An individual's level of lower limb motor function is associated with his or her disability level after stroke, and motor improvement may lead to a better prognosis and quality of life. Data from animal models show that Qizhitongluo (QZTL) capsule facilitates recovery after focal brain injury. We aimed to validate the efficacy and safety of the QZTL capsule for promoting lower limb motor recovery in poststroke patients. In this randomized, multicenter, double-blind, placebo- and active-controlled trial from 13 sites in China, participants with ischemic stroke and Fugl-Meyer motor scale (FMMS) scores of <95 were eligible for inclusion. Patients were randomly assigned in a 2:1:1 ratio to the QZTL group, Naoxintong (NXT) group or placebo group for 12 weeks at 15-28 days after the onset of stroke. The primary outcome was the change in the Lower Limb FMMS (FMMS-LL) score from baseline over the 12-week intervention period. 622 participants were randomly assigned to the QZTL group (309), NXT group (159), or placebo group (154). The FMMS-LL score increased by 4.81 points (95 % CI, 4.27-5.35) in the QZTL group, by 3.77 points (95 % CI, 3.03-4.51) in the NXT group and by 3.00 points (95 % CI, 3.03-4.51) in the placebo group at week 12. The QZTL group showed significantly larger improvements compared with the placebo group at each interview from weeks 4-12 (difference, 0.89 [0.30,1.49] at week 4, P = 0.0032; difference, 1.83[1.01,2.66] at 90 days poststroke, P < 0.0001; difference, 1.81[0.88,2.74] at week 12, P = 0.0001). The QZTL capsule is an effective treatment for lower limb motor impairment. The finding indicates that the QZTL capsule may be used as a potential new strategy for stroke rehabilitation.

Objective: To investigate the changes in the cortical thickness of the region of interest (ROI) and plasma Aβ40, Aβ42, and phosphorylated Tau (P-Tau) concentrations in patients with Alzheimer’s disease (AD) and amnestic mild cognitive impairment (aMCI) as the disease progressed with surface-based morphometry (SBM), to analyze the correlation between ROI cortical thickness and measured plasma indexes and neuropsychological scales, and to explore the clinical value of ROI cortical thickness combined with plasma Aβ40, Aβ42, and P-Tau in the early recognition and diagnosis of AD.Methods: This study enrolled 33 patients with AD, 48 patients with aMCI, and 33 healthy controls (normal control, NC). Concentration changes in plasma Aβ42, Aβ40, and P-Tau collected in each group were analyzed. Meanwhile, the whole brain T1 structure images (T1WI-3D-MPRAGE) of each group of patients were collected, and T1 image in AD-aMCI, AD-NC, and aMCI-NC group were analyzed and processed by SBM technology to obtain brain regions with statistical differences as clusters, and the cortical thickness of each cluster was extracted. Multivariate ordered logistic regression analysis was used to screen out the measured plasma indexes and the indexes with independent risk factors in the cortical thickness of each cluster. Three comparative receiver operating characteristic (ROC) curves of AD-aMCI, AD-NC, and aMCI-NC groups were plotted, respectively, to explore the diagnostic value of multi-factor combined prediction for cognitive impairment. The relationship between cortical thickness and plasma indexes, and between cortical thickness and Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores were clarified by Pearson correlation analysis.Results: Plasma Aβ40, Aβ42, and P-Tau proteins in the NC, aMCI, and AD groups increased with the progression of AD (P < 0.01); cortical thickness reductions in the AD-aMCI groups and AD-NC groups mainly involved the bilateral superior temporal gyrus, transverse temporal gyrus, superior marginal gyrus, insula, right entorhinal cortex, right fusiform gyrus, and cingulate gyrus. However, there were no statistical significances in cortical thickness reductions in the aMCI and NC groups. The cortical thickness of the ROI was negatively correlated with plasma Aβ40, Aβ42, and P-Tau concentrations (P < 0.05), and the cortical thickness of the ROI was positively correlated with MMSE and MoCA scores. Independent risk factors such as Aβ40, Aβ42, P-Tau, and AD-NC cluster 1R (right superior temporal gyrus, temporal pole, entorhinal cortex, transverse temporal gyrus, fusiform gyrus, superior marginal gyrus, middle temporal gyrus, and inferior temporal gyrus) were combined to plot ROC curves. The diagnostic efficiency of plasma indexes was higher than that of cortical thickness indexes, the diagnostic efficiency of ROC curves after the combination of cortical thickness and plasma indexes was higher than that of cortical thickness or plasma indexes alone.Conclusion: Plasma Aβ40, Aβ42, and P-Tau may be potential biomarkers for early prediction of AD. As the disease progressed, AD patients developed cortical atrophy characterized by atrophy of the medial temporal lobe. The combined prediction of these region and plasma Aβ40, Aβ42, and P-Tau had a higher diagnostic value than single-factor prediction for cognitive decline.

Objective. Volume reduction and structural abnormality is the most replicated finding in neuroimaging studies of Alzheimer’s disease (AD). Amnestic mild cognitive impairment (aMCI) is the early stage of AD development. Thus, it is necessary to investigate the link between atrophy of regions of interest (ROIs) in medial temporal lobe, the variation trend of ROI densities and volumes among patients with cognitive impairment, and the distribution characteristics of ROIs in the aMCI group, Alzheimer’s disease (AD) group, and normal control (NC) group. Methods. 30 patients with aMCI, 16 patients with AD, and 30 NC are recruited; magnetic resonance imaging (MRI) brain scans are conducted. Voxel-based morphometry was employed to conduct the quantitative measurement of gray matter densities of the hippocampus, amygdala, entorhinal cortex, and mammillary body (MB). FreeSurfer was utilized to automatically segment the hippocampus into 21 subregions and the amygdala into 9 subregions. Then, their subregion volumes and total volume were calculated. Finally, the ANOVA and multiple comparisons were performed on the above-mentioned data from these three groups. Results. AD had lower GM densities than MCI, and MCI had lower GM densities than NC, but not all of the differences were statistically significant. In the comparisons of AD-aMCI-NC, AD-aMCI, and AD-NC, the hippocampus, amygdala, and entorhinal cortex showed differences in the gray matter densities ( $p<0.05$ ); the differences of mammillary body densities were not significant in the random comparison between these three groups ( $p>0.05$ ). The hippocampus densities and volumes of the subjects from the aMCI group and the AD group were bilaterally symmetric. The gray matter densities of the right side of the entorhinal cortex inside each group and the hippocampus from the NC group were higher than those of the left side ( $p<0.05$ ), and the gray matter densities of the amygdala and mammillary body were bilaterally symmetric in the three groups ( $p>0.05$ ). There were no gender differences of four ROIs in the AD, aMCI, and NC groups ( $p>0.05$ ). The volume differences of the hippocampus presubiculum-body and parasubiculum manifest no statistical significance ( $p>0.05$ ) in the random comparison between these three groups. Volume differences of the left amygdala basal nucleus, the left lateral nucleus, the left cortical amygdala transitional area, the left paravamnion nucleus, and bilateral hippocampal amygdala transition area (HATA) had statistical differences only between the AD group and the NC group ( $p<0.05$ ). Conclusion. Structural defects of medial temporal lobe subfields were revealed in the aMCI and AD groups. Decreased gray matter densities of the hippocampus, entorhinal cortex, and amygdala could distinguish patients with early stage of AD between aMCI and NC. Volume decline of the hippocampus and amygdala subfields could only distinguish AD between NC.

Cerebral amyloid angiopathy-related inflammation (CAA-ri) is a treatable disorder in which seizures may accompany active inflammation. Previous reports hav