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Protective effect of hydrogen sulfide on oxidative stress-induced neurodegenerative diseases 预览
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作者 Rubaiya Tabassum Na Young Jeong Junyang Jung 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期232-241,共10页
Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where r... Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where reactive oxygen species are the main source of oxidative stress. When the normal redox balance is disturbed, deoxyribonucleic acid, lipid, and protein molecules are oxidized under pathological conditions, like diabetes mellitus that leads to diabetic peripheral neuropathy. In diabetes mellitus-induced diabetic peripheral neuropathy, due to hyperglycemia, pancreatic beta cell(β cell) shows resistance to insulin secretion. As a consequence, glucose metabolism is disturbed in neuronal cells which are distracted from providing proper cell signaling pathway. Not only diabetic peripheral neuropathy but also other central damages occur in brain neuropathy. Neurological studies regarding type 1 diabetes mellitus patients with Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis have shown changes in the central nervous system because high blood glucose levels(HbA1 c) appeared with poor cognitive function. Oxidative stress plays a role in inhibiting insulin signaling that is necessary for brain function. Hydrogen sulfide exhibits antioxidant effects against oxidative stress, where cystathionine β synthase, cystathionine γ lyase, and 3-mercaptopyruvate sulfurtransferase are the endogenous sources of hydrogen sulfide. This review is to explore the pathogenesis of diabetes mellitus-induced diabetic peripheral neuropathy and other neurological comorbid disorders under the oxidative stress condition and the anti-oxidative effects of hydrogen sulfide. 展开更多
关键词 Alzheimer's DISEASE amyotrophic lateral SCLEROSIS antioxidant diabetic peripheral NEUROPATHY DNA oxidation hydrogen SULFIDE mitochondrial dysfunction oxidative stress Parkinson's DISEASE reactive oxygen species
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Genetic targeting of astrocytes to combat neurodegenerative disease 预览
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作者 Rachel Kéry Allen P. F. Chen Gregory W. Kirschen 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期199-211,共13页
Astrocytes, glial cells that interact extensively with neurons and other support cells throughout the central nervous system, have recently come under the spotlight for their potential contribution to, or potential re... Astrocytes, glial cells that interact extensively with neurons and other support cells throughout the central nervous system, have recently come under the spotlight for their potential contribution to, or potential regenerative role in a host of neurodegenerative disorders. It is becoming increasingly clear that astrocytes, in concert with microglial cells, activate intrinsic immunological pathways in the setting of neurodegenerative injury, although the direct and indirect consequences of such activation are still largely unknown. We review the current literature on the astrocyte’s role in several neurodegenerative diseases, as well as highlighting recent advances in genetic manipulation of astrocytes that may prove critical to modulating their response to neurological injury, potentially combatting neurodegenerative damage. 展开更多
关键词 Alzheimer's DISEASE amyotrophic lateral SCLEROSIS GLIA immune system inflammation Parkinson's DISEASE reactive ASTROCYTE regeneration
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Hydrogels for neuroprotection and functional rewiring:a new era for brain engineering 预览
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作者 Rocío Fernández-Serra Rebeca Gallego +1 位作者 Paloma Lozano Daniel González-Nieto 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期783-789,共7页
The neurological devastation of neurodegenerative and cerebrovascular diseases reinforces our perseverance to find advanced treatments to deal with these fatal pathologies.High-performance preclinical results have fai... The neurological devastation of neurodegenerative and cerebrovascular diseases reinforces our perseverance to find advanced treatments to deal with these fatal pathologies.High-performance preclinical results have failed at clinical level,as it has been the case for a wide variety of neuroprotective agents and cell-based therapies employed to treat high prevalent brain pathologies such as stroke,Alzheimer’s and Parkinson’s diseases.An unquestionable reality is the current absence of effective therapies to neuroprotect the brain,to arrest neurodegeneration and rewire the impaired brain circuits.Part of the problem might arise from the lack of adequate in vitro and in vivo models and that most of the underlying pathophysiological mechanisms are not yet clarified.Another contributing factor is the lack of efficient systems to sustain drug release at therapeutic concentrations and enhance the survival and function of grafted cells in transplantation procedures.For medical applications the use