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Investigation of a Chinese pedigree with early-onset familial Alzheimer’s disease caused by presenilin 1 p.M233T mutation
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作者 吴思 《中国医学文摘:内科学分册(英文版)》 2019年第2期122-123,共2页
Objective To analyze the clinical presentation andgenotype of a Chinese pedigree with early-onset familialAlzheimer's disease. Methods A pedigree with early-onsetfamilial Alzheimer's disease was recruited. The... Objective To analyze the clinical presentation andgenotype of a Chinese pedigree with early-onset familialAlzheimer's disease. Methods A pedigree with early-onsetfamilial Alzheimer's disease was recruited. The clinicaldata of the proband who was admitted to ShengjingHospital in March 2018 and the family members werecollected. The DNA sequences of 53 dementia relatedgenes were screened using next-generation sequencingtechnology in the blood sample of the proband. The point mutation discovered in the proband was also investigatedin some family members. Results There were five memberswith Alzheimer's disease in the pedigree,includingthe proband,a 42 years old female. The onset age of apedigree member was 33 years and that of the probandwas 37 years. A point mutation from T to C at position698 (M233T) in the exon 7 of presenilin 1 (PS1) genewas found in the proband and two other family memberswho were clinically normal. Conclusion The M233T mutationof PS1 gene can lead to early-onset familialAlzheimer's disease. This family is the first pedigree withM233T mutation of PS1 gene in China,which deservesclinical attention. 展开更多
关键词 Alzheimer a CHINESE PEDIGREE EARLY-ONSET FAMILIAL Alzheimer’s disease
Features of connected speech in patients with mild Alzheimer’s disease
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作者 李妍 《中国医学文摘:内科学分册(英文版)》 2019年第2期125-126,共2页
Objective To explore the features of connectedspeech produced by Chinese mild Alzheimer's disease(AD) patients. Methods Thirty Chinese mild AD patients( eight males and 22 females,and the age was(72. 73 ± 7. ... Objective To explore the features of connectedspeech produced by Chinese mild Alzheimer's disease(AD) patients. Methods Thirty Chinese mild AD patients( eight males and 22 females,and the age was(72. 73 ± 7. 78 ) years) and 30 age-and educationmatchednormal controls from three communities were recruitedin Xuanwu Hospital from January 2018 to May2018. All subjects completed tasks of picture naming,semantic fluency (animal),and Cookie Theft picture description.Picture description was analyzed for speechproduction ( total word output,speech rate,sound errors),lexical content (number of nouns and verbs,proportionof pronouns and verbs,semantic errors),informationcontent (information unit,idea density,efficiency),syntactic structure and complexity (mean length ofutterance,words in sentences,syntactic errors). Differencesbetween the groups were calculated. Associationbetween picture naming,semantic fluency,and measuresin picture descriptions was analyzed. 展开更多
关键词 ALZHEIMER FEATURES CONNECTED speech MILD Alzheimer’s disease
Effect of acupuncture on the ultrastructure of neurons and astrocytes in the hippocampal dentate gyrus in rats with Alzheimer’s disease induced by Aβ1-42
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作者 汤双红 《中国医学文摘:内科学分册(英文版)》 2019年第2期65-66,共2页
Objective To observe the effects of acupuncture at'Baihui'(GV 20) and'Shenshu'(BL 23) on the ultrastructure of hippocampal dentate gyrus in rats with Alzheimer’s disease. Methods Forty SPF Wistar male... Objective To observe the effects of acupuncture at'Baihui'(GV 20) and'Shenshu'(BL 23) on the ultrastructure of hippocampal dentate gyrus in rats with Alzheimer’s disease. Methods Forty SPF Wistar male rats were randomly divided into normal group,sham operation group,model group and acupuncture group,10 rats in each one. 展开更多
关键词 the ULTRASTRUCTURE of NEURONS and ASTROCYTES Alzheimer’s disease INDUCED by A Alzheimer
