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Aim of the study: Parkinson's disease (PD) is a neurodegenerative disorder. It is caused by the degeneration of dopaminergic neurons and the dopamine (DA) deletion in the substantia nigra pars compacta (SNpc). Morphine elevates the level of dopamine in the mesolimbic dopamine system and plays a role in alleviating PD symptoms. However, the molecular mechanism is still unclear. The aim of the study is to investigate the mechanism on morphine alleviating PD symptoms. Materials and methods: The viability of PC12 cells was measured by using MTT assay. The expressions of tyrosine hydroxylase (TH), thioredoxin-1 (Trx-1), CyclinD1 and Cyclin-dependent kinase5 (Cdk5) were detected by Western Blot. Results: In present study, we found that morphine increased the cell viability in PC12 cells. 1-methyl-4-phenylpyridi-nium (MPP+) reduced the cell viability and TH expression, which were reversed by morphine. MPP+ decreased the expressions of Trx-1, CyclinD1, Cdk5, which were restored by morphine. Moreover, the role of morphine in restoring the expressions of Trx-1, CyclinD1 and Cdk5 decreased by MPP+ was abolished by LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt inhibitor. Conclusions: These results suggest that morphine reverses effects induced by MPP þ through activating PI3K/Akt pathway. [ABSTRACT FROM AUTHOR]

Background: Eight-and-a-half syndrome is caused by a lesion in the dorsal tegmentum of the caudal pons involving parapontine reticular formation and median longitudinal fasciculus, as well as the nucleus and/or the fasciculus of the facial nerve. It is characterized by one-and-a-half syndrome and an ipsilateral cranial nerve VII palsy. Also, many variants of eight-and-a-half syndrome have been described, including nine syndrome, thirteen-and-a-half syndrome and fifteen-and-a-half syndrome. Methods: We describe a case of a 49-year-old man who presented with eight-and-a-half syndrome combined with contralateral hemiparesis. We reviewed the literature describing the related spectrum of eight-and-a-half syndrome associated with various etiologies. Results: Brain computed tomography scan revealed a hyperdensity located in the left paramedian aspect of the dorsal pons. T2-weighted magnetic resonance imaging at the 11-month follow-up showed hyperintensity and enlargement of the inferior olivary nuclei, which were compatible with a diagnosis of hypertrophic olivary degeneration. In light of our observations and cases reported in the literature, we categorize the spectrum of eight-and-a-half syndrome into three types, namely classic eight-and-a-half syndrome, eight-and-a-half syndrome variants and eight-and-a-half plus syndrome. Besides, the clinical feature and outcome of the three types are discussed in this article. Conclusions: Recognition of the spectrum of eight-and-a-half syndrome allows precise anatomic localization of the lesion to pontine tegmentum region. [ABSTRACT FROM AUTHOR]

Estrogen has beneficial effects on neurodegenerative disorders and cognitive function of postmenopausal women. Puerarin, isolated from Pueraria lobota, has been classified as a phytoestrogen, which can be highly effective against cerebrovascular diseases. In this study, the effects of puerarin on neural cholinergic system in the brain of ovariectomized guinea pigs were studied. The puerarin at the doses used (15 mg/kg body weight (bw)/day and 30 mg/kg bw/day) for 10 days had the estrogenic activity indicated by the attenuation of the reduction of uterine weight induced by ovariectomy. In brain, puerarin treatment increased choline acetyltransferase (ChAT) activity and expression in hippocampus, and increased ChAT immnuopositive signals in septal diagonal region. Puerarin treatment could suppress the increase of acetylcholinesterase expression and activity to the levels of the intact group, although they were not significantly different from those of the ovariectomized animals. Moreover, puerarin decreased the β-amyloid immunopositive staining in hippocampus. In brief, the present study suggests that puerarin prevents the dysfunction of the neuronal cholinergic system and ameliorates the increase of β-amyloid caused by estrogen deficiency. [ABSTRACT FROM AUTHOR]

Aquaporin 4 (AQP4), usually expressed at astrocytes end-feet, is a main component of the lymph-lymphatic system and promotes paravascular cerebrospinal fluid-interstitial fluid exchange. Moreover, angiotensin II type 1 (AT1) receptor affects amyloid β (Aβ) levels. This study aimed to detect the effect of AT1 receptor deficiency on the blood-brain barrier (BBB) of traumatic brain injury (TBI) mice and the effect on Aβ level and glial lymphatic circulation. TBI model was built using AT1 receptor knockout mice (AT1-KO) and C57BL/6 mice (wild type, WT). BBB integrity was detected by Evans blue extravasation. The expression of the astrocytic water channel AQP4 and astrocyte activation were evaluated with immunofluorescence. The expressions of amyloid precursor protein (APP), junction protein zonula occludens protein-1 (ZO-1) and occludin in mice brain were detected by Western blot (WB). Aβ levels were assayed by enzyme-linked immunosorbent assay (ELISA). AT1 receptor deficiency defended BBB integrity and rescued occludin and ZO-1 decrease in mice brain induced by TBI. AT1-KO mice had less increase of APP expression and Aβ 1–42, Aβ 1–40 levels compared to WT mice under TBI. Moreover, AT1 receptor deficiency was found to significantly inhibit AQP4 depolarization after TBI. T1 receptor deficiency attenuated TBI-induced impairments of BBB by rescuing tight junction proteins and inhibited AQP4 polarization, thus improving the function of glymphatic system to enhance interstitial Aβ clearance in TBI mice brain. [ABSTRACT FROM AUTHOR]