of biomaterials of different compositions and formats has experienced a boom in the last decades.Although the greater complexity of central nervous system has probably conditioned their extensive use with respect to other organs,the number of biomaterials-based applications to treat the injured brain or in the process of being damaged has grown exponentially.Hydrogel-based biomaterials have constituted a turning point in the treatment of cerebral disorders using a new form of advanced therapy.Hydrogels show mechanical properties in the range of cerebral tissue resulting very suitable for local implantation of drugs and cells.It is also possible to fabricate three-dimensional hydrogel constructs with adaptable mesh size to facilitate axonal guidance and elongation.Along this article,we review the current trends in this area highlighting the positive impact of hydrogel-based biomaterials over the exhaustive control of drug delivery,cell engraftment and axonal reinnervation in brain pathologies. 展开更多
关键词 advanced therapies Alzheimer’s DISEASE biomaterials BRAIN HYDROGELS NEUROLOGICAL diseases Parkinson’s DISEASE polymers stroke
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Ethanol extract from Gynostemma pentaphyllum ameliorates dopaminergic neuronal cell death in transgenic mice expressing mutant A53T human alpha-synuclein 预览
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作者 Hyun Jin Park Ting Ting Zhao +4 位作者 Seung Hwan Kim Chong Kil Lee Bang Yeon Hwang Kyung Eun Lee Myung Koo Lee 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期361-368,共8页
Gynostemma(G.) pentaphyllum(Cucurbitaceae) contains various bioactive gypenosides. Ethanol extract from G. pentaphyllum(GP-EX) has been shown to have ameliorative effects on the death of dopaminergic neurons in animal... Gynostemma(G.) pentaphyllum(Cucurbitaceae) contains various bioactive gypenosides. Ethanol extract from G. pentaphyllum(GP-EX) has been shown to have ameliorative effects on the death of dopaminergic neurons in animal models of Parkinson’s disease(PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-and 6-hydroxydopamine. PD patients exhibit multiple symptoms, so PD-related research should combine neurotoxin models with genetic models. In the present study, we investigated the ameliorative effects of GP-EX, including gypenosides, on the cell death of dopaminergic neurons in the midbrain of A53 T α-synuclein transgenic mouse models of PD(A53 T). Both GP-EX and gypenosides at 50 mg/kg per day were orally administered to the A53 T mice for 20 weeks.α-Synuclein-immunopositive cells and α-synuclein phosphorylation were increased in the midbrain of A53 T mice, which was reduced following treatment with GP-EX. Treatment with GP-EX modulated the reduced phosphorylation of tyrosine hydroxylase, extracellular signal-regulated kinase(ERK1/2), Bcl-2-associated death promoter(Bad) at Ser112, and c-Jun N-terminal kinase(JNK1/2) due to α-synuclein overexpression. In the A53 T group, GP-EX treatment prolonged the latency of the step-through passive avoidance test and shortened the transfer latency of the elevated plus maze test. Gypenosides treatment exhibited the effects and efficacy similar to those of GP-EX. Taken together, GP-EX, including gypenosides, has ameliorative effects on dopaminergic neuronal cell death due to the overexpression of α-synuclein by modulating ERK1/2, Bad at Ser112, and JNK1/2 signaling in the midbrain of A53 T mouse model of PD. Further studies are needed to investigate GP-EX as a treatment for neurodegenerative synucleinopathies, including PD. This study was approved by the Animal Ethics Committee of Chungbuk National University(approval No. CBNUA-956-16-01) on September 21, 2016. 展开更多
关键词 A53T α-synuclein genetic mice ERK1/2 GYNOSTEMMA pentaphyllum GYPENOSIDES Parkinson’s disease retention transfer LATENCY time
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Therapeutic importance of hydrogen sulfide in age-associated neurodegenerative diseases 预览
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作者 Rubaiya Tabassum Na Young Jeong Junyang Jung 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期653-662,共10页
Hydrogen sulfide(H2S)is a gasotransmitter that acts as an antioxidant and exhibits a wide variety of cytoprotective and physiological functions in age-associated diseases.One of the major causes of age-related disease... Hydrogen sulfide(H2S)is a gasotransmitter that acts as an antioxidant and exhibits a wide variety of cytoprotective and physiological functions in age-associated diseases.One of the major causes of age-related diseases is oxidative stress.In recent years,the importance of H2S has become clear,although its antioxidant function has not yet been fully explored.The enzymes cystathionineβ-synthase,cystathionineγ-lya-se,and 3-mercaptopyruvate sulfurtransferase are involved in the enzymatic production of H2S.Previously,H2S was considered a neuromodulator,given its role in long-term hippocampal potentiation,but it is now also recognized as an antioxidant in age-related neurodegeneration.Due to aerobic metabolism,the central nervous system is vulnerable to oxidative stress in brain aging,resulting in age-associated degenerative diseases.H2S exerts its antioxidant effect by limiting free radical reactions through the activation of antioxidant enzymes,including superoxide dismutase,catalase,and glutathione peroxidase,which protect against the effects of aging by regulating apoptosis-related genes,including p53,Bax,and Bcl-2.This review explores the implications and mechanisms of H2S as an antioxidant in age-associated neurodegenerative diseases,including Alzheimer’s disease,Parkinson’s disease,Huntington’s disease,and Down syndrome. 展开更多