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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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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Osthole prevents cognitive impairment through modulating neuron cells in Aβ25-35-injected mice 预览
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作者 HOU Xue-qin 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第6期417-418,共2页
OBJECTIVE To investigate the effects of osthole on learning and memory impairment of AD mice induced by injection of Aβ25-35 and the content of Ca2+, GLU and Aβ1-42 in the brain tissue and peripheral blood. METHODS ... OBJECTIVE To investigate the effects of osthole on learning and memory impairment of AD mice induced by injection of Aβ25-35 and the content of Ca2+, GLU and Aβ1-42 in the brain tissue and peripheral blood. METHODS Mice were randomly assigned to sham operation, Aβ25-35, Aβ25-35+Ost-L,Aβ25-35+Ost-M, and Aβ25-35+Ost-H group. Water maze test was performed to assessing spatial learning ability of mice. It is determined that the MDA level and the activity of SOD in the brain tissue of mice in each group by colorimetry. The GLU kit and Ca2 +kit were used to detect the GLU, Ca2 +in tissue and serum. ELISA was used to detect the expression of Aβ1-42 in the hippocampus and serum of mice. HE staining and silver staining were used to detect neuron apoptosis and pathological changes in brain slices and so on. RESULTS(1) Effects of osthole on learning and memory: With the increase of training day,the escape latencies continuously reduced in each experimental group, the escape latencies of the model group was longer on the 1 st, 2 nd, 3 rd, and 5 thdays than the normal group, the difference was statistically significant(day 3 and 4: P<0.05, day 5: P<0.01);compared with the model group, the escaping latency on the 5 thday of the OST low-medium high-dose group was significantly shortened, which was statistically significant(P<0.05).(2) Effects on oxidative stresspathway: the SOD activity of AD mice in the hippocampus model group was lower than that in the normal group, which was statistically significant(P<0.05);The SOD activity in the OST group was higher than that in the model group, which was statistically significant(P<0.05). The MDA content in the model group was significantly higher than that in the normal group(P<0.05). The MDA content in the OST high-dose group was lower than that in the model group, which was statistically significant(P<0.05).(3) Effects of GLU levels on neurotransmitters:the results of the detection of GLU in cortical area and GLU in serum of AD mice in OST dose groups showed that serum GLU leve 展开更多
关键词 OSTHOLE ALZHEIMER disease AΒ25-35 SPATIAL learning and MEMORY
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The local mammalian target of rapamycin (mTOR) modulation: a promising strategy to counteract neurodegeneration 预览
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作者 Diego Dolcetta Roberto Dominici 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1711-1712,共2页
Alzheimer’s disease (AD) and the evolution of the “Amyloid Hypothesis”: The primary risk factor for dementia is aging, as the overwhelming majority of individuals who have the disease (~95%) are 65 years old or old... Alzheimer’s disease (AD) and the evolution of the “Amyloid Hypothesis”: The primary risk factor for dementia is aging, as the overwhelming majority of individuals who have the disease (~95%) are 65 years old or older, and the rate of development of AD doubles roughly every five years from that age, peaking at a nearly 50% population prevalence by the age of 85. The disease is progressive and irreversible, with an average time course of 8 to 10 years. Regardless of catastrophic forecasts for the next decades, its actual prevalence has huge family and social costs. 展开更多
关键词 Alzheimer’s disease primary risk factor family and SOCIAL COSTS
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Low-dose radiation and Alzheimer's disease:Neuronal effects and a potential modality for therapy?
