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Search Results: 1 - 10 of 104458 matches for " Sheng-Di Chen "
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The changing phenotype of microglia from homeostasis to disease
Xiao-Guang Luo, Sheng-Di Chen
Translational Neurodegeneration , 2012, DOI: 10.1186/2047-9158-1-9
Microglia in the aging brain: relevance to neurodegeneration
Xiao-Guang Luo, Jian-Qing Ding, Sheng-Di Chen
Molecular Neurodegeneration , 2010, DOI: 10.1186/1750-1326-5-12
Abstract: Microglia are the representative of immune cells in the relatively immune-privileged central nervous system (CNS) and account for 10% of the total glial cell population in the brain. The initial investigation of microglia came from Rio-Hortega early in the last century, who described microglia as a unique cell type in the CNS with an elongated soma bearing processes extending from both poles of the cell. When severe brain injury happens, microglia cells change their morphology dramatically, migrate to the lesion sites, and proliferate. Proliferated microglia cells phagocytose dying cells and other debris and/or release cytokines to maintain the microenvironment homeostasis and support injured neurons, and thus are beneficial for the neuronal survival. However, in the past decades mounting evidence has also implicated neurotoxic roles of microglia when over-activated in severe injury or neurodegenerative diseases. Hypotheses trying to explain this double-edged feature of microglia have been proposed. Here, we review the senescence-related changes of microglia and focus on their relevance to neurodegeneration.Like macrophages in the periphery, microglia belong to macrophage lineage and are the first and main form of active immune defense in the CNS. Aging of the immune system (immunosenescence) describes a state of profound age-associated changes in the immune system, which contributes to the increased susceptibility to infection of the elderly[1,2]. Although the compromise of adaptive immunity mediated by T and B lymphocytes has gained a significant amount of attention [3-5], the innate system also experiences significant changes with advanced age[2]. As the bridge between adaptive and innate immune system, the aging-associated deterioration of macrophage lineage is of significance. Although not universally consistent, accumulating evidence has demonstrated alterations in macrophage functions in advanced age. In rodents, the cytokine production (interleukin 1 (IL-1),
Current advances in the treatment of Alzheimer's disease: focused on considerations targeting Aβ and tau
Hong-Qi Yang,Zhi-Kun Sun,Sheng-Di Chen
Translational Neurodegeneration , 2012, DOI: 10.1186/2047-9158-1-21
Abstract: Alzheimer’s disease (AD) is a neurodegenerative disorder that impairs mainly the memory and cognitive function in elderly. Extracellular beta amyloid deposition and intracellular tau hyperphosphorylation are the two pathological events that are thought to cause neuronal dysfunction in AD. Since the detailed mechanisms that underlie the pathogenesis of AD are still not clear, the current treatments are those drugs that can alleviate the symptoms of AD patients. Recent studies have indicated that these symptom-reliving drugs also have the ability of regulating amyloid precursor protein processing and tau phosphorylation. Thus the pharmacological mechanism of these drugs may be too simply-evaluated. This review summarizes the current status of AD therapy and some potential preclinical considerations that target beta amyloid and tau protein are also discussed.
Magnetotransport in an aluminum thin film on a GaAs substrate grown by molecular beam epitaxy
Lo Shun-Tsung,Chuang Chiashain,Lin Sheng-Di,Chen Kuang Yao
Nanoscale Research Letters , 2011,
Abstract: Magnetotransport measurements are performed on an aluminum thin film grown on a GaAs substrate. A crossover from electron- to hole-dominant transport can be inferred from both longitudinal resistivity and Hall resistivity with increasing the perpendicular magnetic field B. Also, phenomena of localization effects can be seen at low B. By analyzing the zero-field resistivity as a function of temperature T, we show the importance of surface scattering in such a nanoscale film.