关键词 3-mercaptopyruvate SULFURTRANSFERASE aging antioxidant cystathionineβ-synthase cystathionineγ-lyase GLUTATHIONE hydrogen sulfide NEURODEGENERATIVE disease oxidative stress reactive oxygen species
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Current status and future prospects of stem cell therapy in Alzheimer’s disease 预览
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作者 Fu-Qiang Zhang Jin-Lan Jiang +3 位作者 Jing-Tian Zhang Han Niu Xue-Qi Fu Lin-Lin Zeng 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期242-250,共9页
Alzheimer’s disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only al... Alzheimer’s disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only alleviate the symptoms without curing the disease, which is a serious issue and influences the quality of life of the patients and their caregivers. In recent years, stem cell technology has provided new insights into the treatment of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Currently, the main sources of stem cells include neural stem cells, embryonic stem cells, mesenchymal stem cells, and induced pluripotent stem cells. In this review, we discuss the pathophysiology and general treatment of Alzheimer’s disease, and the current state of stem cell transplantation in the treatment of Alzheimer’s disease. We also assess future challenges in the clinical application and drug development of stem cell transplantation as a treatment for Alzheimer’s disease. 展开更多
关键词 Alzheimer's disease β-amyloid drug development embryonic STEM CELLS induced PLURIPOTENT STEM CELLS mesenchymal STEM CELLS nerve REGENERATION NEURAL REGENERATION NEURAL STEM CELLS NEURODEGENERATIVE disorders STEM cell therapy
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Novel pluripotent stem cell lines for enriched grafting in Parkinson's disease 预览
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作者 Agustin Cota-Coronado Lachlan H.Thompson N.Emmanuel Diaz-Martinez 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期255-256,共2页
Parkinson's disease (PD) is the second most common neurodegenerative disease, affecting 1% of the population over 55 years of age and up to 4% of the population over 80 years of age (Blesa et al., 2012). This prog... Parkinson's disease (PD) is the second most common neurodegenerative disease, affecting 1% of the population over 55 years of age and up to 4% of the population over 80 years of age (Blesa et al., 2012). This progressive and neurodegenerative condition results from an excessive loss of dopaminergic neurons (50-70%) of the substantia nigra pars compacta, leading to a significant decrease in dopamine (DA) levels in the striatum and consequently a functional deterioration of motor circuity (Blesa et al., 2012;Nielsen et al., 2016). 展开更多
关键词 Parkinson's DISEASE STRIATUM NEURODEGENERATIVE
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Increased intron retention is linked to Alzheimer's disease 预览
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作者 Chin-Tong Ong Swarnaseetha Adusumalli 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期259-260,共2页
Intron retention in aging and Alzheimer's disease (AD): AD is an age-related neurodegenerative disorder with pathological accumulation of amyloid plaque (Masters et al., 2015), which can be classified into familia... Intron retention in aging and Alzheimer's disease (AD): AD is an age-related neurodegenerative disorder with pathological accumulation of amyloid plaque (Masters et al., 2015), which can be classified into familial and sporadic form. In familial AD, mutations in genes encoding either amyloid precursor protein or presenilin (PS1 and PS2) cause overproduction of amyloid-42 molecules and early onset of dementia. 展开更多
关键词 RETENTION Alzheimer's DISEASE DEMENTIA
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Determining the mechanism behind yoga's effects on preventing the symptoms of Alzheimer's disease 预览
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作者 Adithy Hassan Meghan Robinson Stephanie M. Willerth 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期261-262,共2页
Background on the relationship between meditation/yoga practice and its effect on Alzheimer's disease (AD): Dementia refers to a variety of conditions that affect the normal function of the brain, leading to sympt... Background on the relationship between meditation/yoga practice and its effect on Alzheimer's disease (AD): Dementia refers to a variety of conditions that affect the normal function of the brain, leading to symptoms like memory loss, issues with problem solving, difficulty in processing thoughts and disordered language (McKhann et al., 2011). 展开更多