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作者 Feng Li Liu Qiang +1 位作者 Wang Bing Cai Lu 《中华放射医学与防护杂志》 CAS CSCD 北大核心 2019年第8期581-589,共9页
Exposure to low-dose radiation(LDR,mostly less than 100 mGy)may reduce the vulnerability of exposed tissues to subsequent high-dose radiation(HDR)-induced damage,a phenomenon known as adaptive responses,which occurs v... Exposure to low-dose radiation(LDR,mostly less than 100 mGy)may reduce the vulnerability of exposed tissues to subsequent high-dose radiation(HDR)-induced damage,a phenomenon known as adaptive responses,which occurs via mechanisms including anti-inflammation and anti-oxidation.Alzheimer′s disease(AD)is a type of dementia that causes problems with memory,thinking,and behavior.Using the available literature,this review will examine whether there is any effect of LDR on AD.The available evidence shows that although LDR can alter the expression of some genes related to AD such as Apbb1,Lrp1,and Il1α,these alterations do not cause AD-like syndromes in animals,suggesting that LDR may also simultaneously upregulate several protective mechanisms that prevent the eventual development of AD.Furthermore,LDR seems capable of improving the symptoms of AD,as evidenced by the experience of an 81-year-old female AD patient.This patient was diagnosed with AD more than 10 years ago and gradually progressed to advanced AD in 2015,despite routine treatment.The patient then received about 12 computed tomography scans(about 40 mGy each)up until Nov.2017,which significantly improved her quality of life and reduced several AD symptoms.The improvement in this patient′s medical condition led to a few recent clinical trials investigating the effects of LDR on AD.To date,there is no efficient therapy available for AD,thus whether exposure to LDR at 100 mGy can provide a preventive or therapeutic effect for AD is an important issue.If LDR is a potential treatment for AD,as suggested by this reported case,this non-invasive approach would also bear the merit that it would be unlikely to cause a significant radiation health risk,as the LDR could be delivered locally to the head without any impact on other organs. 展开更多
关键词 LOW-DOSE radiation Alzheimer's disease Adaptive response HORMESIS NEURONAL STIMULATION
Potential preventive disease-modifying pharmacological strategies to delay late onset Alzheimer’s disease 预览
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作者 Miren Ettcheto Oriol Busquets Antoni Camins 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1721-1725,共5页
Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular ... Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated Tau protein.Over the years,AD has been classified in two subgroups:early onset or familial AD and late onset or sporadic AD.On the one hand,familial AD has been described to be the result of genetic mutations that cause,in some cases,for the overproduction of amyloid β.On the other,the cause of late onset or sporadic AD is still unclear even though several hypotheses have been proposed to explain the process of severe and progressive memory and cognitive loss.In the present review,some of the current hypotheses that try to explain the origin of late onset or sporadic AD have been summarized.Also,their potential implication in the development of new drugs for the presymptomatic treatment of late onset or sporadic AD has been considered. 展开更多
关键词 Alzheimer's DISEASE BETA-SECRETASE NEUROINFLAMMATION Tau amyloid N-METHYL-D-ASPARTATE glutamate
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正念冥想对阿尔茨海默病患者的认知能力及元认知水平影响 预览
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作者 谭红珠 《山西医药杂志》 CAS 2019年第12期1515-1517,共3页
阿尔茨海默病(Alzheimer′s disease,AD),是一种老年常见的进行性损害神经系统疾病,目前其病因有待进一步研究。临床症状[1]多为记忆力下降、认知能力下降、功能障碍等痴呆性表现,而上述表现会给患者及家人带来沉重的经济和社会负担。... 阿尔茨海默病(Alzheimer′s disease,AD),是一种老年常见的进行性损害神经系统疾病,目前其病因有待进一步研究。临床症状[1]多为记忆力下降、认知能力下降、功能障碍等痴呆性表现,而上述表现会给患者及家人带来沉重的经济和社会负担。临床上缺少有效的药物及手术护理方法,优质护理可以减慢神经系统损害速度,具有重要意义。正念冥想是通过集中自我注意力调节身心的活动,重点关注此时此刻的感觉、体验此时此刻的经历,需要个体全身心的投入其中并接纳。研究证实[2],正念冥想可以加强认知能力、提高注意力、改善心理状态等。另有研究证实[3],正念冥想在一定程度上可以重塑大脑网络,增强记忆功能。抑郁症、创伤后应激障碍等患者接受正念冥想可以取得较好效果,但是鲜有研究报道正念冥想对AD患者的效果,本研究笔者就正念冥想对AD患者的认知能力及元认知水平展开报道,供临床参考。 展开更多
关键词 阿尔茨海默病患者 认知能力 元认知 冥想 ALZHEIMER 创伤后应激障碍 神经系统疾病 临床症状