History, Present, and Progress of Frontotemporal Dementia in China: A Systematic Review
Ru-Jing Ren,Yue Huang,Gang Xu,Chun-Bo Li,Qi Cheng,Sheng-Di Chen,Gang Wang
International Journal of Alzheimer's Disease , 2012, DOI: 10.1155/2012/587215
Abstract: We aim to provide an overview of clinical and demographical features and neuropathological research on frontotemporal dementia (FTD) from China over the past decade. We reviewed the demographic features, clinical presentations, and neuropathology of the FTD-spectrum disorders from the 49 cases in China published since 1998. On the basis of these findings, we retrospect the history and speculate on future progress in terms of FTD in China. We found that most published papers comprise case reports with a few retrospective studies with small sample sizes. Behavior variant FTD (bvFTD) was the most common diagnostic subtype, of which 35% were associated with amyotrophic lateral sclerosis or Parkinsonian syndrome. More than 47% patients with FTD had age onset before 65. There were no differences in age of onset and sex distribution between diagnostic subtypes. The spectrum of neuropathological diagnosis of bvFTD was frontotemporal lobe degeneration (FTLD) with tau protein or ubiquitin-immunopositive inclusions, and FTLD without intracellular inclusions. Median survival in bvFTD was 14 years. This paper provides an overview of the current status and pointers for future research directions of FTD in China. 1. Introduction Frontotemporal dementia (FTD) is a clinically and pathologically heterogeneous syndrome, characterized by progressive decline in behavior or language functions associated with frontal and temporal lobe degeneration (FTLD) [1–4]. Although FTD was first described in the early 1900s as an early-onset disorder presenting before the age of 65, it has only recently been appreciated as a leading cause of dementia, and to be more common than previously recognized in advanced age [5]. Extensive worldwide studies on FTD have been conducted, including epidemiological investigations, cohort, and retrospective studies [6–8]. An interesting study, in terms of the distribution of FTD across four ethnic groups, claimed that it was as common in Asians as Caucasians [9]. Unfortunately, the epidemiological and demographic characteristics of FTD in China have not been investigated to date, where millions of patients suffer from Alzheimer’s disease (AD) [10, 11]. Given that FTD is the second most common early-onset dementia after AD in the west [1–4], the epidemiology of FTD of China is of considerable interest. Since the introduction of standardized clinical diagnostic criteria for FTD [12] into China, there has been an increasing interest in each of the three clinical variants: bvFTD [13–28], semantic dementia (SD) [29–31], and progressive noninfluent aphasia
Retraction: Dopaminergic regeneration by neurturin-overexpressing c17.2 neural stem cells in a rat model of Parkinson's disease
Wei-Guo Liu, Xi-Jing Wang, Guo-Qiang Lu, Biao Li, Gang Wang, Sheng-Di Chen
Molecular Neurodegeneration , 2009, DOI: 10.1186/1750-1326-4-45
Dopaminergic regeneration by neurturin-overexpressing c17.2 neural stem cells in a rat model of Parkinson's disease
Wei-Guo Liu, Xi-Jing Wang, Guo-Qiang Lu, Biao Li, Gang Wang, Sheng-Di Chen
Molecular Neurodegeneration , 2007, DOI: 10.1186/1750-1326-2-19
Abstract: After intrastriatal grafting, NTN-c17.2 cells differentiated and gradually downregulated nestin expression, while the grafts stably overexpressed NTN. Further, an observation of rotational behavior and the contents of neurotransmitters tested by high-performance liquid chromatography showed that the regenerative effect of the NTN-c17.2 group was significantly better than that of the Mock-c17.2 group, and the regenerative effect of the Mock-c17.2 group was better than that of the PBS group. Further research through reverse-transcriptase polymerase chain reaction assays and in vivo histology revealed that the regenerative effect of Mock-c17.2 and NTN-c17.2 cell grafts may be attributed to the ability of NSCs to produce neurotrophic factors and differentiate into tyrosine hydroxylase-positive cells.The transplantation of NTN-c17.2 can exert neuroregenerative effects in the rat model of PD, and the delivery of NTN by NSCs may constitute a very useful strategy in the treatment of PD.A pathologic feature of Parkinson's disease (PD) is the loss of melanized dopaminergic neurons within the substantia nigra (SN) pars compacta coupled with depletion of striatal dopamine. This is responsible for the major motor features of the disease [1]. Current symptomatic treatments involving dopaminergic replacement therapy and deep brain stimulation (DBS) therapy cannot prevent further neurodegeneration and disease progression [2,3].In recent years, researchers have searched for preventative and curative strategies, leading to the development of certain novel therapeutic approaches. Most of these approaches are based on strategies of neuroprotection, whereby dopaminergic neurons are prevented from dying, and neuroregeneration, whereby dead or injured neurons are supplemented by transplantation [4-7].Neurturin (NTN) is a member of the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophic factors. NTN acts on dopaminergic neurons through a receptor complex composed of l
Erythropoietin prevents PC12 cells from beta-amyloid-induced apoptosis via PI3K?Akt pathway
Sun Zhi-Kun, Yang Hong-Qi, Wang Zhi-Quan, Pan Jing, Hong Zhen, Chen Sheng-Di
Translational Neurodegeneration , 2012, DOI: 10.1186/2047-9158-1-7