关键词 EFFECTS YOGA Alzheimer's DISEASE
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Alteration of functional connectivity in patients with Alzheimer’s disease revealed by resting-state functional magnetic resonance imaging 预览
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作者 Jie Zhao Yu-Hang Du +2 位作者 Xue-Tong Ding Xue-Hu Wang Guo-Zun Men 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期285-292,共8页
The main symptom of patients with Alzheimer’s disease is cognitive dysfunction. Alzheimer’s disease is mainly diagnosed based on changes in brain structure. Functional connectivity reflects the synchrony of function... The main symptom of patients with Alzheimer’s disease is cognitive dysfunction. Alzheimer’s disease is mainly diagnosed based on changes in brain structure. Functional connectivity reflects the synchrony of functional activities between non-adjacent brain regions, and changes in functional connectivity appear earlier than those in brain structure. In this study, we detected resting-state functional connectivity changes in patients with Alzheimer’s disease to provide reference evidence for disease prediction. Functional magnetic resonance imaging data from patients with Alzheimer’s disease were used to show whether particular white and gray matter areas had certain functional connectivity patterns and if these patterns changed with disease severity. In nine white and corresponding gray matter regions, correlations of normal cognition, early mild cognitive impairment, and late mild cognitive impairment with blood oxygen level-dependent signal time series were detected. Average correlation coefficient analysis indicated functional connectivity patterns between white and gray matter in the resting state of patients with Alzheimer’s disease. Functional connectivity pattern variation correlated with disease severity, with some regions having relatively strong or weak correlations. We found that the correlation coefficients of five regions were 0.3–0.5 in patients with normal cognition and 0–0.2 in those developing Alzheimer’s disease. Moreover, in the other four regions, the range increased to 0.45–0.7 with increasing cognitive impairment. In some white and gray matter areas, there were specific connectivity patterns. Changes in regional white and gray matter connectivity patterns may be used to predict Alzheimer’s disease;however, detailed information on specific connectivity patterns is needed. All study data were obtained from the Alzheimer’s Disease Neuroimaging Initiative Library of the Image and Data Archive Database. 展开更多
关键词 Alzheimer's disease blood oxygen level-dependent signal correlation coefficient FUNCTIONAL connectivity pattern FUNCTIONAL magnetic resonance imaging GRAY MATTER RESTING state white MATTER
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Action of trichostatin A on Alzheimer’s disease-like pathological changes in SH-SY5Y neuroblastoma cells 预览
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作者 Li-Hua Li Wen-Na Peng +2 位作者 Yu Deng1 Jing-Jing Li Xiang-Rong Tian 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期293-301,共9页
The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effe... The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the nuclear factor erythroid 2-related factor 2(Nrf2) and Kelch-like epichlorohydrin-related protein-1(Keap1) signaling pathway, amyloid β-peptide 25–35(Aβ25–35) was used to induce Alzheimer’s disease-like pathological changes in SH-SY5 Y neuroblastoma cells. Cells were then treated with trichostatin A. The effects of trichostatin A on the expression of Keap1 and Nrf2 were detected by real-time quantitative polymerase chain reaction, western blot assays and immunofluorescence. Total antioxidant capacity and autophagy activity were evaluated by total antioxidant capacity assay kit and light chain 3-I/II levels, respectively. We found that trichostatin A increased cell viability and Nrf2 expression, and decreased Keap1 expression in SH-SY5 Y cells. Furthermore, trichostatin A increased the expression of Nrf2-related target genes, such as superoxide dismutase, NAD(P)H quinone dehydrogenase 1 and glutathione S-transferase, thereby increasing the total antioxidant capacity of SH-SY5 Y cells and inhibiting amyloid β-peptide-induced autophagy. Knockdown of Keap1 in SH-SY5 Y cells further increased trichostatin A-induced Nrf2 expression. These results indicate that the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the Keap1-Nrf2 pathway. The mechanism for this action may be that trichostatin A increases cell viability and the antioxidant capacity of SH-SY5 Y cells by alleviating Keap1-mediated inhibition Nrf2 signaling, thereby alleviating amyloid β-peptide-induced cell damage. 展开更多
关键词 Alzheimer's disease amyloid-β peptide autophagy KEAP1 signal neurocytotoxicity oxidative stress damage SH-SY5Y cells total antioxidant capacity transcription factor Nrf2 TSA
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MicroRNAs in blood and cerebrospinal fluid as diagnostic biomarkers of multiple sclerosis and to monitor disease progression 预览
