4,077 research outputs found

    Resolution enhancement, noise suppression, and joint T2* decay estimation in dual-echo sodium-23 MR imaging using anatomically-guided reconstruction

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    Purpose: Sodium MRI is challenging because of the low tissue concentration of the 23 Na nucleus and its extremely fast biexponential transverse relaxation rate. In this article, we present an iterative reconstruction framework using dual-echo 23Na data and exploiting anatomical prior information (AGR) from high-resolution, low-noise, 1 H MR images. This framework enables the estimation and modeling of the spatially-varying signal decay due to transverse relaxation during readout (AGRdm), which leads to images of better resolution and reduced noise resulting in improved quantification of the reconstructed 23Na images. Methods: The proposed framework was evaluated using reconstructions of 30 noise realizations of realistic simulations of dual echo twisted projection imaging (TPI) 23 Na data. Moreover, three dual echo 23 Na TPI brain data sets of healthy controls acquired on a 3T Siemens Prisma system were reconstructed using conventional reconstruction, AGR and AGRdm. Results: Our simulations show that compared to conventional reconstructions, AGR and AGRdm show improved bias-noise characteristics in several regions of the brain. Moreover, AGR and AGRdm images show more anatomical detail and less noise in the reconstructions of the experimental data sets. Compared to AGR and the conventional reconstruction, AGRdm shows higher contrast in the sodium concentration ratio between gray and white matter and between gray matter and the brain stem. Conclusion: AGR and AGRdm generate 23 Na images with high resolution, high levels of anatomical detail, and low levels of noise, potentially enabling high-quality 23 Na MR imaging at 3T.Comment: 19 pages, 8 figures, 2 table

    Reward circuitry is perturbed in the absence of the serotonin transporter

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    The serotonin transporter (SERT) modulates the entire serotonergic system in the brain and influences both the dopaminergic and norepinephrinergic systems. These three systems are intimately involved in normal physiological functioning of the brain and implicated in numerous pathological conditions. Here we use high-resolution magnetic resonance imaging (MRI) and spectroscopy to elucidate the effects of disruption of the serotonin transporter in an animal model system: the SERT knock-out mouse. Employing manganese-enhanced MRI, we injected Mn^(2+) into the prefrontal cortex and obtained 3D MR images at specific time points in cohorts of SERT and normal mice. Statistical analysis of co-registered datasets demonstrated that active circuitry originating in the prefrontal cortex in the SERT knock-out is dramatically altered, with a bias towards more posterior areas (substantia nigra, ventral tegmental area, and Raphé nuclei) directly involved in the reward circuit. Injection site and tracing were confirmed with traditional track tracers by optical microscopy. In contrast, metabolite levels were essentially normal in the SERT knock-out by in vivo magnetic resonance spectroscopy and little or no anatomical differences between SERT knock-out and normal mice were detected by MRI. These findings point to modulation of the limbic cortical–ventral striatopallidal by disruption of SERT function. Thus, molecular disruptions of SERT that produce behavioral changes also alter the functional anatomy of the reward circuitry in which all the monoamine systems are involved

    Altered Neurocircuitry in the Dopamine Transporter Knockout Mouse Brain

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    The plasma membrane transporters for the monoamine neurotransmitters dopamine, serotonin, and norepinephrine modulate the dynamics of these monoamine neurotransmitters. Thus, activity of these transporters has significant consequences for monoamine activity throughout the brain and for a number of neurological and psychiatric disorders. Gene knockout (KO) mice that reduce or eliminate expression of each of these monoamine transporters have provided a wealth of new information about the function of these proteins at molecular, physiological and behavioral levels. In the present work we use the unique properties of magnetic resonance imaging (MRI) to probe the effects of altered dopaminergic dynamics on meso-scale neuronal circuitry and overall brain morphology, since changes at these levels of organization might help to account for some of the extensive pharmacological and behavioral differences observed in dopamine transporter (DAT) KO mice. Despite the smaller size of these animals, voxel-wise statistical comparison of high resolution structural MR images indicated little morphological change as a consequence of DAT KO. Likewise, proton magnetic resonance spectra recorded in the striatum indicated no significant changes in detectable metabolite concentrations between DAT KO and wild-type (WT) mice. In contrast, alterations in the circuitry from the prefrontal cortex to the mesocortical limbic system, an important brain component intimately tied to function of mesolimbic/mesocortical dopamine reward pathways, were revealed by manganese-enhanced MRI (MEMRI). Analysis of co-registered MEMRI images taken over the 26 hours after introduction of Mn^(2+) into the prefrontal cortex indicated that DAT KO mice have a truncated Mn^(2+) distribution within this circuitry with little accumulation beyond the thalamus or contralateral to the injection site. By contrast, WT littermates exhibit Mn^(2+) transport into more posterior midbrain nuclei and contralateral mesolimbic structures at 26 hr post-injection. Thus, DAT KO mice appear, at this level of anatomic resolution, to have preserved cortico-striatal-thalamic connectivity but diminished robustness of reward-modulating circuitry distal to the thalamus. This is in contradistinction to the state of this circuitry in serotonin transporter KO mice where we observed more robust connectivity in more posterior brain regions using methods identical to those employed here

    K-Bayes Reconstruction for Perfusion MRI I: Concepts and Application

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    Despite the continued spread of magnetic resonance imaging (MRI) methods in scientific studies and clinical diagnosis, MRI applications are mostly restricted to high-resolution modalities, such as structural MRI. While perfusion MRI gives complementary information on blood flow in the brain, its reduced resolution limits its power for detecting specific disease effects on perfusion patterns. This reduced resolution is compounded by artifacts such as partial volume effects, Gibbs ringing, and aliasing, which are caused by necessarily limited k-space sampling and the subsequent use of discrete Fourier transform (DFT) reconstruction. In this study, a Bayesian modeling procedure (K-Bayes) is developed for the reconstruction of perfusion MRI. The K-Bayes approach (described in detail in Part II: Modeling and Technical Development) combines a process model for the MRI signal in k-space with a Markov random field prior distribution that incorporates high-resolution segmented structural MRI information. A simulation study was performed to determine qualitative and quantitative improvements in K-Bayes reconstructed images compared with those obtained via DFT. The improvements were validated using in vivo perfusion MRI data of the human brain. The K-Bayes reconstructed images were demonstrated to provide reduced bias, increased precision, greater effect sizes, and higher resolution than those obtained using DFT
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