Phase imaging with multiple phase-cycled balanced steady-state free precession at 9.4 T.

While phase imaging with a gradient echo (GRE) sequence is popular, phase imaging with balanced steady-state free precession (bSSFP) has been underexplored. The purpose of this study was to investigate anatomical and functional phase imaging with multiple phase-cycled bSSFP, in expectation of increasing spatial coverage of steep phase-change regions of bSSFP. Eight different dynamic 2D pass-band bSSFP studies at four phase-cycling (PC) angles and two TE /TR values were performed on rat brains at 9.4 T with electrical forepaw stimulation, in comparison with dynamic 2D GRE. Anatomical and functional phase images were obtained by averaging the dynamic phase images and mapping correlation between the dynamic images and the stimulation paradigm, and were compared with their corresponding magnitude images. Phase imaging with 3D pass-band and 3D transition-band bSSFP was also performed for comparison with 3D GRE phase imaging. Two strategies of combining the multiple phase-cycled bSSFP phase images were also proposed. Contrast between white matter and gray matter in bSSFP phase images significantly varied with PC angle and became twice as high as that of GRE phase images at a specific PC angle. With the same total scan time, the combined bSSFP phase images provided stronger phase contrast and visualized neuronal fiber-like structures more clearly than the GRE phase images. The combined phase images of both 3D pass-band and 3D transition-band bSSFP showed phase contrasts stronger than those of the GRE phase images in overall brain regions, even at a longer TE of 20 ms. In contrast, phase functional MRI (fMRI) signals were weak overall and mostly located in draining veins for both bSSFP and GRE. Multiple phase-cycled bSSFP phase imaging is a promising anatomical imaging technique, while its usage as fMRI does not seem desirable with the current approach.

Central artery stiffness, baroreflex sensitivity, and brain white matter neuronal fiber integrity in older adults.

Cerebral hypoperfusion elevates the risk of brain white matter (WM) lesions and cognitive impairment. Central artery stiffness impairs baroreflex, which controls systemic arterial perfusion, and may deteriorate neuronal fiber integrity of brain WM. The purpose of this study was to examine the associations among brain WM neuronal fiber integrity, baroreflex sensitivity (BRS), and central artery stiffness in older adults. Fifty-four adults (65 ± 6 years) with normal cognitive function or mild cognitive impairment (MCI) were tested. The neuronal fiber integrity of brain WM was assessed from diffusion metrics acquired by diffusion tensor imaging. BRS was measured in response to acute changes in blood pressure induced by bolus injections of vasoactive drugs. Central artery stiffness was measured by carotid-femoral pulse wave velocity (cfPWV). The WM diffusion metrics including fractional anisotropy (FA) and radial (RD) and axial (AD) diffusivities, BRS, and cfPWV were not different between the control and MCI groups. Thus, the data from both groups were combined for subsequent analyses. Across WM, fiber tracts with decreased FA and increased RD were associated with lower BRS and higher cfPWV, with many of the areas presenting spatial overlap. In particular, the BRS assessed during hypotension was strongly correlated with FA and RD when compared with hypertension. Executive function performance was associated with FA and RD in the areas that correlated with cfPWV and BRS. These findings suggest that baroreflex-mediated control of systemic arterial perfusion, especially during hypotension, may play a crucial role in maintaining neuronal fiber integrity of brain WM in older adults.

Spatial Distribution of Parvalbumin-Positive Fibers in the Mouse Brain and Their Alterations in Mouse Models of Temporal Lobe Epilepsy and Parkinson's Disease.

Parvalbumin interneurons belong to the major types of GABAergic interneurons. Although the distribution and pathological alterations of parvalbumin interneuron somata have been widely studied, the distribution and vulnerability of the neurites and fibers extending from parvalbumin interneurons have not been detailly interrogated. Through the Cre recombinase-reporter system, we visualized parvalbumin-positive fibers and thoroughly investigated their spatial distribution in the mouse brain. We found that parvalbumin fibers are widely distributed in the brain with specific morphological characteristics in different regions, among which the cortex and thalamus exhibited the most intense parvalbumin signals. In regions such as the striatum and optic tract, even long-range thick parvalbumin projections were detected. Furthermore, in mouse models of temporal lobe epilepsy and Parkinson's disease, parvalbumin fibers suffered both massive and subtle morphological alterations. Our study provides an overview of parvalbumin fibers in the brain and emphasizes the potential pathological implications of parvalbumin fiber alterations.

Altered globotriaosylceramide accumulation and mucosal neuronal fiber density in the colon of the Fabry disease mouse model.

BACKGROUND: Fabry disease (FD) is a hereditary X-linked metabolic storage disorder characterized by deficient or absent lysosomal α-galactosidase A (α-Gal A) activity. This deficiency causes progressive accumulation of glycosphingolipids, primarily globotriaosylceramide (Gb3), in nearly all organ systems. Gastrointestinal (GI) symptoms can be very debilitating and are among the most frequent and earliest of the disease. As the pathophysiology of these symptoms is poorly understood, we carried out a morphological and molecular characterization of the GI tract in α-Gal A knockout mice colon in order to reveal the underlying mechanisms. METHODS: Here, we performed the first morphological and biomolecular characterization of the colon wall structure in the GI tract of the α-Gal A knock-out mouse (α-Gal A -/0), a murine model of FD. KEY RESULTS: Our data show a greater thickness of the gastrointestinal wall in α-Gal A (-/0) mice due to enlarged myenteric plexus' ganglia. This change is paralleled by a marked Gb3 accumulation in the gastrointestinal wall and a decreased and scattered pattern of mucosal nerve fibers. CONCLUSIONS AND INFERENCES: The observed alterations are likely to be a leading cause of gut motor dysfunctions experienced by FD patients and imply that the α-Gal A (-/0) male mouse represents a reliable model for translational studies on enteropathic pain and GI symptoms in FD.