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作者 Bridget Martinez Philip V.Peplow 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期606-619,共14页
Multiple sclerosis is a chronic autoimmune disease of the central nervous system.It is the main cause of non-traumatic neurological disability in young adults.Multiple sclerosis mostly affects people aged 20–50 years... Multiple sclerosis is a chronic autoimmune disease of the central nervous system.It is the main cause of non-traumatic neurological disability in young adults.Multiple sclerosis mostly affects people aged 20–50 years;however,it can occur in young children and much older adults.Factors identified in the distribution of MS include age,gender,genetics,environment,and ethnic background.Multiple sclerosis is usually associated with progressive degrees of disability.The disease involves demyelination of axons of the central nervous system and causes brain and spinal cord neuronal loss and atrophy.Diagnosing multiple sclerosis is based on a patient’s medical history including symptoms,physical examination,and various tests such as magnetic resonance imaging,cerebrospinal fluid and blood tests,and electrophysiology.The disease course of multiple sclerosis is not well correlated with the biomarkers presently used in clinical practice.Blood-derived biomarkers that can detect and distinguish the different phenotypes in multiple sclerosis may be advantageous in personalized treatment with disease-modifying drugs and to predict response to treatment.The studies reviewed have shown that the expression levels of a large number of miRNAs in peripheral blood,serum,exosomes isolated from serum,and cerebrospinal fluid are altered in multiple sclerosis and can distinguish the disease phenotypes from each other.Further studies are warranted to independently validate these findings so that individual or pairs of miRNAs in serum or cerebrospinal fluid can be used as potential diagnostic markers for adult and pediatric multiple sclerosis and for monitoring disease progression and response to therapy. 展开更多
关键词 clinically isolated syndrome CSF disease PROGRESSION EXOSOMES humans microRNA multiple SCLEROSIS PERIPHERAL blood PHENOTYPES serum
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Characteristic response of striatal astrocytes to dopamine depletion 预览
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作者 Yao-Feng Zhu Wei-Ping Wang +5 位作者 Xue-Feng Zheng Zhi Chen Tao Chen Zi-Yun Huang Lin-Ju Jia Wan-Long Lei 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期724-730,共7页
Astrocytes and astrocyte-related proteins play important roles in maintaining normal brain function,and also regulate pathological processes in brain diseases and injury.However,the role of astrocytes in the dopamine-... Astrocytes and astrocyte-related proteins play important roles in maintaining normal brain function,and also regulate pathological processes in brain diseases and injury.However,the role of astrocytes in the dopamine-depleted striatum remains unclear.A rat model of Parkinson’s disease was therefore established by injecting 10μL 6-hydroxydopamine(2.5μg/μL)into the right medial forebrain bundle.Immunohistochemical staining was used to detect the immunoreactivity of glial fibrillary acidic protein(GFAP),calcium-binding protein B(S100B),and signal transducer and activator of transcription 3(STAT3)in the striatum,and to investigate the co-expression of GFAP with S100B and STAT3.Western blot assay was used to measure the protein expression of GFAP,S100B,and STAT3 in the striatum.Results demonstrated that striatal GFAP-immunoreactive cells had an astrocytic appearance under normal conditions,but that dopamine depletion induced a reactive phenotype with obvious morphological changes.The normal striatum also contained S100B and STAT3 expression.S100B-immunoreactive cells were uniform in the striatum,with round bodies and sparse,thin processes.STAT3-immunoreactive cells presented round cell bodies with sparse processes,or were darkly stained with a large cell body.Dopamine deprivation induced by 6-hydroxydopamine significantly enhanced the immunohistochemical positive reaction of S100B and STAT3.Normal striatal astrocytes expressed both S100B and STAT3.Striatal dopamine deprivation increased the number of GFAP/S100B and GFAP/STAT3 double-labeled cells,and increased the protein levels of GFAP,S100B,and STAT3.The present results suggest that morphological changes in astrocytes and changes in expression levels of astrocyte-related proteins are involved in the pathological process of striatal dopamine depletion.The study was approved by Animal Care and Use Committee of Sun Yat-sen University,China(Zhongshan Medical Ethics 2014 No.23)on September 22,2014. 展开更多
关键词 6-HYDROXYDOPAMINE ASTROCYTE dopamine depletion DOPAMINERGIC neurons Parkinson’s disease SIOOB STAT3 STRIATUM
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Early active immunization with Aβ3–10-KLH vaccine reduces tau phosphorylation in the hippocampus and protects cognition of mice 预览
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作者 Jin-Chun Wang Kun Zhu +3 位作者 Hui-Yi Zhang Guo-Qing Wang Hui-Ying Liu Yun-Peng Cao 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期519-527,共9页
