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Effect of Panax notoginseng saponins on the expression of beta-amyloid protein in the cortex of the parietal lobe and hippocampus, and spatial learning and memory in a mouse model of senile dementia 被引量:9
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作者 Zhenguo Zhong Dengpan Wu Liang Lu Jinsheng Wang Wenyan Zhang Zeqiang Qu 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第12期1297-1303,共7页
BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheime... BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer's disease. OBJECTIVE: Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein (App) and β -amyloid (A β ), to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 (SAMP8) and compare the effects with huperzine A. DESIGN, TIME AND SETTING: A completely randomized grouping design, controlled animal experiment was performed in the Center for Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS: Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups: PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. (batch No.: Z53021485, Yuxi, Yunan Province, China). Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. (batch No.: 20040801, Zhejiang, China). METHODS: The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES: After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency (time-to-platform), and the percentage of swimming time spent in each quadrant. The number of A β 1-40, A β 1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content ofApp, tau, acetylcholinesterase, and synaptophysin (Syp) was tested by real time PCR and RT-PCR. RESULTS: The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group (P 〈 0.05). The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of A β 1-40, A β 1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group (P 〈 0.05). CONCLUSION: These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer's disease. The therapeutic effects of PNS for Alzheimer's disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A. 展开更多
关键词 Alzheimer's disease Panax notoginseng saponins learning and memory β -amyloid precursor protein 1-40 β -amyloid precursor protein 1-42 amyloid β -peptide SYNapTOPHYSIN senescence accelerated mouse-prone 8
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miR-15b-5p targeting amyloid precursor protein is involved in the anti-amyloid eflect of curcumin in swAPP695-HEK293 cells 被引量:3
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作者 Hong-Ying Liu Xian Fu +4 位作者 You-Fu Li Xian-Liang Li Zhen-Yu Ma Ying Zhang Qing-Chun Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第9期1603-1609,共7页
Curcumin exerts a neuroprotective effect on Alzheimer’s disease;however,it is not known whether microRNAs are involved in this protective effect.This study was conducted using swAPP695-HEK293 cells as an Alzheimer’s... Curcumin exerts a neuroprotective effect on Alzheimer’s disease;however,it is not known whether microRNAs are involved in this protective effect.This study was conducted using swAPP695-HEK293 cells as an Alzheimer’s disease cell model.swAPP695-HEK293 cells were treated with 0,0.5,1,2,5,and 10μM curcumin for 24 hours.The changes in miR-15b-5p,miR-19a-3p,miR-195-5p,miR-101-3p,miR-216b-5p,miR-16-5p and miR-185-5p expression were assessed by real-time quantitative polymerase chain reaction.The mRNA and protein levels of amyloid precursor protein,amyloid-β40 and amyloid-β42 were evaluated by quantitative real-time polymerase chain reaction,western blot assays and enzyme-linked immunosorbent assays.swAPP695-HEK293 cells were transfected with miR-15b-5p mimic,or treated with 1μM curcumin 24 hours before miR-15b-5p inhibitor transfection.The effects of curcumin on amyloid precursor protein,amyloid-β40 and amyloid-β42 levels were evaluated by western blot assays and enzyme-linked immunosorbent assay.Luciferase assays were used to analyze the interaction between