Abstract: The protective effect of Epo was studied in differentiated PC12 cells treated with Abeta. The viability of the cells, the apoptosis of the cells and the level of Bax, Bcl-2, cleaved caspase-3 and cleaved PARP expression were detected by MTT, Hoechst 33258 staining and Western blotting respectively.20 μM Abeta (25-35) could induce a decreased viability and a increased apoptosis in PC12 cell in a time-dependent manner. However, 20 μM Abeta (35-25) had no effect on cell viability and apoptosis. Western blot analysis also showed that Abeta(25-35) treatment could decrease the expression of Bcl-2 (P < 0.05) and increase the expression of Bax (P < 0.05), Cleaved casapase-3 (P < 0.05), and Cleaved PARP (P < 0.05). The pretreatment of Epo could effectively reverse all the above changes induced by Abeta(25-35) (P < 0.05). Furthermore, the protective effect of Epo could be blocked by PI3K inhibitor LY294002 (P < 0.05).Epo prevented cell injuries in PC12 cells exposed to the Abeta(25-35) and this effect may depend on the PI3K?Akt pathway. Our study provided an important evidence for the potential application of Epo in the therapy of Alzheimer's disease.Apoptosis is a particular type of programmed cell death controlled by precise intrinsic genetic programme in order to regulate cell population. Among the mechanisms of cell death, apoptosis has been proposed to explain the cell loss observed in many neurodegenerative disorders including Alzheimer's disease (AD) [1-3]. AD is a neurodegenerative disorder of the central nervous system (CNS), which correlate with the appearance of neurofibrillary tangles (NFTs) and senile plaques (SPs) [4]. The major component of SPs is beta-amyloid peptide (Abeta), which is believed to be the most probable cause of AD [3,5]. Many studies have shown that Abeta can directly induce neuronal death via apoptosis [2,6,7].Erythropoietin (Epo) was originally characterized as the principal regulator of erythropoiesis [8]. Many experimental studies have shown
Using Gastrocnemius sEMG and Plasma α-Synuclein for the Prediction of Freezing of Gait in Parkinson's Disease Patients
Xiao-Ying Wang, Wen-Yan Kang, Qiong Yang, Lin-Yuan Zhang, Sheng-Di Chen, Jun Liu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089353
Abstract: Freezing of gait (FOG) is a complicated gait disturbance in Parkinson's disease (PD) and a relevant subclinical predictor algorithm is lacking. The main purpose of this study is to explore the potential value of surface electromyograph (sEMG) and plasma α-synuclein levels as predictors of the FOG seen in PD. 21 PD patients and 15 normal controls were recruited. Motor function was evaluated using the Unified Parkinson's Disease Rating Scale (UPDRS) and Freezing of gait questionnaire (FOG-Q). Simultaneously, gait analysis was also performed using VICON capture system in PD patients and sEMG data was recorded as well. Total plasma α-synuclein was quantitatively assessed by Luminex assay in all participants. Recruited PD patients were classified into two groups: PD patients with FOG (PD+FOG) and without FOG (PD-FOG), based on clinical manifestation, the results of the FOG-Q and VICON capture system. PD+FOG patients displayed higher FOG-Q scores, decreased walking speed, smaller step length, smaller stride length and prolonged double support time compared to the PD-FOG in the gait trial. sEMG data indicated that gastrocnemius activity in PD+FOG patients was significantly reduced compared to PD-FOG patients. In addition, plasma α-synuclein levels were significantly decreased in the PD+FOG group compared to control group; however, no significant difference was found between the PD+FOG and PD-FOG groups. Our study revealed that gastrocnemius sEMG could be used to evaluate freezing gait in PD patients, while plasma α-synuclein might discriminate freezing of gait in PD patients from normal control, though no difference was found between the PD+FOG and PD-FOG groups.
CD200-CD200R dysfunction exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of Parkinson's disease
Shi Zhang, Xi-Jin Wang, Li-Peng Tian, Jing Pan, Guo-Qiang Lu, Ying-Jie Zhang, Jian-Qing Ding, Sheng-Di Chen
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-154
Abstract: 6-hydroxydopamine (6-OHDA)-lesioned rats were used as an animal model of PD. CD200R-blocking antibody (BAb) was injected into striatum to block the engagement of CD200 and CD200R. The animals were divided into three groups, which were treated with 6-OHDA/Veh (PBS), 6-OHDA/CAb (isotype control antibody) or 6-OHDA/BAb, respectively. Rotational tests and immunohistochemistry were employed to evaluate motor deficits and dopaminergic neurodegeneration in animals from each group. HPLC analysis was used to measure monoamine levels in striatum. Morphological analysis and quantification of CD11b- (or MHC II-) immunoreactive cells were performed to investigate microglial activation and possible neuroinflammation in the substantia nigra (SN). Finally, ELISA was employed to assay protein levels of proinflammatory cytokines.Compared with 6-OHDA/CAb or 6-OHDA/Veh groups, rats treated with 6-OHDA/BAb showed a significant increase in counts of contralateral rotation and a significant decrease in TH-immunoreactive (TH-ir) neurons in SN. A marked decrease in monoamine levels was also detected in 6-OHDA/BAb-treated rats, in comparison to 6-OHDA/Veh-treated ones. Furthermore, remarkably increased activation of microglia as well as up-regulation of proinflammatory cytokines was found concomitant with dopaminergic neurodegeneration in 6-OHDA/BAb-treated rats.This study shows that deficits in the CD200-CD200R system exacerbate microglial activation and dopaminergic neurodegeneration in a 6-OHDA-induced rat model of PD. Our results suggest that dysfunction of CD200-CD200R signalling may be involved in the aetiopathogenesis of PD.Parkinson's disease (PD) is the second most common neurodegenerative disease in the world, and is characterized by dopaminergic neuron loss in the substantia nigra pars compacta (SNpc) [1]. PD was first described by James Parkinson in 1817, and the aetiology of PD still remains unknown. However, emerging investigations suggest that multiple factors, both genetic an
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