Active and passive anti-Aβimmunotherapies have successfully been used for the prevention and treatment of Alzheimer’s disease animal models.However,clinical use of these immunotherapies is not effective,because the ... Active and passive anti-Aβimmunotherapies have successfully been used for the prevention and treatment of Alzheimer’s disease animal models.However,clinical use of these immunotherapies is not effective,because the vaccination is administered too late.At 1 month of age,100μL of Aβ3–10-KLH peptide(vaccine,2μg/μL)was subcutaneously injected into the neck of an amyloid precursor protein/presenilin-1/tau transgenic(3×Tg-AD)mouse model.Aβ3–10-KLH peptide was re-injected at 1.5,2.5,3.5,4.5,5.5,and 6.5 months of age.Serum levels of Aβantibody were detected by enzyme-linked immunosorbent assay,while spatial learning and memory ability were evaluated by Morris water maze.Immunohistochemistry was used to detect total tau with HT7 and phosphorylated tau with AT8(phosphorylation sites Ser202 and Thr205)and AT180(phosphorylation site Thr231)antibodies in the hippocampus.In addition,western blot analysis was used to quantify AT8 and AT180 expression in the hippocampus.The results showed that after vaccine injection,mice produced high levels of Aβantibody,cognitive function was significantly improved,and total tau and phosphorylated tau levels were significantly reduced.These findings suggest that early active immunization with Aβ3–10-KLH vaccine can greatly reduce tau phosphorylation,thereby mitigating the cognitive decline of 3×Tg-AD mice.This study was approved by the Animal Ethics Committee of China Medical University,China(approval No.103-316)on April 2,2016. 展开更多
关键词 3×Tg-AD Aβ3–10-KLH VACCINE Alzheimer’s disease amyloid precursor protein AMYLOID-BETA cognitive DECLINE tau phosphorylation transgenic mouse
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Effect of stromal cell-derived factor-1/CXCR4 axis in neural stem cell transplantation for Parkinson’s disease 预览
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作者 Jiao-Tian Xu Yuan Qian +7 位作者 Wei Wang Xiao-Xiang Chen Yang Li Yu Li Zhi-Yong Yang Xiao-Bin Song Di Lu Xing-Li Deng 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期112-119,共8页
Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still unclear.Stromal cell-derived factor-1 and its receptor,ch... Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still unclear.Stromal cell-derived factor-1 and its receptor,chemokine receptor 4(CXCR4),are important regulators of cell migration.We speculated that the CXCR4/stromal cell-derived factor 1 axis may be involved in the therapeutic effect of neural stem cell transplantation in the treatment of Parkinson’s disease.A Parkinson’s disease rat model was injected with 6-hydroxydopamine via the right ascending nigrostriatal dopaminergic pathway,and then treated with 5μL of neural stem cell suspension(1.5×104/L)in the right substantia nigra.Rats were intraperitoneally injected once daily for 3 days with 1.25 mL/kg of the CXCR4 antagonist AMD3100 to observe changes after neural stem cell transplantation.Parkinson-like behavior in rats was detected using apomorphine-induced rotation.Immunofluorescence staining was used to determine the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Using quantitative real-time polymerase chain reaction,the mRNA expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra were measured.In addition,western blot assays were performed to analyze the protein expression of stromal cell-derived factor-1 and CXCR4.Our results demonstrated that neural stem cell transplantation noticeably reduced apomorphine-induced rotation,increased the mRNA and protein expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra,and enhanced the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Injection of AMD3100 inhibited the aforementioned effects.These findings suggest that the stromal cell-derived factor-1/CXCR4 axis may play a significant role in the therapeutic effect of neural stem cell transplantation in a rat model of Parkinson’s disease.This study was approved by the Animal Care and Use Committee of Kunming 展开更多
关键词 AMD3100 CORPUS STRIATUM CXCR4 neural stem cells Parkinson’s disease STROMAL cell-derived factor-1 substantia nigra
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Challenges in studying geographic atrophy (GA) age-related macular degeneration:the potential of a new mouse model with GA-like features 预览
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作者 J. Arjuna Ratnayaka Andrew J. Lotery 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期863-864,共2页
