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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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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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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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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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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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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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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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Alzheimer’s disease, neural stem cells and neurogenesis:cellular phase at single-cell level 预览
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作者 Mehmet Ilyas Cosacak Prabesh Bhattarai Caghan Kizil 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期824-827,共4页
Alzheimer’s disease cannot be cured as of yet.Our current understanding on the causes of Alzheimer’s disease is limited.To develop treatments,experimental models that represent a particular cellular phase of the dis... Alzheimer’s disease cannot be cured as of yet.Our current understanding on the causes of Alzheimer’s disease is limited.To develop treatments,experimental models that represent a particular cellular phase of the disease and more rigorous scrutiny of the cellular pathological mechanisms are crucial.In recent years,Alzheimer’s disease research underwent a paradigm shift.According to this tendency,Alzheimer’s disease is increasingly being conceived of a disease where not only neurons but also multiple cell types synchronously partake to manifest the pathology.Knowledge on every cell type adds an alternative approach and hope for the efforts towards the treatment.Neural stem cells and their neurogenic ability are making an appearance as a new aspect of the disease manifestation based on the recent findings that neurogenesis reduces dramatically in Alzheimer’s disease patients compared to healthy individuals.Therefore,understanding how neural stem cells can form new neurons in Alzheimer’s disease brains holds an immense potential for clinics.However,this provocative idea requires further evidence and tools for investigation.Recently,single cell sequencing appeared as a revolutionary tool to understand cellular programs in unprecedented resolution and it will undoubtedly facilitate comprehensive investigation of different cell types in Alzheimer’s disease.In this mini-review,we will touch upon recent studies that use single cell sequencing for investigating cellular response in Alzheimer’s disease and some consideration pertaining to the utilization of neural regeneration for Alzheimer’s disease research. 展开更多
关键词 Alzheimer's disease mouse NEURAL regeneration NEURAL stem CELL NEUROGENESIS neuron single CELL sequencing ZEBRAFISH
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Natural stilbenes effects in animal models of Alzheimer’s disease 预览
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作者 Aline Freyssin Guylène Page +1 位作者 Bernard Fauconneau Agnès Rioux Bilan 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期843-849,共7页
Alzheimer’s disease is one of the most frequent neurodegenerative diseases.This pathology is characterized by protein aggregates,mainly constituted by amyloid peptide and tau,leading to neuronal death and cognitive i... Alzheimer’s disease is one of the most frequent neurodegenerative diseases.This pathology is characterized by protein aggregates,mainly constituted by amyloid peptide and tau,leading to neuronal death and cognitive impairments.Drugs currently proposed to treat this pathology do not prevent neurodegenerative processes and are mainly symptomatic therapies.However,stilbenes presenting multiple pharmacological effects could be good potential therapeutic candidates.The aim of this review is to gather the more significant papers among the broad literature on this topic,concerning the beneficial effects of stilbenes (resveratrol derivatives) in animal models of Alzheimer’s disease.Indeed,numerous studies focus on cellular models,but an in vivo approach remains of primary importance since in animals (mice or rats,generally),bioavailability and metabolism are taken into account,which is not the case in in vitro studies.Furthermore,examination of memory ability is feasible in animal models,which strengthens the relevance of a compound with a view to future therapy in humans.This paper is addressed to any researcher who needs to study untested natural stilbenes or who wants to experiment the most effective natural stilbenes in largest animals or in humans.This review shows that resveratrol,the reference polyphenol,is largely studied and seems to have interesting properties on amyloid plaques,and cognitive impairment.However,some resveratrol derivatives such as gnetin C,trans-piceid,or astringin have never been tested on animals.Furthermore,pterostilbene is of particular interest,by its improvement of cognitive disorders and its neuroprotective role.It could be relevant to evaluate this molecule in clinical trials. 展开更多