miR-15b-5p and the 3′-untranslated region of amyloid precursor protein.The results show that amyloid precursor protein and amyloid-βexpression were enhanced in swAPP695-HEK293 cells compared with HEK293 parental cells.Curcumin suppressed the expression of amyloid precursor protein and amyloid-βand up-regulated the expression of miR-15b-5p in swAPP695-HEK293 cells.In addition,we found a negative association of miR-15b-5p expression with amyloid precursor protein and amyloid-βlevels in the curcumin-treated cells.Luciferase assays revealed that miR-15b-5p impaired the luciferase activity of the plasmid harboring the 3′-untranslated region of amyloid precursor protein.These findings indicate that curcumin down-regulates the expression of amyloid precursor protein and amyloid-βin swAPP695-HEK293 cells,which was partially mediated by miR-15b-5p via targeting of the 3′-untranslated region of amyloid precursor protein. 展开更多
关键词 nerve REGENERATION Alzheimer’s disease natural plant drug CURCUMINOIDS miRNAs amyloid precursor protein amyloid 3′-untranslated region LUCIFERASE assays neurons neural REGENERATION
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法舒地尔通过促进线粒体自噬抑制NLRP3炎性小体激活改善APP/PS1转基因小鼠认知功能
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作者 刘怀绢 章培军 +3 位作者 于婧文 王记委 尉杰忠 郭敏芳 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2024年第8期696-703,共8页
目的基于线粒体自噬和含pyrin结构域核苷酸结合寡聚结构域样受体家族蛋白3(NLRP3)炎性小体(inflammasome)途径探究法舒地尔改善淀粉样前体蛋白/早老素1(APP/PS1)转基因小鼠认知功能障碍的机制。方法APP/PS1小鼠分为模型组以及治疗组,C57... 目的基于线粒体自噬和含pyrin结构域核苷酸结合寡聚结构域样受体家族蛋白3(NLRP3)炎性小体(inflammasome)途径探究法舒地尔改善淀粉样前体蛋白/早老素1(APP/PS1)转基因小鼠认知功能障碍的机制。方法APP/PS1小鼠分为模型组以及治疗组,C57BL/6小鼠为对照组。治疗组每日腹腔注射25 mg/kg的法舒地尔,连续2个月,对照组和模型组注射同等体积的生理盐水。水迷宫和Y迷宫实验检测小鼠行为学;尼氏染色法和神经元特异性核抗原(NeuN)免疫荧光组织化学染色评估神经元的数量和形态,原位末端转移酶标记技术(TUNEL)染色检测神经元凋亡;免疫荧光组织化学染色检测P62和NLRP3的表达;实时荧光定量PCR检测第10号染色体缺失的磷酸酶和张力蛋白同源物(PTEN)诱导的推定激酶1(PINK1)、帕金森病蛋白(Parkin)和NLRP3 mRNA的表达水平;Western blot法检测PINK1、Parkin、P62、微管相关蛋白1轻链3(LC3)、NLRP3、含C末端胱天蛋白酶活化和募集结构域凋亡相关斑点样蛋白(ASC)和白细胞介素18(IL-18)的表达。结果水迷宫和Y迷宫结果显示,治疗组小鼠认知行为明显改善,其空间记忆和探索能力显著提高;尼氏染色结果和NeuN免疫荧光组织化学染色结果显示,与对照组相比,模型组小鼠神经元数量减少,尼氏小体减少,法舒地尔治疗后神经元的形态和数量均有所改善,TUNEL染色结果还表明,法舒地尔治疗后APP/PS1小鼠脑组织中凋亡细胞数减少;与对照组相比,模型组PINK1、Parkin表达减少,P62、LC3、NLRP3、ASC和IL-18表达增加,法舒地尔治疗后PINK1、Parkin和LC3表达增加,P62、NLRP3、ASC和IL-18表达减少。结论法舒地尔可以改善APP/PS1小鼠的认知功能,并改善其神经元损伤,其机制可能与促进线粒体自噬进而抑制NLRP3炎性小体的激活有关。 展开更多
关键词 阿尔茨海默病 淀粉样前体蛋白/早老素1(apP/PS1)小鼠 法舒地尔 线粒体自噬 炎性小体(inflammasome)
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Optimization of Insulin Rapid Amyloid Fibrosis Conditions
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作者 黄晨 刘耀嘉 +5 位作者 李依萌 张凯 陈祥 马树涛 李真 陈婷 《Journal of Donghua University(English Edition)》 CAS 2023年第4期370-376,共7页
Amyloid fibers are now considered as one of the possible therapeutic targets of neurodegenerative diseases due to their unique physicochemical properties and toxicity. To efficiently trace in real time how the drug in... Amyloid fibers are now considered as one of the possible therapeutic targets of neurodegenerative diseases due to their unique physicochemical properties and toxicity. To efficiently trace in real time how the drug inhibits protein amyloid fibrosis, it is necessary to study the conditions for rapid amyloid fibrosis. Insulin is selected as the model protein in vitro to explore the process of amyloid formation. The effects of the molar concentration of NaCl, pH and reaction temperature in the single-factor experiment are discussed and the response surface analysis is carried out. Amyloid fibrosis is labeled by Thioflavin-T(ThT). The optimal molar concentration of NaCl, pH and reaction temperature for insulin rapid amyloid fibrosis are 50.0 mmol/L, 2.02 and 54℃, respectively. With the addition of 0.1 mmol/L phenol, the half-time of insulin amyloid fibrosis is shortened from 5.4 h to 1.7 h. The insulin rapid amyloid fibrosis system provides a new approach for screening the protein amyloid fibrosis inhibitors. 展开更多
