Assessment of functional and structural brain abnormalities with resting-state functional MRI in patients with vestibular neuronitis.

BACKGROUND: Vestibular neuritis (VN) is a disorder manifesting as acute, isolated, spontaneous vertigo. There are few comprehensive studies on the changes in related functional and structural brain regions. PURPOSE: To evaluate alterations in spontaneous neural activity, functional connectivity (FC), and gray matter volume (GMV) in patients with VN. MATERIAL AND METHODS: A total of 24 patients with VN and 22 age- and sex-matched healthy controls underwent resting-state functional magnetic resonance imaging (rs-fMRI) and three-dimensional T1-weighted anatomical imaging. We calculated the amplitude of low frequency fluctuation (ALFF), regional homogeneity (ReHo), and degree centrality (DC) to discern local brain abnormalities. The most abnormal brain region was selected as the region of interest (ROI) for FC analysis based on ALFF and ReHo values after Bonferroni correction. Voxel-based morphometry (VBM) was used to assess differences in GMV. RESULTS: Patients with VN, compared to healthy controls, showed increased ALFF (P < 0.001), ReHo values (P = 0.002, <0.001), and DC (P = 0.013) in the left lingual gyrus and right postcentral gyrus. FC analysis demonstrated enhanced connectivity between the left lingual gyrus and the left superior frontal gyrus, and decreased connectivity with the right insula gyrus, right and left supramarginal gyrus (P = 0.012, 0.004, <0.001, 0.014). In addition, GMV was reduced in the bilateral caudate (P = 0.022, 0.014). CONCLUSIONS: Patients with VN exhibit abnormal spontaneous neural activity and changes in ALFF, ReHo, DC, GMV, and FC. Understanding these functional and structural brain abnormalities may elucidate the underlying mechanisms of VN.

The mechanism behind activation of the Nod-like receptor family protein 3 inflammasome in Parkinson's disease.

Previous studies have shown that the ATP-P2X4 receptor signaling pathway mediates the activation of the Nod-like receptor family protein 3 (NLRP3) inflammasome. The NLRP3 inflammasome may promote renal interstitial inflammation in diabetic nephropathy. As inflammation also plays an important role in the pathogenesis of Parkinson's disease, we hypothesized that the ATP-P2X4 receptor signaling pathway may activate the NLRP3 inflammasome in Parkinson's disease. A male rat model of Parkinson's disease was induced by stereotactic injection of 6-hydroxydopamine into the pars compacta of the substantia nigra. The P2X4 receptor and the NLRP3 inflammasome (interleukin-1ß and interleukin-18) were activated. Intracerebroventricular injection of the selective P2X4 receptor antagonist 5-(3-bromophenyl)-1,3-dihydro-2H-benzofuro[3,2-e]-1,4-diazepin-2-one (5-BDBD) or knockdown of P2X4 receptor expression by siRNA inhibited the activation of the NLRP3 inflammasome and alleviated dopaminergic neurodegeneration and neuroinflammation. Our results suggest that the ATP-P2X4 receptor signaling pathway mediates NLRP3 inflammasome activation, dopaminergic neurodegeneration, and dopamine levels. These findings reveal a novel role of the ATP-P2X4 axis in the molecular mechanisms underlying Parkinson's disease, thus providing a new target for treatment. This study was approved by the Animal Ethics Committee of Qingdao University, China, on March 5, 2015 (approval No. QYFYWZLL 26119).