关键词 Alzheimer's disease AMYLOID animal models cognitive impairment inflammation NATURAL STILBENES NEUROPROTECTION RESVERATROL tau
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Can mouse models mimic sporadic Alzheimer’s disease? 预览
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作者 Bettina MFoidl Christian Humpel 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期401-406,共6页
Alzheimer’s disease(AD)is a progressive neurodegenerative disorder and the most common form of dementia worldwide.As age is the main risk factor,>97%of all AD cases are of sporadic origin,potentiated by various ri... Alzheimer’s disease(AD)is a progressive neurodegenerative disorder and the most common form of dementia worldwide.As age is the main risk factor,>97%of all AD cases are of sporadic origin,potentiated by various risk factors associated with life style and starting at an age>60 years.Only<3%of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2,and symptoms already start at an age<30 years.In order to study progression of AD,as well as therapeutic strategies,mouse models are state-of-the-art.So far many transgenic mouse models have been developed and used,with mutations in the APP or presenilin or combinations(3×Tg,5×Tg).However,such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop.Several risk genes,such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD,but also many risk factors associated with life style(e.g.,diabetes,hypercholesterolemia,stress)may play a role.In this review we discuss the current situation regarding AD mouse models,and the problems to develop a sporadic mouse model of AD. 展开更多
关键词 Alzheimer’s disease BETA-AMYLOID cerebral AMYLOID ANGIOPATHY cognitive impairment SPORADIC and genetic mouse models tau vascular risk factors
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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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20S proteasome and glyoxalase 1 activities decrease in erythrocytes derived from Alzheimer’s disease patients 预览
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作者 Hui Lv Gui-Yuan Wei +4 位作者 Can-Shou Guo Yu-Feng Deng Yong-Ming Jiang Ce Gao Chong-Dong Jian 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期178-183,共6页
As a result of accumulating methylglyoxal and advanced glycation end products in the brains of patients with Alzheimer’s disease,it is considered a protein precipitation disease.The ubiquitin proteasome system is one... As a result of accumulating methylglyoxal and advanced glycation end products in the brains of patients with Alzheimer’s disease,it is considered a protein precipitation disease.The ubiquitin proteasome system is one of the most important mechanisms for cells to degrade proteins,and thus is very important for maintaining normal physiological function of the nervous system.This study recruited 48 individuals with Alzheimer’s disease(20 males and 28 females aged 75±6 years)and 50 healthy volunteers(21 males and 29 females aged 72±7 years)from the Affiliated Hospital of Youjiang Medical University for Nationalities(Baise,China)between 2014 and 2017.Plasma levels of malondialdehyde and H2O2 were measured by colorimetry,while glyoxalase 1 activity was detected by spectrophotometry.In addition,20S proteasome activity in erythrocytes was measured with a fluorescent substrate method.Ubiquitin and glyoxalase 1 protein expression in erythrocyte membranes was detected by western blot assay.The results demonstrated that compared with the control group,patients with Alzheimer’s disease exhibited increased plasma malondialdehyde and H2O2 levels,and decreased glyoxalase 1 activity;however,expression level of glyoxalase 1 protein remained unchanged.Moreover,activity of the 20S proteasome was decreased and expression of ubiquitin protein was increased in erythrocytes.These findings indicate that proteasomal and glyoxalase activities may be involved in the occurrence of Alzheimer’s disease,and erythrocytes may be a suitable tissue for Alzheimer’s disease studies.This study was approved by the Ethics Committee of Youjiang Medical University for Nationalities(approval No.YJ12017013)on May 3,2017. 展开更多
关键词 20S proteasomal activity Alzheimer’s disease erythrocytes GLYOXALASE 1 H2O2 MALONDIALDEHYDE nerve regeneration total UBIQUITIN
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Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer’s disease 预览