Loss of central vision critical to everyday activities such as reading,face-recognition and driving due to damage in the central retina (the macula) is the leading cause of irreversible blindness amongst adults in the... Loss of central vision critical to everyday activities such as reading,face-recognition and driving due to damage in the central retina (the macula) is the leading cause of irreversible blindness amongst adults in the developed world.This condition,termed age-related macular degeneration (AMD),is a complex,chronic degenerative disease driven by a combination of genetic and lifestyle risk factors.Early signs of retinal changes in people as young as 30–40 years have been reported,although these individuals appear to be asymptomatic.However,by the age of 65,the disease is present in ~3% of individuals,which increases dramatically to affect 1/3 of individuals by the eighth decade of life.Early to intermediate AMD is estimated to affect ~150 million individuals globally,with another 10 million individuals suffering from end-stage,sight-threatening forms.These terminal stages are broadly grouped into dry (geographic atrophy,GA) or wet (choroidal neovascular,CNV) AMD (Sarks et al.,1988;Bird et al.,2014),with similar frequencies reported in patients.Recent advances in identifying genetic risk factors,including our discoveries in this field,indicate an initial shared pathology before progressing to aforementioned late-stage phenotypes.Currently,GA patients have no effective treatment,which may in part be due to the lack of good in vivo models for GA studies.Here,we summarize our new findings that describe an altogether new mouse model with GA-like features which shows progressive outer retinal pathology (Ibbett et al.,2019) that can be used to gain novel insights into GA and potentially as a tool for drug development. 展开更多
关键词 MACULA central VISION DEGENERATIVE disease
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Navigating the dynamic landscape of alpha-synuclein morphology:a review of the physiologically relevant tetrameric conformation 预览
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作者 Heather RLucas Ricardo DFernández 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期407-415,共9页
N-acetylatedα-synuclein(αSyn)has long been established as an intrinsically disordered protein associated with a dysfunctional role in Parkinson’s disease.In recent years,a physiologically relevant,higher order conf... N-acetylatedα-synuclein(αSyn)has long been established as an intrinsically disordered protein associated with a dysfunctional role in Parkinson’s disease.In recent years,a physiologically relevant,higher order conformation has been identified as a helical tetramer that is tailored by buried hydrophobic interactions and is distinctively aggregation resistant.The canonical mechanism by which the tetramer assembles remains elusive.As novel biochemical approaches,computational methods,pioneering purification platforms,and powerful imaging techniques continue to develop,puzzling information that once sparked debate as to the veracity of the tetramer has now shed light upon this new counterpart inαSyn neurobiology.Nuclear magnetic resonance and computational studies on multimericαSyn structure have revealed that the protein folding propensity is controlled by small energy barriers that enable large scale reconfiguration.Alternatively,familial mutations ablate tetramerization and reconfigure polymorphic fibrillization.In this review,we will discuss the dynamic landscape ofαSyn quaternary structure with a focus on the tetrameric conformation. 展开更多
关键词 ALPHA-SYNUCLEIN amyloid FIBRILS intrinsically disordered PROTEIN MULTIMER N-ACETYLATION oligomer Parkinson’s disease PROTEIN folding PROTEIN structure TETRAMER
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A mimetic peptide ofα2,6-sialyllactose promotes neuritogenesis 预览
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作者 Shuang-Xi Chen Jia-Hui He +3 位作者 Yong-Jian Mi Hui-Fan Shen Melitta Schachner Wei-Jiang Zhao 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1058-1065,共8页
Oxidative stress contributes to the pathogenesis of neurodegenerative diseases.With the aim to find reagents that reduce oxidative stress,a phage display library was screened for peptides mimicking a2,6-sialyllactose(... Oxidative stress contributes to the pathogenesis of neurodegenerative diseases.With the aim to find reagents that reduce oxidative stress,a phage display library was screened for peptides mimicking a2,6-sialyllactose(6'-SL),which is known to beneficially influence neural functions.Using Sambucus nigra lectin,which specifically binds to 6'-SL,we screened a phage display library and found a peptide comprising identical sequences of 12 amino acids.Mimetic peptide,reverse peptide and scrambled peptide were tested for inhibition of 6'-SL binding to the lectin.Indeed,lectin binding to 6'-SL was inhibited by the most frequently identified mimetic peptide,but not by the reverse or scrambled peptides,showing that this peptide mimics 6'-SL.Functionally,mimetic peptide,but not the reverse or scrambled peptides,increased viability and expression of neural cell adhesion molecule L1 in SK-N-SH human neuroblastoma cells,and promoted survival and neurite outgrowth of cultured mouse cerebellar granule neurons challenged by H_20_2-induced oxidative stress.The combined results indicate that the 6'-SL mimetic peptide promotes neuronal survival and neuritogenesis,thus raising hopes for the treatment of neurodegenerative diseases.This study was approved by the Medical Ethics Committee of Shantou University Medical College,China(approval No.SUMC 2014-004)on February 20,2014. 展开更多