关键词 amyloid fibrosis response surface analysis INSULIN model protein
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SfAp参与调控白背飞虱的翅发育
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作者 杨熙彬 雷庆 +3 位作者 龙慧 龙贵云 杨洪 金道超 《昆虫学报》 CAS CSCD 北大核心 2024年第10期1299-1306,共8页
【目的】Apterous(Ap)属于LIM结构域家族的发育调控蛋白。本研究旨在探究Ap基因在白背飞虱Sogatella furcifera翅发育中的作用。【方法】基于白背飞虱基因组和转录组数据库,采用RT-PCR验证SfAp的cDNA序列并进行生物信息学分析;利用RT-q... 【目的】Apterous(Ap)属于LIM结构域家族的发育调控蛋白。本研究旨在探究Ap基因在白背飞虱Sogatella furcifera翅发育中的作用。【方法】基于白背飞虱基因组和转录组数据库,采用RT-PCR验证SfAp的cDNA序列并进行生物信息学分析;利用RT-qPCR检测SfAp在白背飞虱不同发育阶段(1-5龄若虫和雌雄成虫)和成虫不同组织(头、胸、腹、足、翅、体壁、脂肪体和肠道)中的表达量;通过RNAi技术靶向沉默3龄若虫SfAp后观察白背飞虱的生长发育情况,并统计RNAi后的存活率、总死亡率和翅畸形率,采用RT-qPCR测定翅发育信号通路关键基因(鞣化激素基因SfBurs-α和SfBurs-β、Hippo信号通路基因SfHippo和SfSal、Wnt信号通路基因SfWg、Hedgehog信号通路基因SfHh和SfDpp及SfHOW)的表达量。【结果】克隆获得了白背飞虱SfAp(GenBank登录号:PP901867)的开放阅读框,长1287 bp,编码428个氨基酸的蛋白质,其编码蛋白质预测的分子量为47.41 kD,理论等电点为8.99,SfAp含有典型的LIM保守结构域;SfAp与褐飞虱Nilaparvata lugens的NlAp亲缘关系最近,氨基酸序列一致性达84.86%。发育表达谱结果显示,SfAp在4龄若虫前表达量较高,随后逐渐下降,到5龄第3天若虫期表达量显著升高,成虫羽化后表达量下降;组织表达谱结果表明,SfAp在成虫胸部中表达量最高,其次是在腹部、脂肪体和肠道中高量表达。显微注射dsSfAp导致羽化成虫表现出翅不伸展及畸形,并且翅发育相关基因SfBurs-α,SfBurs-β,SfHippo,SfSal,SfWg,SfHh,SfDpp和SfHOW的表达也被显著抑制。【结论】SfAp通过影响翅发育信号通路关键基因的表达量,进而影响白背飞虱的翅伸展及发育过程。 展开更多
关键词 白背飞虱 LIM结构域家族 发育调节蛋白 ap基因 表达谱分析 翅发育
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Effects of natural cerebrolysin on protective proteins and pro-apoptotic molecules in mesenchymal stem cells following beta-amyloid peptide1-40-induced endoplasmic reticulum stress 被引量:1
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作者 Yinghong Li Zhengzhi Wu +4 位作者 Ming Li Xiaoli Zhang Min Yang Manyin Chen Andrew C. J.Huang O 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第12期986-993,共8页
BACKGROUND: Studies have demonstrated that β-amyloid peptide (Aβ), a characteristic pathological product of Alzheimer's disease (AD), results in neuronal endoplasmic reticulum stress (ERS). However, the mech... BACKGROUND: Studies have demonstrated that β-amyloid peptide (Aβ), a characteristic pathological product of Alzheimer's disease (AD), results in neuronal endoplasmic reticulum stress (ERS). However, the mechanisms of traditional Chinese medicine against ERS in AD are poorly understood. OBJECTIVE: To measure expression levels of protective proteins (GRP78 and GRP94) of ER molecular partners and pro-apoptotic Caspase-12 ER membrane expression following application of traditional Chinese medicine natural cerebrolysin (NC) to treat Aβ1-40-induced ERS. DESIGN, TIME AND SETTING: A parallel-controlled study was performed at the Institute of Integrated Western and Traditional Chinese Medicine, Shenzhen Hospital of Southern Medical University between September 2006 and November 2008. MATERIALS: Sprague Dawley male rats, 6-8 weeks old, were used to harvest tibial and femoral bone marrow. Isolation and purification of mesenchymal stem cells (MSCs) were established from the whole bone marrow by removing non-adherent cells in primary and passage cultures. Aβ1-40 was provided by Sigma, USA. NC was provided by Shenzhen Institute of Integrated Chinese and Western Medicine, China. NC was predominantly composed of Renshen (Radix Ginseng), Tianma (Rhizoma Gastrodiae), and Yinxingye (Ginkgo Leaf) in a proportion of 1 : 2: 2. Following conventional water extraction technology, an extract (1 : 20) was prepared. Six adult, male, New Zealand rabbits underwent intragastric administration of NC extract (0.976 g/kg per day) for 1 month to prepare NC-positive serum, and the remaining 6 rabbits received intragastric administration of physiological saline to prepare normal blank serum. METHODS: A total of 500 nmol/L Aβ1-40 was used to establish ERS models of primary cultured MSCs. AD cell models were incubated with different doses of NC-positive serum (2.5%, 5%, and 10%). MSCs treated with normal blank serum served as normal blank controls. MAIN OUTCOME MEASURES: Reverse transcription-polymerase chain reaction and fluorescent