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Potential therapeutic roles of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease 预览
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作者 Bhaskar C. Das Somsankar Dasgupta Swapan K. Ray 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期1880-1892,共13页
All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to a... All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to activate specific signaling pathways in the cells. Retinoic acid signaling is extremely important in the central nervous system. Impairment of retinoic acid signaling pathways causes severe pathological processes in the central nervous system, especially in the adult brain. Retinoids have major roles in neural patterning, differentiation, axon outgrowth in normal development, and function of the brain. Impaired retinoic acid signaling results in neuroinflammation, oxidative stress, mitochondrial malfunction, and neurodegeneration leading to progressive Alzheimer’s disease, which is pathologically characterized by extra-neuronal accumulation of amyloid plaques(aggregated amyloid-beta) and intra-neurofibrillary tangles(hyperphosphorylated tau protein) in the temporal lobe of the brain. Alzheimer’s disease is the most common cause of dementia and loss of memory in old adults. Inactive cholinergic neurotransmission is responsible for cognitive deficits in Alzheimer’s disease patients. Deficiency or deprivation of retinoic acid in mice is associated with loss of spatial learning and memory. Retinoids inhibit expression of chemokines and neuroinflammatory cytokines in microglia and astrocytes, which are activated in Alzheimer’s disease. Stimulation of retinoic acid receptors and retinoid X receptors slows down accumulation of amyloids, reduces neurodegeneration, and thereby prevents pathogenesis of Alzheimer’s disease in mice. In this review, we described chemistry and biochemistry of some natural and synthetic retinoids and potentials of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease. 展开更多
关键词 Alzheimer's disease AMYLOID PLAQUES neurofibrillary TANGLES NEUROINFLAMMATION NEURODEGENERATION RETINOIDS
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Small interfering RNA delivery to the neurons near the amyloid plaques for improved treatment of Alzheimer’s disease
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作者 Qian Guo Xiaoyao Zheng +10 位作者 Peng Yang Xiaoying Pang Kang Qian Pengzhen Wang Shuting Xu Dongyu Sheng Liuchang Wang Jinxu Cao Wei Lu Qizhi Zhang Xinguo Jiang 《药学学报:英文版》 CSCD 2019年第3期590-603,共14页
Gene therapy represents a promising treatment for the Alzheimer’s disease(AD). However,gene delivery specific to brain lesions through systemic administration remains big challenge. In our previous work, we have deve... Gene therapy represents a promising treatment for the Alzheimer’s disease(AD). However,gene delivery specific to brain lesions through systemic administration remains big challenge. In our previous work, we have developed an siRNA nanocomplex able to be specifically delivered to the amyloid plaques through surface modification with both CGN peptide for the blood–brain barrier(BBB)penetration and QSH peptide for β-amyloid binding. But, whether the as-designed nanocomplex could indeed improve the gene accumulation in the impaired neuron cells and ameliorate AD-associated symptoms remains further study. Herein, we prepared the nanocomplexes with an siRNA against β-site amyloid precursor protein-cleaving enzyme 1(BACE1), the rate-limiting enzyme of Aβ production, as the therapeutic siRNA of AD. The nanocomplexes exhibited high distribution in the Aβ deposits-enriched hippocampus, especially in the neurons near the amyloid plaques after intravenous administration. In APP/PS1 transgenic mice, the nanocomplexes down-regulated BACE1 in both mRNA and protein levels,as well as Aβ and amyloid plaques to the level of wild-type mice. Moreover, the nanocomplexes significantly increased the level of synaptophysin and rescued memory loss of the AD transgenic mice without hematological or histological toxicity. Taken together, this work presented direct evidences that the design of precise gene delivery to the AD lesions markedly improves the therapeutic outcome. 展开更多
关键词 siRNA delivery NEURONS AMYLOID PLAQUES BACE1 gene Alzheimer’s disease
Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer’s disease 预览