关键词 central nervous system cerebellar granule neurons mimetic peptide neural cell adhesion molecule L1 NEURITOGENESIS neurodegenerative disease neuronal survival oxidative stress phage display Sambucus nigra lectin α2 6-sialyllactose
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Stem cell therapy for Parkinson’s disease:safety and modeling 预览
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作者 Theo Stoddard-Bennett Renee Reijo Pera 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期36-40,共5页
For decades,clinicians have developed medications and therapies to alleviate the symptoms of Parkinson’s disease,but no treatment currently can slow or even stop the progression of this localized neurodegeneration.Fo... For decades,clinicians have developed medications and therapies to alleviate the symptoms of Parkinson’s disease,but no treatment currently can slow or even stop the progression of this localized neurodegeneration.Fortunately,sparked by the genetic revolution,stem cell reprogramming research and the advancing capabilities of personalization in medicine enable forward-thinking to unprecedented patient-specific modeling and cell therapies for Parkinson’s disease using induced pluripotent stem cells(iPSCs).In addition to modeling Parkinson’s disease more accurately than chemically-induced animal models,patient-specific stem cell lines can be created,elucidating the effects of genetic susceptibility and sub-populations’differing responses to in vitro treatments.Sourcing cell therapy with iPSC lines provides ethical advantages because these stem cell lines do not require the sacrifice of human zygotes and genetically-specific drug trails can be tested in vitro without lasting damage to patients.In hopes of finally slowing the progression of Parkinson’s disease or re-establishing function,iPSC lines can ultimately be corrected with gene therapy and used as cell sources for neural transplantation for Parkinson’s disease.With relatively localized neural degeneration,similar to spinal column injury,Parkinson’s disease presents a better candidacy for cell therapy when compared to other diffuse degeneration found in Alzheimer’s or Huntington’s Disease.Neurosurgical implantation of pluripotent cells poses the risk of an innate immune response and tumorigenesis.Precautions,therefore,must be taken to ensure cell line quality before transplantation.While cell quality can be quantified using a number of assays,a yielding a high percentage of therapeutically relevant dopaminergic neurons,minimal de novo genetic mutations,and standard chromosomal structure is of the utmost importance.Current techniques focus on iPSCs because they can be matched with donors using human leukocyte antigens,thereby reducing the sever 展开更多
关键词 alpha SYNUCLEIN animal model cell therapy DOPAMINERGIC neurons induced PLURIPOTENT STEM CELLS NEURODEGENERATION Parksinson’s disease STEM CELLS
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Selective serotonin reuptake inhibitors and Alzheimer’s disease 预览
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作者 Bernadette Mdawar Elias Ghossoub Rita Khoury 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期41-46,共6页
Given the failure to develop disease-modifying therapies for Alzheimer’s disease(AD),strategies aiming at preventing or delaying the onset of the disease are being prioritized.While the debate regarding whether depre... Given the failure to develop disease-modifying therapies for Alzheimer’s disease(AD),strategies aiming at preventing or delaying the onset of the disease are being prioritized.While the debate regarding whether depression is an etiological risk factor or a prodrome of AD rages on,a key determining factor may be the timing of depression onset in older adults.There is increasing evidence that untreated early-onset depression is a risk factor and that late-onset depression may be a catalyst of cognitive decline.Data from animal studies have shown a beneficial impact of selective serotonin reuptake inhibitors on pathophysiological biomarkers of AD including amyloid burden,tau deposits and neurogenesis.In humans,studies focusing on subjects with a prior history of depression also showed a delay in the onset of AD in those treated with most selective serotonin reuptake inhibitors.Paroxetine,which has strong anticholinergic properties,was associated with increased mortality and mixed effects on amyloid and tau deposits in mice,as well as increased odds of developing AD in humans.Although most of the data regarding selective serotonin reuptake inhibitors is promising,findings should be interpreted cautiously because of notable methodological heterogeneity between studies.There is thus a need to conduct large scale randomized controlled trials with long follow up periods to clarify the dose-effect relationship of specific serotonergic antidepressants on AD prevention. 展开更多
关键词 Alzheimer’s disease AMYLOIDOGENESIS animal models ANTIDEPRESSANT depression onset delay prevention selective SEROTONIN REUPTAKE inhibitor SSRI
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