immunocytochemistry were respectively used to measure mRNA and protein expression levels of GRP78, GRP94, and Caspase-12 in MSCs. RESULTS: Following Aβ1-40 exposure, mRNA and protein expression levels of GRP78 and GRP94, as well as Caspase-12, significantly increased (P 〈 0.05), suggesting successful establishment of ERS models. Following NC-positive serum application, mRNA and protein expression levels of GRP78 and GRP94 in MSCs significantly increased (P 〈 0.05 or P 〈 0.01). However, mRNA and protein expression levels of Caspase-12 significantly decreased (P 〈 0.05, or P 〈 0.01) compared with the ERS model group. These effects were dose-dependent. CONCLUSION: NC downregulated Caspase-12 expression and upregulated GRP78 and GRP94 expression in MSCs in a dose-dependent manner under the state of Aβ1-40-induced ERS. 展开更多
关键词 endoplasmic reticulum stress amyloid beta protein 1-40 Alzheimer's Disease natural cerebrolysin protective effect mesenchymal stem cells
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槲皮素对N2a/APP细胞的神经保护作用机制
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作者 郭敏 彭亚倩 +2 位作者 张婷 唐智 齐晓岚 《贵州医科大学学报》 CAS 2024年第9期1249-1258,共10页
目的探究槲皮素在稳定表达人瑞典淀粉样蛋白前体蛋白APP695的小鼠神经母细胞瘤N2a细胞中神经保护作用的机制。方法采用稳转APP695瑞士突变的N2a细胞(N2a/APP)为研究对象,通过CCK-8法检测槲皮素对N2a/APP细胞活力的影响;选择不同浓度槲... 目的探究槲皮素在稳定表达人瑞典淀粉样蛋白前体蛋白APP695的小鼠神经母细胞瘤N2a细胞中神经保护作用的机制。方法采用稳转APP695瑞士突变的N2a细胞(N2a/APP)为研究对象,通过CCK-8法检测槲皮素对N2a/APP细胞活力的影响;选择不同浓度槲皮素处理N2a/APP细胞,并用蛋白质印迹法(Western blot)法检测槲皮素处理后N2a/APP细胞内β-淀粉样蛋白前体蛋白(APP)、25kDa突触关联蛋白(SNAP25)、突触素(Synaptophysin,SYP)和突触后致密区蛋白95(PSD95)、细胞外调节蛋白激酶(ERK1/2)通路蛋白、丝氨酸/苏氨酸蛋白激酶B(AKT)通路蛋白、胱氨酸/谷氨酸逆向转运系统的轻链亚基(xCT)蛋白及NADPH氧化酶4(NOX4)蛋白的表达水平;使用流式细胞术检测槲皮素处理后细胞活性氧自由基(ROS)和线粒体膜电位变化,免疫荧光法检测槲皮素处理后N2a/APP细胞内脂质过氧化和DNA损伤程度。结果槲皮素处理N2a/APP细胞后,APP表达显著降低,SNAP25和Synaptophysin表达明显升高,磷酸化ERK1/2水平显著降低,磷酸化AKT水平升高,NOX4表达降低,xCT表达明显升高,线粒体膜电位恢复,氧化应激、脂质过氧化和DNA氧化损伤程度降低,差异均有统计学意义(P<0.05)。结论槲皮素对N2a/APP细胞的神经保护作用机制可能与ERK1/2和AKT通路减轻氧化应激、恢复受损突触和损伤线粒体的功能有关。 展开更多
关键词 阿尔兹海默症 槲皮素 淀粉样前体蛋白 线粒体功能障碍 氧化应激
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基于GEO数据库构建APP、APBA和APBB家族的胃癌预后评估模型
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作者 李文诗 俞思琦 +4 位作者 王梦欧 吴歆姝 包博文 车晓芳 郑春雷 《锦州医科大学学报》 CAS 2024年第5期48-54,共7页
目的基于淀粉样β前体蛋白(amyloid beta precursor protein,APP)家族、淀粉样β前体蛋白结合蛋白A(amyloid beta precursor protein binding family A,APBA)家族和淀粉样β前体蛋白结合蛋白B(amyloid beta precursor protein binding f... 目的基于淀粉样β前体蛋白(amyloid beta precursor protein,APP)家族、淀粉样β前体蛋白结合蛋白A(amyloid beta precursor protein binding family A,APBA)家族和淀粉样β前体蛋白结合蛋白B(amyloid beta precursor protein binding family B,APBB)家族构建胃癌预后评估模型。方法从基因表达综合(gene expression omnibus,GEO)数据库下载GSE62254胃癌数据集作为训练集,GSE15459作为验证集。利用Cox回归分析筛选APP家族、APBA家族和APBB家族中胃癌预后的独立危险因素;分别建立基于三家族独立预后因素的风险评分1(risk score 1,RS1)、RS1联合病理学参数的RS2、传统TNM分期的RS3;卡方检验分析RS1与胃癌患者临床病理特征的关系;利用单细胞在线分析网站,分析纳入RS1模型的基因在不同细胞亚群中的表达情况;利用CIBERSORT分析RS1对不同免疫细胞浸润的影响;利用基因集富集分析(gene set enrichment analysis,GSEA)进行通路富集分析。结果APLP2、APBB1、APBB2是胃癌患者预后的独立危险因素(P<0.05),基于三者的风险评分RS1高组患者生存期明显短于RS1低组患者。联合临床病理学参数的Cox回归分析显示,N分期、M分期、Lauren分型和RS1是胃癌患者预后的独立危险因素(P<0.05)。基于此构建的RS2(AUC=0.767)比仅基于T分期、N分期、M分期构建的RS3(AUC=0.719)预测准确率提高了4.8%。RS1和肿瘤T分期呈正相关(P<0.05),RS1高组CD4静息细胞浸润较高,激活细胞浸润较低,M2巨噬细胞浸润较高。GSEA通路分析显示,高RS1组患者富集于MAPK、MTOR和WNT等通路。结论本研究成功构建了基于APP、APBA和APBB家族的胃癌预后评估模型,该模型能够较准确地判断胃癌患者预后。 展开更多
关键词 胃癌 apP apBA家族 apBB家族 风险评分
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APP、BMPs在OSCC中的表达及与临床病理学因素的相关性研究
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作者 裴雷杰 范新昊 +2 位作者 朱向宇 刘钟月 吴娜 《现代科学仪器》 2024年第2期94-97,共4页
目的:分析淀粉样前体蛋白(APP)与骨形成蛋白(BMPs)在口腔鳞状细胞癌(OSCC)中的表达及与临床病理学因素相关性。测定75例OSCC癌组织及其配对的癌旁正常组织标本中APP、BMPs表达水平。结果:OSCC癌组织中的APP、BMP-2阳性表达率及mRNA表达... 目的:分析淀粉样前体蛋白(APP)与骨形成蛋白(BMPs)在口腔鳞状细胞癌(OSCC)中的表达及与临床病理学因素相关性。测定75例OSCC癌组织及其配对的癌旁正常组织标本中APP、BMPs表达水平。结果:OSCC癌组织中的APP、BMP-2阳性表达率及mRNA表达均高于癌旁正常组织(P<0.05);APP、BMP-2表达与OSCC临床分期、淋巴结转移有关(P<0.05);临床分期Ⅲ期、颈部淋巴转移及APP、BMP-2 mRNA高表达是OSCC不良预后的危险因素(P<0.05)。结论APP与BMPs与OSCC临床分期及淋巴结转移有关,可判断OSCC预后。 展开更多
关键词 口腔鳞状细胞癌 淀粉样前体蛋白 骨形成蛋白 临床病理学 相关性