Primary central nervous system lymphoma, a rare primary intracranial tumor, is highly malignant and usually associated with poor prognosis. Recent years, owing to the remarkable progress in intervention techniques, survival time reported has been significantly prolonged. Strategies targeting alleviation and remission are primarily depended on the early diagnosis. However, due to the heterogeneity of the clinical symptoms and imaging features, the disease is frequently misdiagnosed especially in the early phase, rendering a delay of optimal treatment. Herein, we reported the case of a 61-year-old man who was initially misdiagnosed as demyelinating encephalopathy. MRI images showed multifocal lesions across the cerebral cortex and deep white matter, which are not strengthened on contrast enhancements. In respect of clinical symptoms, no significant progress was observed over about 11 months. Finally, the diagnosis was revealed by brain biopsy. After reviewing all the images of the patient, we found that the corpus callosum was involved early in the course of the disease. Therefore, for multifocal intracranial lesions involving the corpus callosum, we should always be vigilant about the possibility of primary central nervous system lymphoma. Histopathological examination of brain biopsy is helpful for early definitive diagnosis. [ABSTRACT FROM AUTHOR]

Purpose: This study is to investigate the relationship between thyroid function and Parkinson's disease (PD). Materials and Methods: Totally 77 PD patients were included, who were divided into tremor-dominant-type (TDT), akinetic-rigid-type (ART) and mixed-type (MXT) subgroups. Parkinsonism severity and stage was assessed by modified H-Y stage. Thyroid-stimulating hormone (TSH), fT3 and fT4 levels were detected to analyze thyroid function. Parameters of thyroid homeostasis, including thyroid's secretory capacity (SPINA-GT), the total deiodinase activity (SPINA-GD) and Jostel's TSH index and the thyrotroph thyroid hormone sensitivity index (TTSI), were calculated and compared. Results: Thyroid hormone levels in PD patients were lower than normal controls. Patients with TDT/MXT had significantly higher fT4 level than those with ART. TSH levels were 1.73 ± 0.93 and 2.06 ± 1.04 ulU/ml for patients with TDT/MXT and ART, respectively. The patients in the TDT/MXT group had significantly lower SPINA-GD while significantly higher SPINA-GT than ART group. The fT3 level was significantly higher in early group than advanced group. TSH index in the early group was significantly higher than the advanced group. The fT4 level was negatively correlated with UPDRS motor score. Univariate and multivariable logistic regression analysis indicated that fT4 was positively correlated with PD motor subtype, which disappeared after adjusting for confounding factors. The fT3 level was negatively correlated with PD disease severity, even after adjusting for confounding factors. In female PD patients, fT4 level in TDT/MXT group was significantly higher than ART group. Male PD patients had higher fT4 levels in early patients than advanced patients. Percentage of patients exhibiting ART was decreased significantly in higher fT4 level subgroups. With the increase of TSH index and TTSI, the proportion of advanced PD patients gradually decreased. The proportion of PD patients with TDT/MXT motor subtype gradually increased with the quartiles of SPINA-GT. Conclusion: Thyroid hormone levels and structural parameters of thyroid homeostasis are correlated with motor subtype and disease severity in euthyroid patients with PD. [ABSTRACT FROM AUTHOR]

Purpose: Evidence has shown that propofol may cause widespread apoptotic neurodegeneration. Hypoxic preconditioning has been demonstrated to provide neuroprotection and brain recovery from both acute and chronic neurodegeneration in several cellular and animal models. However, the mechanism has not been well elucidated. Therefore, the present study was designed to investigate the expression of glucose transporters (GLUT1 and GLUT3) and mitochondrial division and fusion (Drp1 and Mfn2) proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity. Methods: Propofol (100 mg/kg) was given to 7-day-old Sprague-Dawley rats; in some rats, hypoxic preconditioning was administered before intraperitoneal propofol injection by subjecting rats to five cycles of 10 min of hypoxia (8% O2) and 10 min of normoxia (21% O2). Then, the rats were allowed to breathe room air for 2 h. Neuronal mitochondrial morphology was observed by transmission electron microscopy. ATP content was detected using an ATP assay kit. The expression levels of GLUT1, GLUT3, pDrp1, Drp1 and Mfn2 were detected by Western blot, and the expression levels of GLUT1 and GLUT3 were further examined by immunohistochemistry. Results: Propofol damaged mitochondria, and decreased ATP content and GLUT3 and pDrp1 protein expression. However, our results suggested that hypoxic preconditioning could attenuate propofol neurotoxicity by reducing mitochondrial damage and increasing ATP content and pDrp1, GLUT1 and GLUT3 protein expression. Conclusion: Hypoxic preconditioning reduced propofol-induced damage in the hippocampus of neonatal rats by attenuating the increase in mitochondrial division and decrease in GLUT3 expression. [ABSTRACT FROM AUTHOR]