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作者 Edwin E. Reza-Zaldivar Mercedes A. Hernández-Sapiéns +6 位作者 Yanet K. Gutiérrez-Mercado Sergio Sandoval-ávila Ulises Gomez-Pinedo Ana L. Márquez-Aguirre Estefanía Vázquez-Méndez Eduardo Padilla-Camberos Alejandro A. Canales-Aguirre 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1626-1634,共9页
Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived e... Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived exosomes on neurogenesis and cognitive capacity in a mouse model of Alzheimer’s disease.Alzheimer’s disease mouse models were established by injection of beta amyloid 1?42 aggregates into dentate gyrus bilaterally.Morris water maze and novel object recognition tests were performed to evaluate mouse cognitive deficits at 14 and 28 days after administration.Afterwards,neurogenesis in the subventricular zone was determined by immunofluorescence using doublecortin and PSA-NCAM antibodies.Results showed that mesenchymal stem cells-derived exosomes stimulated neurogenesis in the subventricular zone and alleviated beta amyloid 1?42-induced cognitive impairment,and these effects are similar to those shown in the mesenchymal stem cells.These findings provide evidence to validate the possibility of developing cell-free therapeutic strategies for Alzheimer’s disease.All procedures and experiments were approved by Institutional Animal Care and Use Committee(CICUAL)(approval No.CICUAL 2016-011)on April 25,2016. 展开更多
关键词 Alzheimer’s DISEASE neurodegenerative DISEASE COGNITIVE impairment memory Alzheimer’s DISEASE MOUSE model mesenchymal stem cell EXOSOMES NEUROGENESIS COGNITIVE improvement cell-free therapy neural regeneration
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Characteristics and advantages of adenoassociated virus vector-mediated gene therapy for neurodegenerative diseases 预览
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作者 Yuan Qu Yi Liu +2 位作者 Ahmed Fayyaz Noor Johnathan Tran Rui Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第6期931-938,共8页
Common neurodegenerative diseases of the central nervous system are characterized by progressive damage to the function of neurons,even leading to the permanent loss of function.Gene therapy via gene replacement or ge... Common neurodegenerative diseases of the central nervous system are characterized by progressive damage to the function of neurons,even leading to the permanent loss of function.Gene therapy via gene replacement or gene correction provides the potential for transformative therapies to delay or possibly stop further progression of the neurodegenerative disease in affected patients.Adeno-associated virus has been the vector of choice in recent clinical trials of therapies for neurodegenerative diseases due to its safety and efficiency in mediating gene transfer to the central nervous system.This review aims to discuss and summarize the progress and clinical applications of adeno-associated virus in neurodegenerative disease in central nervous system.Results from some clinical trials and successful cases of central neurodegenerative diseases deserve further study and exploration. 展开更多
关键词 nerve REGENERATION central nervous system gene therapy NEURODEGENERATIVE DISEASE viral vector ADENO-ASSOCIATED virus Alzheimer’s DISEASE Parkinson’s DISEASE Huntington’s DISEASE amyotrophic lateral SCLEROSIS spinal muscular atrophy neural REGENERATION
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自噬在神经退行性疾病中的调控作用 预览
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作者 徐宏睿(综述) 曾常茜(审校) 《临床与病理杂志》 2019年第9期2074-2078,共5页
自噬过程受到一系列复杂信号分子的调控。基础水平的自噬在清除异常积聚的蛋白质、受损的细胞器、维持细胞自身内环境的稳定和细胞生存中扮演着重要角色。自噬水平的上调或者降低与神经退行性疾病的发生发展有密切联系。调节自噬可以有... 自噬过程受到一系列复杂信号分子的调控。基础水平的自噬在清除异常积聚的蛋白质、受损的细胞器、维持细胞自身内环境的稳定和细胞生存中扮演着重要角色。自噬水平的上调或者降低与神经退行性疾病的发生发展有密切联系。调节自噬可以有效清除神经细胞中异常折叠积聚的蛋白质,从而缓解疾病进展。随着近几年对自噬现象和机制研究的不断深入,促进或者逆转自噬可能是一种治疗神经退行性疾病的有效策略和途径。 展开更多
关键词 自噬 神经退行性疾病 帕金森病 阿尔茨海默病 肌萎缩性侧索硬化症 亨廷顿氏舞蹈病 癫痫
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自噬在神经退行性疾病中的作用研究进展 预览
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作者 肖昊翔 李天 +1 位作者 彭帆 杨阳 《解放军医学杂志》 CAS CSCD 北大核心 2019年第4期341-346,共6页
自噬是细胞内溶酶体介导的降解错误折叠蛋白及衰老损伤细胞器的生命过程,广泛存在于真核细胞中。自噬在维持细胞稳态和物质能量再循环中具有重要作用。近年来,在许多组织和器官中发现了自噬的特殊功能。值得注意的是,自噬在神经退行性... 自噬是细胞内溶酶体介导的降解错误折叠蛋白及衰老损伤细胞器的生命过程,广泛存在于真核细胞中。自噬在维持细胞稳态和物质能量再循环中具有重要作用。近年来,在许多组织和器官中发现了自噬的特殊功能。值得注意的是,自噬在神经退行性疾病中的作用越来越被人们所重视。神经元自噬功能紊乱和异常蛋白质聚集折叠是神经退行性疾病的主要病理改变。研究表明,自噬调节与阿尔茨海默病淀粉样蛋白、帕金森病路易小体和亨廷顿病中亨廷顿蛋白等的清除具有密切联系。此外,天然药物包括白藜芦醇、海藻糖、姜黄素等已被证明在神经退行性疾病中通过调控自噬发挥着积极作用。因此,进一步了解自噬的机制对神经退行性疾病的治疗至关重要。现对自噬的分子机制及其在神经退行性疾病中的进展作一综述,旨在为神经退行性疾病的临床治疗提供参考。 展开更多
关键词 自噬 神经退行性疾病 阿尔兹海默症 帕金森病 亨廷顿病
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The Physiopathological Crossroads of Aging 预览