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Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer's disease 被引量:2
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作者 Sara H.Mokhtar Min Joung Kim +14 位作者 Kylie A.Magee Pei Mun Aui Speros Thomas Maha M.Bakhuraysah Amani A.Alrehaili Jae Young Lee David L.Steer Rachel Kenny Catriona Mc Lean Michael F.Azari Antonis Birpanagos Ewlina Lipiec Philip Heraud Bayden Wood Steven Petratos 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第6期1066-1080,共15页
Alzheimer’s disease(AD)is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles.Prior to the development of these characteristic pathological hallmarks of AD,ante... Alzheimer’s disease(AD)is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles.Prior to the development of these characteristic pathological hallmarks of AD,anterograde axonal transport is impaired.However,the key proteins that initiate these intracellular impairments remain elusive.The collapsin response mediator protein-2(CRMP-2)plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2releases kinesin-1.Here,we tested the hypothesis that amyloid-beta(Aβ)-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1(an anterograde axonal motor transport protein)in AD.We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site.Additionally,in the transgenic Tg2576 mouse model of familial AD(FAD)that exhibits Aβaccumulation in the brain with age,we found substantial co-localization of p T555CRMP-2and dystrophic neurites.In SH-SY5Y differentiated neuronal cultures,Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1.The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation.These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function,leading to neuronal defects. 展开更多
关键词 amyloid-beta protein kinases collapsin response mediator protein MICROTUBULES KINESIN TUBULIN
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Effects of Ginsenoside Rg1 on nuclear factor-kappa B activity in beta amyloid protein-treated neural cells 被引量:2
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作者 Yunbo Chen Dapeng Zhang Mei Feng Qi Wang Shuyi Cheng Weixiong Liang Zehuai Wen 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第8期590-596,共7页
BACKGROUND: Modern pharmacological studies have shown that Ginsenoside Rgl is one of the active components of ginseng that promote intelligence in the nervous system. Ginsenoside Rgl can improve memory and learning i... BACKGROUND: Modern pharmacological studies have shown that Ginsenoside Rgl is one of the active components of ginseng that promote intelligence in the nervous system. Ginsenoside Rgl can improve memory and learning in mouse models of β-amyloid protein (Aβ)-induced dementia. OBJECTIVE: To investigate whether effects of Ginsenoside Rgl against Aβ are associated with activity of nuclear factor-kappa B (NF-κB). DESIGN, TIME AND SETTING: The randomized performed at the DME Center, Institute of Clinica controlled, cell biological experiment was Pharmacology, Guangzhou University of Chinese Medicine, China from July 2005 to May 2006. MATERIALS: Beta-amyloid fragment 25-35 (Aβ25-35) was supplied by the Neural Biochemical Laboratory, Xuanwu Hospital, Capital Medical University, China. Ginsenoside Rgl was obtained from National Institute for the Control of Pharmaceutical and Biological Products, China. Rabbit anti-rat NF-κB p65 antibody was purchased from Santa Cruz Biotechnology, USA. METHODS: Hippocampal neurons and cortical astrocytes of neonatal Sprague Dawley rats were harvested and treated with various concentrations (0, 5, 10, 20, and 40 μmol/L) of Aβ for 6, 12, and 24 hours to establish cellular models of Alzheimer's disease. Cellular models were pretreated with various concentrations of Ginsenoside Rgl (1,2, 4, 8, and 16 μmol/L). According to cell morphology and activity, the following conditions were selected: 40 μmol/L Aβ for 24 hours, as well as 2, 4, and 8 μmol/L