AMRI has continued its investigation into the mechanisms that generate anatomical and functional contrast in MRI scans. In susceptibility-weighted MRI, a technique for anatomical MRI that provides unique contrast and high spatial resolution at high magnetic field, the major contributors to contrast between healthy brain tissues have been revealed and quantitified. However, quantification of these contributions remains difficult and remaining uncertainties are 1) what is the distribution of susceptibility compounds on the cellular level;and 2) what is the molecular mechanism that creates exchange-induced NMR frequency shifts. In the 2010-2011 review year, AMRI has made some progress towards addressing the cellular mechanism underlying susceptibility contrast. Specifically, by studying marmoset brain at diiference orientations relative to the magnetic field it was found that magnetic susceptibility effects are the major contributor to T2* relaxation at high field (7Tesla), that this contribution is orientation dependent, and that pure dipolar effects that underlie T2 relaxation contribute to a lesser extent. These relaxation effects are attributed to myelin. In addition, it was found that this susceptibility effect is also reflected in the T2* decay curve and cause multi-component relaxation behavior. These findings suggest the possibility of studying the brains myelin content through T2* relaxation, which is potentially important for demyelinating diseases such as MS. In addition, it was found that in MS, strong susceptibility effects that occur in the periphery of some MS lesions are caused by elecated iron in macrophages and microglia. In functional MRI, contrast mechanisms were further investigated by performing physiological and neuronal challenges. It was found that respiratory challenges cause a spatially dependent blood-oxygen-level change accross the brain observable from both the amplitude and timing of the response. The regional dependence in the timing suggest that the underlying vascular dilation is caused by a vasoactive agent that resides in the arterial vasculature and originates from regions significantly upstream from the cerbral cortex. In addition, it was found that substantial downstream effects occur in the venous vasculature due to passive vasodilation.

Project Start
Project End
Budget Start
Budget End
Support Year
5
Fiscal Year
2011
Total Cost
$1,592,200
Indirect Cost
City
State
Country
Zip Code
Jiang, Xu; van Gelderen, Peter; Duyn, Jeff H (2017) Spectral characteristics of semisolid protons in human brain white matter at 7 T. Magn Reson Med 78:1950-1958
Shmueli, K; Dodd, S J; van Gelderen, P et al. (2017) Investigating lipids as a source of chemical exchange-induced MRI frequency shifts. NMR Biomed 30:
Duyn, Jeff H; Schenck, John (2017) Contributions to magnetic susceptibility of brain tissue. NMR Biomed 30:
Duyn, Jeff H (2017) Studying brain microstructure with magnetic susceptibility contrast at high-field. Neuroimage :
Chang, Catie; Leopold, David A; Schölvinck, Marieke Louise et al. (2016) Tracking brain arousal fluctuations with fMRI. Proc Natl Acad Sci U S A 113:4518-23
Chang, Catie; Raven, Erika P; Duyn, Jeff H (2016) Brain-heart interactions: challenges and opportunities with functional magnetic resonance imaging at ultra-high field. Philos Trans A Math Phys Eng Sci 374:
van Gelderen, Peter; Jiang, Xu; Duyn, Jeff H (2016) Effects of magnetization transfer on T1 contrast in human brain white matter. Neuroimage 128:85-95
Mandelkow, Hendrik; de Zwart, Jacco A; Duyn, Jeff H (2016) Linear Discriminant Analysis Achieves High Classification Accuracy for the BOLD fMRI Response to Naturalistic Movie Stimuli. Front Hum Neurosci 10:128
Li, Xiaozhen; van Gelderen, Peter; Sati, Pascal et al. (2015) Detection of demyelination in multiple sclerosis by analysis of [Formula: see text] relaxation at 7 T. Neuroimage Clin 7:709-14
Yao, Bing; Ikonomidou, Vasiliki N; Cantor, Fredric K et al. (2015) Heterogeneity of Multiple Sclerosis White Matter Lesions Detected With T2*-Weighted Imaging at 7.0 Tesla. J Neuroimaging 25:799-806

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