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Objective To evaluate whether bone marrow stromal cells (BMSCs) transplantation can improve the cognitive function of aged rats with vascular dementia. Methods Thirty rats were equally ramdomized into normal control group and 4 treatment groups; the 4 treatment groups received subcutaneous injection of D-galactose (D-gal) for 4 weeks; and then, two-vessel occlusion (2VO) was performed in 3 of the treatment groups; and 24 h after 2VO, D-gal+2VO+saline group and D-gal+2VO+BMSCs group were subjected to stereotactic injection of normal saline and BMSCs into the subventricular zone (SVZ), respectively. The cognitive function was examined by Morris water maze test 6 weeks after stereotactic injection; immunofluorescence staining was employed to observe the transplantation ratio of BMSCs to neurons. Results Increased times and distances during Morris water maze in rats of the D-gal+2VO group, D-gal+2VO+saline group and D-gal+2VO+BMSCs group were noted as compared with those in the controls, indicating that the cognitive function of rats in these 3 groups was obviously impaired; these rats had the characteristics of having vascular dementia.Transplanted BMSCs in the D-gal+2VO+BMSCs group distributed around the lateral ventricles, and acquired the phenotypes of neurons (2%) and astrocyte (1%) 6 weeks after the transplantation. In addition, compared with that in rats of the D-gal+2VO group and D-gal+2VO+saline group, the cognitive dysfunction of rats in the D-gal+2VO+BMSCs group was improved (needing less time and swimming shorter distance, no difference in speed of swimming). Conclusion The D-gal injection plus 2VO can result in cognitive dysfunction of rats, and the engrafted BMSCs may exhibit the beneficial effect on cognitive function.Neural function remolding caused by interaction between BMSCs and host brain may be responsible for the function improvement

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<p><b>BACKGROUND</b>Neuropathologically, Alzheimer disease (AD) is characterized by the presence of extracellular plaques enriched in beta-amyloid peptides; however, the mechanism by which it results in the neurotoxicity is uncertain. The purpose of this study was to investigate whether it would prompt the progress of Alzheimer disease via enhancement of aberrant phosphorylated tau that results from its increased kinase gene expression.</p><p><b>METHODS</b>Twenty-four male rats were divided into three groups, and each group had 8 rats: control, sham-operated, and Abeta(25-35) injected AD model groups. AD rat models were created by unilateral injections of Abeta(25-35) into the amygdala. The hyperphosphorylated tau protein was estimated by immunohistochemistry with paired helical filament-1 (PHF-1) antibody and paired helical filament-tau (AT8) antibody. The expressions of glycogen synthase kinase-3beta (GSK-3beta) and p38 mitogen-activated protein kinase (P(38)MAPK) mRNA were observed by in situ hybridization.</p><p><b>RESULTS</b>Compared with the control and sham-operated groups, the evaluation of paired AT8 and paired helical filament-1 (PHF-1) in the cortexes and hippocampus of the AD model group showed the numbers of AT8 and PHF-1 positive cells, as well as the optical density (OD) values of the proteins were significantly higher (AT8: in CA2: 0.318 +/- 0.037 vs. 0.135 +/- 0.028, 0.136 +/- 0.031; in frontal cortex: 0.278 +/- 0.040 vs. 0.130 +/- 0.028, 0.190 +/- 0.037. PHF-1: in CA2: 0.386 +/- 0.034 vs. 0.139 +/- 0.010, 0.193 +/- 0.041; in frontal cortex: 0.395 +/- 0.050 vs. 0.159 +/- 0.030, 0.190 +/- 0.044, respectively, P < 0.01); the number of GSK-3beta mRNA and P(38)MAPK mRNA positive cells of the AD model group, as well as the OD values, also increased significantly in the cortexes, hippocampus (GSK-3beta-mRNA: in CA2: 0.384 +/- 0.012 vs. 0.190 +/- 0.015, 0.258 +/- 0.064; in frontal cortex: 0.398 +/- 0.018 vs. 0.184 +/- 0.031, 0.218 +/- 0.049. P(38)MAPK mRNA: in CA2: 0.409 +/- 0.038 vs. 0.161 +/- 0.041, 0.189 +/- 0.035; in frontal cortex: 0.423 +/- 0.070 vs. 0.160 +/- 0.032, 0.203 +/- 0.053, respectively, P < 0.01).</p><p><b>CONCLUSION</b>Unilateral injection of Abeta(25-35) into the rat amygdala increases the generation of aberrant phosphorylated tau by increasing GSK-3beta and P(38)MAPK gene expression, that accelerates the process of Alzhemer's disease.</p>