Ginsenoside Rg1. NF-κB activity was observed using immunofluorescence and cytochemical staining. MAIN OUTCOME MEASURES: Morphology and viability of hippocampal neurons and cortical astrocytes, and activities of NF-κB were measured. RESULTS: Hippocampal neuron activity was significantly greater in the normal and 2 and 4 μmol/L Ginsenoside Rgl groups compared with the model group (P 〈 0.05). Astrocyte activity was significantly greater in the normal, 1,2, 4, 8, and 16 μmol/L Ginsenoside Rgl groups compared with the model group (P 〈 0.05). NF-κB activity of hippocampal neurons was significantly greater in the normal, 2, 4, and 8 μmol/L Ginsenoside Rgl groups compared with the model group (P 〈 0.01). NF-κB activity of astrocytes was significantly less in the normal, 2, 4, and 8 μmol/L Ginsenoside Rgl groups compared with the model group (P 〈 0.01 or P 〈 0.05). No significant difference in NF-κB activity was determined between the 2 μmol/L Ginsenoside Rgl and normal groups (P 〉 0.05). CONCLUSION: Ginsenoside Rgl protected neural cells by upregulating NF-κB activity in neurons and downregulating NF-κB activity in astrocytes. Ginsenoside Rgl (2 μmol/L) maintained cell activity and NF-κB activity at normal levels. 展开更多
关键词 Ginsenoside Rgl Alzheimer's disease β-amyloid protein nuclear factor-κB NEUROPROTECTION
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THE PROTECTIVE EFFECTS OF THE TOTAL SAPONIN OF DIPSACUS ASPEROIDES ON THE APOPTOSIS OF HIPPOCAMPAL NEURONS INDUCED BY β-AMYLOID PROTEIN 被引量:2
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作者 钱亦华 杨杰 +4 位作者 胡海涛 刘勇 杨广德 曹云新 任惠民 《Journal of Pharmaceutical Analysis》 SCIE CAS 2004年第1期30-34,共5页
Objective To investigate the effects of the total saponin of Dipsacus asperoides (tSDA) and ginsenoside Rb1 (GRb1) on the apoptosis of primary cultured hippocampal neurons induced by β-amyloid protein (Aβ). Methods... Objective To investigate the effects of the total saponin of Dipsacus asperoides (tSDA) and ginsenoside Rb1 (GRb1) on the apoptosis of primary cultured hippocampal neurons induced by β-amyloid protein (Aβ). Methods Primary cultured hippocampal neurons, the cultures were pretreated with tSDA and GRb1 on 10d for 24 hours respectively. Then the cultures were treated with 35 μmol·L -1 Aβ25-35 for 24 hours, observed the changing of survival rate of neurons and the apoptosis of neurons with biochemical analysis combining immunofluorescent cytochemical double-staining technique. Results Hippocampal neurons were treated with 35 μmol·L -1 Aβ for 24 hours, and survival rate of neurons downed to 52.6%. When neurons were pretreated by tSDA and GRb1, survival rate of neurons increased 11% to 15%. The findings of immunofluorescent cytochemical double-staining indicated that apoptotic neurons were obviously more than that of the blank group, reaching 43.9%.When neurons were pretreated by tSDA and GRb1, apoptotic neurons were downed to 16.6%, 10.8% respectively. Conclusion tSDA had the same effects as GRb1, protecting the neurons, antagonizing neurotoxicity of Aβ, increasing survival rate of neurons, and reducing apoptotic neurons induced by Aβ. 展开更多
关键词 total saponin of Dipsacus asperoides β-amyloid protein cell culture apOPTOSIS Alzheimer's disease
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BACE1 inhibitors:A promising therapeutic approach for the management of Alzheimer’s disease
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作者 Richa Arya Smita Jain +5 位作者 Sarvesh Paliwal Kirtika Madan Swapnil Sharma Achal Mishra Prashant Tiwari Sunil Kumar Kadiri 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2024年第9期369-381,共13页