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作者 J. Lasierra-Cirujeda P. Coronel +4 位作者 M. J. Aza Pascual-Salcedo M. Gimeno M. M. Aza Pascual Salcedo A. Lasierra-Iba?ez C. Lasala-Aza 《生物科学与医学(英文)》 2019年第6期102-128,共27页
Stress, inflammation and Plasminogen activator inhibitor 1 (PAI-1) are key mechanisms throughout the development of aging, constituting a crossroad in the most frequent pathologies that accompany it. Among metabolic p... Stress, inflammation and Plasminogen activator inhibitor 1 (PAI-1) are key mechanisms throughout the development of aging, constituting a crossroad in the most frequent pathologies that accompany it. Among metabolic processes, obesity, metabolic syndrome and type 2 diabetes mellitus are included and Alzheimer’s disease among the neurodegenerative processes. Stress is a mechanism of defense of the organism against exogenous and endogenous actions called stressors. In the case of low intensity stimuli, the organism responds with actions aimed at a physiological adaptation (Homeostasis). On the other hand, when a high intensity (experimental level) or chronic stimulus (oxidative stress) is repeated, structural and functional changes are observed in different organs with activation of the hypothalamus-pituitary-adrenal axis, the renin angiotensin system and the sympathetic nervous system, stimulating the production of hormones that release cytokines with proin-flammatory/antiinflammatory properties that play an important role in the previously mentioned pathologies, as well as a marked increase in PAI-1, a gene regulated by stress and by cytokines, with manifest action at the origin of thromboembolic disease, so frequent in aging. The objective of this review is to highlight the importance of the binomial stress and PAI-1 in aging and in the pathologies that accompany it. Because PAI-1 is part of the pathology and complications in aging, some authors suggest the study of PAI-1 inhibitors to achieve its physiological levels, as part of the treatment of these diseases. 展开更多
关键词 Aging. Oxidative Stress PLASMINOGEN Activator Inhibitor 1 TRANSFORMING Growth Factor Beta 1 GLUTATHIONE Alzheimer’s Disease
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Computational Assessment and Pharmacological Property Breakdown of Eight Patented and Candidate Drugs against Four Intended Targets in Alzheimer’s Disease 预览
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作者 Bishajit Sarkar Syed Sajidul Islam +4 位作者 Md. Asad Ullah Sohana Hossain Md. Nazmul Islam Prottoy Yusha Araf Masuma Afrin Taniya 《生命科学与技术进展(英文)》 2019年第11期405-430,共26页
Alzheimer’s Disease (AD) is the most prevalent age-related dementia. AD can be caused by abnormal processing of amyloid precursor protein (APP) or by oxidative stress or may be due to the actions of kinases or the de... Alzheimer’s Disease (AD) is the most prevalent age-related dementia. AD can be caused by abnormal processing of amyloid precursor protein (APP) or by oxidative stress or may be due to the actions of kinases or the degeneration and loss of functions of neurons in the brain. Although various treatments have already gained success in the in vitro studies, however, till now not a single satisfactory drug has been proven that can cure this disease permanently till now. In this study, the best possible drug has been determined from a group of drug molecules using methods of molecular docking. Molecular docking is a computational approach which helps to determine the best molecule from a group of molecules which may bind with the highest affinity with the intended target by mimicking the original biological environment in a computer. The tested drug molecules in this experiment are the disease modifying agents, capable of inhibiting a particular protein involving in the AD pathway. Eight drug molecules (ligands)-memantine (-4.075 Kcal/mol), hymenialdisine (-8.079 Kcal/mol), tideglusib (-6.445 Kcal/mol), kenpaullone (-7.545 Kcal/mol), dihydrospiro[dibenzo[a,d][7]annulene-5,4’-imidazol] (-4.742 Kcal/mol), harmine (-7.57 Kcal/mol), harmol (-6.583 Kcal/mol) and 1-Methyl-4-Phenylpyridinium (-5.214 Kcal/mol), have been docked successfully against four targets (proteins)-N-Methyl-D-Aspartate Receptor (NMDAR), glycogen synthase kinase-3β (GSK-3β), beta-secretase (β-secretase) and dual specificity tyrosine (Y)-phosphorylation-regulated kinase 1A (DYR-K1A) in this experiment which are intended targets in current AD treatment approaches. Investigation of docking results, druglikeness properties and ADME/T testing results suggest that the best findings of this experiment are memantine, hymenialdisine, dihydrospiro[dibenzo[a,d][7]annulene-5,4’-imi- dazol] and harmol, that could be the best possible drugs for the treatment of AD. 展开更多
关键词 Alzheimer’s Disease Harmol Β-SECRETASE DOCKING Tau Protein Β-AMYLOID
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