Objective: Plasma high hypersensitive C-reactive protein (hs-CRP) levels are associated with risk and prognosis of vascular diseases. The clinical implications of markedly elevated hs-CRP levels are more discovered in the onset and development of stroke. The aim of this study is to determine the association of plasma hs-CRP levels on the prognosis in patients with acute ischemic stroke. Methods: Retrospective analysis of a single-center database of consecutive cases for acute cerebral infarction (ACI) from January 1 2012 to December 30 2016 was performed. Significant predictors of the dependent variable variance were identified by standard linear, univariate and multivariate, or binary logistic regression modeling. Multivariate regression analysis was introduced to investigate the relationship between plasma hs-CRP levels at admission and change in National Institutes of Health Stroke Scale (NIHSS) score at discharge. Results: The percentages of hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, body mass index (BMI) and chronic kidney disease were raised with the increase of hs-CRP plasma concentration at admission among all patients (p < 0.05). ACI patients with large-artery atherosclerosis had an increasing percentage with the increase of hs-CRP mean value (p < 0.05). The initial NIHSS scores, the acute infection rate and age advance also increased with the increase of hs-CRP plasma concentration at admission (p < 0.05). The ratio of neurological improvement increased with the decrease of plasma hs-CRP concentration (p < 0.05). The neurological deterioration and poor prognosis increased with the increase of plasma hs-CRP concentration (p < 0.05). Conclusion: High plasma hs-CRP levels are associated with worse outcomes in the ACI patients. Monitoring plasma hs-CRP levels and cutting down the elevated plasma hs-CRP levels will be beneficial in screening and treatment decisions for the prognosis of acute ischemic stroke. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the effect of rimonabant, a cannabinoid receptor type 1 antagonist, on calcium/calmodulin- dependent protein kinase II and cannabinoid receptor type 1 in chronic intermittent hypoxia. Materials and methods: Healthy male rats were divided into control group, intermittent hypoxia group for 4 or 6 weeks, hypoxic intervention group that received rimonabant (1 mg/kg/d) before exposure to hypoxia for 4 or 6 weeks (n = 10/group). Morphological changes and expressions of the two indexes in the cerebral hippocampus cells were determined by haematoxylin-eosin staining and immunohistochemistry, respectively. Results: In the intermittent hypoxia group at 4 weeks, the hippocampal cells were damaged with sparse cytoplasm and unclear boundaries, which are even worse at 6 weeks. In contrast, the hippocampal cells of the hypoxic intervention group were neatly arranged at 4 weeks. At 6 weeks, cells were larger with scarce cytoplasm and nuclear changes indicative of cell death. Calcium/calmodulin-dependent protein kinase II and cannabinoid receptor type 1 expression in the cerebral hippocampus was elevated in the intermittent hypoxia group at 4 weeks with even greater at 6 weeks. Cannabinoid receptor type 1 expression was reduced in the hypoxic intervention group compared to the intermittent hypoxia group. Correlation analysis revealed significant positive correlation of them in the intermittent hypoxia group. Conclusions: Chronic intermittent hypoxia induced structural damage in the hippocampus and increased cannabinoid receptor type 1 and calcium/calmodulin-dependent protein kinase II expression, which may mediate cognitive impairment associated with chronic intermittent hypoxia. Rimonabant had a protective effect against chronic intermittent hypoxia. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to compare serum leptin, apolipoprotein A1 (ApoA1), apolipoprotein J (ApoJ) and apolipoprotein H (ApoH) levels in males with obstructive sleep apnea and hypopnea syndrome (OSAHS) to those in healthy control subjects and to examine the possible relation between neurocognitive performance and these factors/serum markers in the subjects. Methods: In this observational, cross-sectional study, a full-night polysomnography and sensitive neuropsychological assessment were performed on 50 newly diagnosed Chinese male patients and 30 healthy subjects. Fasting blood samples were used to measure leptin and ApoA1, ApoH and ApoJ levels using ELISA. Results: Compared with normal control subjects, OSAHS patients have significantly lower levels of ApoA1 and higher levels of leptin, ApoH and ApoJ. After adjustment for age, years of education, body mass index (BMI) and apnea--hypopnea index, leptin and ApoA1 were associated with global cognitive function, and leptin level was positively correlated with inhibition reaction time. ApoJ was negatively correlated with visual reproduction and logical memory performance. Multiple regression analysis shows that from age, BMI, education year, biomarker levels and the parameters of PSG, only the variables of leptin and education year added to the prediction of the Montreal cognitive assessment score in a statistically significant way. Conclusions: Abnormal expression of leptin and apolipoproteins and poor performance on neuropsychological tests were observed in patients with OSAHS. There is also an association between serum leptin, ApoA1, and ApoJ levels and cognitive performance in the patients. [ABSTRACT FROM AUTHOR]