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作者 Ning Li Yang Li +3 位作者 Li-Juan Li Ke Zhu Yan Zheng Xiao-Min Wang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第6期1037-1045,共9页
Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory,and plasticity deficits play a key role in dementia caused by Alzheimer’s disease.However,the mechanis... Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory,and plasticity deficits play a key role in dementia caused by Alzheimer’s disease.However,the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer’s disease remain unclear.In the present study,Alzheimer’s disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration,as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer’s disease-like diseases.APP/PS1 double transgenic(5XFAD;Jackson Laboratory)mice and their littermates(wild-type,controls)were used in this study.Additional 6-weekold and 10-week-old 5XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus.For 10-week-old 5XFAD mice and wild-type mice,the left hippocampus was used for electrophysiological recording,and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels.The results revealed that,compared with wild-type mice,6-week-old 5XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus.Another set of 5XFAD mice began to show attenuation at the age of 10 weeks,and a large quantity of amyloid beta protein was accumulated in hippocampal cells.The location ofα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased.These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer’s disease.The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Capital Medical University,China on December 17,2015(approval No.AE 展开更多
关键词 nerve REGENERATION Alzheimer’s disease SYNAPTIC plasticity hippocampus learning and memory long-term POTENTIATION βamyloid glutamate receptor SYNAPTIC strength neural REGENERATION
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New perspectives in iron chelation therapy for the treatment of Parkinson’s disease 预览
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作者 Marco T. Nunez Pedro Chana-Cuevas 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期1905-1906,共2页
Neurodegenerative diseases with an iron accumulation component: A wide variety of neurological diseases are characterized by the accumulation of iron in different areas of the central nervous system, include Parkinson... Neurodegenerative diseases with an iron accumulation component: A wide variety of neurological diseases are characterized by the accumulation of iron in different areas of the central nervous system, include Parkinson’s disease, Huntington disease, Alzheimer’s disease, Friedreich’s ataxia, amyotrophic lateral sclerosis, pantothenate kinase-associated neurodegeneration and other neuropathologies associated with brain iron accumulation (Hayflick et al., 2018). 展开更多
关键词 PARKINSON HUNTINGTON Friedreich ALZHEIMER
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经颅多普勒超声对阿尔茨海默症患者脑血流参数变化的研究及其临床意义分析 预览
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作者 魏珍 童剑飞 《全科医学临床与教育》 2019年第8期739-741,共3页
随着人口老龄化现象的加重,我国阿尔茨海默症(alzheimer disease,AD)患者日渐增多[1]。AD会对患者的身心健康、生活质量造成严重的影响,同时会给家庭与社会带来沉重的负担[2]。因此,对AD患者尽早进行诊断有利于为临床治疗方案制定、预... 随着人口老龄化现象的加重,我国阿尔茨海默症(alzheimer disease,AD)患者日渐增多[1]。AD会对患者的身心健康、生活质量造成严重的影响,同时会给家庭与社会带来沉重的负担[2]。因此,对AD患者尽早进行诊断有利于为临床治疗方案制定、预防措施实施提供一定的依据。 展开更多
关键词 阿尔茨海默症 临床意义 经颅多普勒超声 患者 参数变化 脑血流 ALZHEIMER 人口老龄化
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Effects of Acupuncture on Alzheimer's Disease: Evidence from Neuroimaging Studies
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作者 YU Chao-chao MA Chao-yang +4 位作者 WANG Hua KONG Li-hong ZHAO Yan SHEN Feng WU Miao 《中国结合医学杂志:英文版》 SCIE CAS CSCD 2019年第8期631-640,共10页