Alzheimer’s disease is a neurological disorder marked by the accumulation of amyloid beta(Aβ)aggregates,resulting from mutations in the amyloid precursor protein.The enzymeβ-secretase,also known asβ-site amyloid p... Alzheimer’s disease is a neurological disorder marked by the accumulation of amyloid beta(Aβ)aggregates,resulting from mutations in the amyloid precursor protein.The enzymeβ-secretase,also known asβ-site amyloid precursor protein cleaving enzyme 1(BACE1),plays a crucial role in generating Aβpeptides.With no targeted therapy available for Alzheimer’s disease,inhibiting BACE1 aspartic protease has emerged as a primary treatment target.Since 1999,compounds demonstrating potential binding to the BACE1 receptor have advanced to human trials.Structural optimization of synthetically derived compounds,coupled with computational approaches,has offered valuable insights for developing highly selective leads with drug-like properties.This review highlights pivotal studies on the design and development of BACE1 inhibitors as anti-Alzheimer’s disease agents.It summarizes computational methods employed in facilitating drug discovery for potential BACE1 inhibitors and provides an update on their clinical status,indicating future directions for novel BACE1 inhibitors.The promising clinical results of Elenbecestat(E-2609)catalyze the development of effective,selective BACE1 inhibitors in the future. 展开更多
关键词 BACE1 inhibitors amyloid precursor protein Β-SECRETASE Structure-based drug design 3D-QSAR β-amyloid precursor protein
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Telencephalin protects Paju cells from beta-amyloid protein-induced apoptosis 被引量:1
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作者 Heping Yang Dapeng Wu +3 位作者 Xiaojie Zhang Xiang Wang Yi Peng Zhiping Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第29期2251-2255,共5页
Previous studies have confirmed that telencephalin (TLN) is a neural glycoprotein that protects axonal disruption induced by the beta-amyloid protein (Aβ42/35) in the neural crest-derived tumor cell line Paju. Th... Previous studies have confirmed that telencephalin (TLN) is a neural glycoprotein that protects axonal disruption induced by the beta-amyloid protein (Aβ42/35) in the neural crest-derived tumor cell line Paju. The present study investigated the effects of TLN on neuronal degeneration induced by Aβ42 in the differentiated Paju cell line. Results demonstrated that after cultivating cells in Aβ42 medium, the survival rate of Paju-TLN cells was significantly higher than that of Paju-neo cells, and that apoptotic rate was noticeably reduced. These results indicate that TLN reduces Paju cell apoptosis induced by Aβ42. 展开更多
关键词 telencephalin/intercellular adhesion molecule-5 beta-amyloid protein neuroprotective effect apOPTOSIS Alzheimer's disease neural regeneration
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Congophilic fibrils in the glomeruli with polyclonal immunoglobulin gamma staining-another cause for diagnostic overlap:A case report
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作者 Maria Bernadette Che-Ying Chow Lucas Bushrow +3 位作者 Irmeen Siddiqui April Chiu Mirza Hamirani Anjali A Satoskar 《World Journal of Clinical Cases》 SCIE 2024年第17期3200-3205,共6页
BACKGROUND Glomerulopathy with fibrillary deposits is not uncommon in routine nephropathology practice,with amyloidosis and fibrillary glomerulonephritis being the two most frequently encountered entities.Renal amyloi... BACKGROUND Glomerulopathy with fibrillary deposits is not uncommon in routine nephropathology practice,with amyloidosis and fibrillary glomerulonephritis being the two most frequently encountered entities.Renal amyloid heavy and light chain(AHL)is relatively uncommon and its biopsy diagnosis is usually limited to cases that show strong equivalent staining for a single immunoglobulin(Ig)heavy chain and a single light chain,further supported by mass spectrometry(MS)and serum studies for monoclonal protein.But polyclonal light chain staining can pose a challenge.CASE SUMMARY Herein we present a challenging case of renal AHL with polyclonal and polytypic Ig gamma(IgG)staining pattern by immunofluorescence.The patient is a 62-yearold Caucasian