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<p><b>BACKGROUND</b>Aging is an important risk factor for vascular dementia, and D-galactose (D-gal) injection can simulate the pathology of aging. Two-vessel occlusion of common carotid arteries (2VO) is the most popular model for vascular dementia. This study was aimed to investigate the possibility of D-gal injection plus 2VO simulating cognitive impairment of aging vascular dementia; and whether transplanted bone marrow stromal cells (BMSCs) can improve the cognitive function induced by D-gal injection plus 2VO.</p><p><b>METHODS</b>Totally 30 male Sprague-Dawley rats were divided into 5 groups equivalently: control group, D-gal group, D-gal + 2VO group, D-gal + 2VO + saline water group, and D-gal + 2VO + BMSCs group. Aging hypoperfusion rats were created by subcutaneous injection of D-gal and occlusion of two common carotid arteries. BMSCs or saline water was stereotactically transplanted into the subventricular zone as treatment vehicles at 24 hours post operation. Two-way repeat analysis of variance (ANOVA) was used for significance analysis of 5 groups at 6 weeks post transplantation; moreover, Tamhane's test (equal variance not assumed) and least significant difference (LSD) test (equal variance assumed) were used for pairwise comparison in Morris water maze (MWM).</p><p><b>RESULTS</b>Transplanted BMSCs distributed around the lateral ventricles and acquired the phenotypes of neurons and astrocytes. In terms of swimming path distance and escape latency in MWM, D-gal + 2VO + BMSC group showed significant improvement than the D-gal + 2VO group but was still obviously worse than the control group (both P < 0.05). There was no significant difference in swimming speed for all 5 groups.</p><p><b>CONCLUSIONS</b>D-gal plus 2VO induces cognitive dysfunction. The engrafted BMSCs exhibit the beneficial effect on cognitive function via promotion interactively with host brain.</p>

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Objective To investigate the dynamic changes of serum levels of neuron-specific enolase(NSE),endothelin(ET)and calcitonin gene-related peptide(CGRP)and their clinical significance in the elderly patients with acute cerebral infarction.Methods One hundred and twenty elderly patients with acute cerebral infarction(ACI),60 elderly patients with lacunar infarct,60 elderly patients with hypertension and 60 elderly patients with cerebral artherosclerosis were enrolled. The areas of infarction were measured and the venous blood samples at different times were collected after cerebral infarction to determine the concentrations of NSE,ET and CGRP by radioimmunoassay. Results There were dynamic changes of the plasma levels of NSE,ET and CGRP.In the early time the plasma levels of NSE and ET of the elderly patients with acute cerebral infarction were significantly higher than those of the elderly patients with cerebral artherosclerosis,or with hypertension,or with lacunar infarct(P＜0.01,P＜0.01,P＜0.05,respectively),and were gradually declined along with timing.In ACI group,the level of NSE began to increase gradually after 24 hours,reached the highest in 2 days,and decreased to normal after 14 days,but the level of ET was always higher than those in the cerebral artherosclerosis and hypertension groups.The ET levels in lacunar infarct and hypertension groups were also significantly higher than in the cerebral artherosclerosis group(P＜0.01).However,when compared with the cerebral artherosclerosis and hypertension groups,the plasma concentrations of CGRP in cerebral infarction and lacunar infarct groups were obviously lower(P＜0.01),and increased gradually.We also found the larger the infarction area,the lower the level of CGRP.Conclusions The NSE,ET and CGRP concentrations are associated closely with acute cerebral infaction.Monitoring the level of NSE is applicable for early diagnosis of cerebral infarction.