As the worldwide population ages, the prevalence of Alzheimer's disease (AD) increases. However, the results of promising medications have been unsatisfactory. Chinese acupuncture has a long history of treating de... As the worldwide population ages, the prevalence of Alzheimer's disease (AD) increases. However, the results of promising medications have been unsatisfactory. Chinese acupuncture has a long history of treating dementia, but lack of evidence from well-designed randomized controlled trials that validate its efficacy and safety, as well as its lack of clear underlying mechanisms, contribute to its limited application in clinical practice. In recent years, brain imaging technologies, such as functional magnetic resonance imaging and positron emission tomography, have been used to assess brain responses to acupuncture in a dynamic, visual, and objective way. These techniques are frequently used to explore neurological mechanisms of responses to acupuncture in AD and provide neuroimaging evidence as well as starting points to elucidate the possible mechanisms. This review summarizes the existing brain imaging evidence that explains the effects of acupuncture for AD and analyzes brain responses to acupuncture at cognitive-related acupoints [Baihui (GV 20), Shenmen (HT 7), Zusanli (ST 36), Neiguan (PC 6), and Taixi (KI 3)] from perspectives of acupoint specificity and acupoint combinations. Key issues and directions to consider in future studies are also put forward. This review should deepen our understanding of how brain imaging studies can be used to explore the underlying mechanisms of acupuncture in AD. 展开更多
关键词 ACUPUNCTURE Alzheimer's disease brain response ACUPOINT SPECIFICITY NEUROIMAGING
Electro-acupuncture therapy to improve spatial learning and memory in APPswe/ PS1dE9 transgenic mice through the inhibition of the TLR4/MyD88 signaling pathway 预览
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作者 Menghan Lu Ning Ding +4 位作者 Xin Wang Jin Cao Jing Jiang Yushan Gao Zhigang Li 《中医科学杂志(英文)》 2019年第2期184-192,共9页
Objective:To determine whether electro-acupuncture (EA) therapy could improve the cognitive functions of amyloid precursor protein Swedish mutation (APPswe)/presenilin 1 deleted in exon 9 (PS1dE9) mice and examine whe... Objective:To determine whether electro-acupuncture (EA) therapy could improve the cognitive functions of amyloid precursor protein Swedish mutation (APPswe)/presenilin 1 deleted in exon 9 (PS1dE9) mice and examine whether EA treatment could attenuate neuroinflammation by targeting the toll-like receptor 4 (TLR4)/myeloid differentiation primary response factor 88 (MyD88) signaling pathway.Methods:Twenty-seven double transgenic APPswe/PS1dE9 mice were randomly allocated into three groups:an Alzheimer's disease model group (AD group),a medication group (M group) and an EA treatment group (EA group).Each group contained nine mice,and nine wild-type mice were used in a normal group (N group).The animals in the M group were treated with oral administrations of 0.92 mg/kg donepezil hydrochloride for 15 days.For animals in the EA group,EA treatments were used on the Yintang (GV 29) and Baihui (GV 20) acupoints for 20 minutes,and the Shuigou (GV 26) acupoint was pricked without needle retention following EA treatments.Following treatments,the spatial learning and memory of the mice were measured using the Morris water maze test.The expression levels of TLR4,MyD88,nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) were analyzed by immunohistochemical staining and western blot.Results:The escape latencies of the M and EA groups were significantly lower than those of the AD group (vs M,P =.002;vs EA,P <.001).Moreover,compared with the AD group,the numbers of platform crossings was higher (vs M,P =.038;vs EA,P =.008) and the latency time for target quadrants was longer (vs M,P =.002;vs EA,P =.001) in the M and EA groups (P <.05).Furthermore,in the M and EA groups,the expression levels of TLR4,MyD88,NF-κB and iNOS decreased significantly compared with those of the AD group (all P <.01).Conclusion:EA treatment enhanced the memory and learning abilities of APPswe/PS1dE9 mice by regulating the TLR4/MyD88 inflammatory signaling pathway. 展开更多
关键词 ELECTRO-ACUPUNCTURE (EA) TLR4 Alzheimer's disease (AD) MICROGLIA NF-κB
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Activation of α7 nAChR by PNU improves synaptic and cognitive function through restoring the expression of synaptic-associated proteins 预览
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作者 WANG Xiao-lin DENG Yu-xin +5 位作者 GAO Yu-mei DONG Yang-ting WANG Fan GUAN Zhi-zhong HONG Wei QI Xiao-lan 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第6期474-475,共2页
