging techniques; (iii) results of sodium MRI application in clinical studies; and (iv) future perspectives.mixedPetracca, M; Fleysher, L; Oesingmann, N; Inglese, M.Petracca, M; Fleysher, L; Oesingmann, N; Inglese, MARIA MATILD

Brain Metabolite Proton T2 Mapping at 3.0 T in Relapsing-Remitting Multiple Sclerosis1

For 3.0-T T2-weighted MR imaging in relapsing-remitting multiple sclerosis, one T2 signal per metabolite suffices in any brain region, irrespective of disease duration, thus validating the hypothesis that the spectroscopic signal intensity changes predominantly represent metabolite levels and not T2 weighting

The substrate of increased cortical FA in MS: A 7T post-mortem MRI and histopathology study

Background: Using diffusion tensor imaging (DTI), it was previously found that demyelinated gray matter (GM) lesions have increased fractional anisotropy (FA) when compared to normal-appearing gray matter (NAGM) in multiple sclerosis (MS). The biological substrate underlying this FA change is so far unclear; both neurodegenerative changes and microglial activation have been proposed as causal contributors. Objective: To test the proposed hypothesis that microglia activation is responsible for increased FA in cortical GM lesions. Methods: We investigated post-mortem cortical DTI changes in hemispheric, coronally cut sections and investigated the underlying histopathology using immunohistochemistry. Results: Overall, there were few activated microglia/macrophages, and no difference between GM lesions and NAGM was observed. However, cell density was increased in GM lesions compared to NAGM (309.67 ± standard deviation (SD) 124.44 vs 249.95 ± SD 56.75, p = 0.002). Conclusion: FA increase was not due to lesional and non-lesional differences in microglia activation and/or proliferation. We found an increase in general cellular density without a notable difference in cellular size, that is, tissue compaction, as a possible alternative explanation