OBJECTIVE Alzheimer disease(AD) is the most common type of dementia and is featured by the accumulation of β-amyloid peptide(Aβ) in the brain. The Alpha 7 nicotinic acetylcholine receptor family(α7 nAChR) was widel... OBJECTIVE Alzheimer disease(AD) is the most common type of dementia and is featured by the accumulation of β-amyloid peptide(Aβ) in the brain. The Alpha 7 nicotinic acetylcholine receptor family(α7 nAChR) was widely considered to interact with that Aβ, mediate neuroprotection and improve cognitive performance. However, the mechanisms underlying these interactions remain elusive. The present study aimed to determine how this interaction contribute to AD pathology. METHODS In vitro model of AD(primary culture of mice hippocampus treated with Aβ) and in vivo, a mouse model of AD(APPswe/PSEN1 d E9 double transgenic mice, APP/PS1_DT mice) were used to study to the possible inter-action of α7 nAChR and Aβ in the pathogenesis of AD. In vitro experiments, the primary hippocampal neurons cell was exposed to Aβ1-42 peptides in combination with PNU. In vivo experiments, different drugs/operations was applied to APP/PS1_DT mice for setting up of the following groups: WP group, wild-type C57 mice treated with PNU(α7 nAChR specific agonist);AP group, APP/PS1_DT mice treated with PNU;APP/PS1 group, the APP/PS1_DT mice injected intraperitoneally with the same amount of normal saline for 5 d;Control group, wild-type C57 mice injected intraperitoneally with the same amount of normal saline for 5 d. A transmission electron microscope was used to observed the synaptic morphological changes of hippocampal neurons. Reverse transcription quantitative PCR(RT-q PCR) and Western blot analysis were used to detect the expression levels of synaptic-associated proteins(SYN, SNAP25 etc). The learning and memory abilities of mice were detected by Morris water maze. RESULTS In vitro, it was found that α7 nAChR acts as an anti-Aβ-induced synaptic injury to nerve cell by increased the expression of synaptic-associated proteins and attenuated apoptosis induced by Aβ oligomers. In vivo, α7 nAChR attenuated synaptic loss induced by Aβ1-42, reduced the deposition of Aβ1-42 in the hippocampus and maintained the integrity of synaptic stru 展开更多
关键词 α7 NACHR Β-AMYLOID peptide SYNAPTIC CaM-CaMKⅡ-CREB signalling pathway ALZHEIMER disease
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The Glutamatergic Postrhinal Cortex–Ventrolateral Orbitofrontal Cortex Pathway Regulates Spatial Memory Retrieval
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作者 Xinyang Qi Zhanhong Jeff Du +7 位作者 Lin Zhu Xuemei Liu Hua Xu Zheng Zhou Cheng Zhong Shijiang Li Liping Wang Zhijun Zhang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第3期447-460,共14页
A deficit in spatial memory has been taken as an early predictor of Alzheimer’s disease(AD) or mild cognitive impairment(MCI). The uncinate fasciculus(UF) is a long-range white-matter tract that connects the anterior... A deficit in spatial memory has been taken as an early predictor of Alzheimer’s disease(AD) or mild cognitive impairment(MCI). The uncinate fasciculus(UF) is a long-range white-matter tract that connects the anterior temporal lobe with the orbitofrontal cortex(OFC)in primates. Previous studies have shown that the UF impairment associated with spatial memory deficits may be an important pathological change in aging and AD, but its exact role in spatial memory is not well understood. The pathway arising from the postrhinal cortex(POR) and projecting to the ventrolateral orbitofrontal cortex(vlOFC)performs most of the functions of the UF in rodents.Although the literature suggests an association between spatial memory and the regions connected by the POR–vlOFC pathway, the function of the pathway in spatialmemory is relatively unknown. To further illuminate the function of the UF in spatial memory, we dissected the POR–vlOFC pathway in mice. We determined that the POR–vlOFC pathway is a glutamatergic structure, and that glutamatergic neurons in the POR regulate spatial memory retrieval. We also demonstrated that the POR–vlOFC pathway specifically transmits spatial information to participate in memory retrieval. These findings provide a deeper understanding of UF function and dysfunction related to disorders of memory, as in MCI and AD. 展开更多
关键词 Spatial memory Postrhinal CORTEX Ventrolateral orbitofrontal CORTEX MILD cognitive IMPAIRMENT Alzheimer's disease
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