male who presented to an outside institution with a serum creatinine of up to 8.1 mg/dL and nephrotic range proteinuria.Despite the finding of a polyclonal and polytypic staining pattern on immunofluorescence,ultrastructural study of the renal biopsy demonstrated the presence of fibrils with a mean diameter of 10 nm.Congo red was positive while DNAJB9 was negative.MS suggested a diagnosis of amyloid AHL type with IgG and lambda,but kappa light chains were also present supporting the immunofluorescence staining results.Serum immunofixation studies demonstrated IgG lambda monoclonal spike.The patient was started on chemotherapy.The chronic renal injury however was quite advanced and he ended up needing dialysis shortly after.CONCLUSION Tissue diagnosis of AHL amyloid can be tricky.Thorough confirmation using other available diagnostic techniques is recommended in such cases. 展开更多
关键词 Heavy and light chain amyloid Fibrillary glomerulonephritis DNAJB9 Serum immunofixation protein electrophoresis Mass spectrometry Congo red Case report
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Treadmill exercise in combination with acousto-optic and olfactory stimulation improves cognitive function in APP/PS1 mice through the brain-derived neurotrophic factor-and Cygb-associated signaling pathways
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作者 Biao Xiao Chaoyang Chu +6 位作者 Zhicheng Lin Tianyuan Fang Yuyu Zhou Chuxia Zhang Jianghui Shan Shiyu Chen Liping Li 《Neural Regeneration Research》 SCIE CAS 2025年第9期2706-2726,共21页
A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigati... A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease. 展开更多
关键词 acousto-optic stimulation adult neurogenesis Alzheimer's disease amyloid precursor protein/presenilin 1 mice amyloid-beta deposition brain cell apoptosis cognitive impairment depression-like behavior involuntary treadmill exercise olfactory stimulation serum metabolites
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Telencephalin protects PAJU cells from amyloid beta protein-induced apoptosis by activating the ezrin/radixin/moesin protein family/phosphatidylinositol-3-kinase/protein kinase B pathway
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作者 Heping Yang Dapeng Wu +3 位作者 Xiaojie Zhang Xiang Wang Yi Peng Zhiping Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第28期2189-2198,共10页
Telencephalin is a neural glycoprotein that reduces apoptosis induced by amyloid beta protein in the human neural tumor cell line PAJU. In this study, we examined the role of the ezrin/radixin/moesin protein family/ph... Telencephalin is a neural glycoprotein that reduces apoptosis induced by amyloid beta protein in the human neural tumor cell line PAJU. In this study, we examined the role of the ezrin/radixin/moesin protein family/phosphatidylinositol-3-kinase/protein kinase B pathway in this process. Western blot analysis demonstrated that telencephalin, phosphorylated ezrin/radixin/moesin and phosphatidylinositol-3-kinase/protein kinase B were not expressed in PAJU cells transfected with empty plasmid, while they were expressed in PAJU cells transfected with a telencephalin expression plasmid. After treatment with 1.0 nM amyloid beta protein 42, expression of telencephalin and phosphorylated phosphatidylinositol-3-kinase/protein kinase B in the transfected cells gradually diminished, while levels of phosphorylated ezrin/radixin/moesin increased. In addition, the high levels of telencephalin, phosphorylated ezrin/radixin/moesin and phosphatidylinositol-3-kinase/protein kinase B expression in PAJU cells transfected with a telencephalin expression plasmid could be suppressed by the phosphatidylinositol-3-kinase inhibitor LY294002. These findings indicate that telencephalin activates the ezrin/radixin/moesin family/phosphatidylinositol-3-kinase/protein kinase B pathway and protects PAJU cells from amyloid beta protein-induced apoptosis. 展开更多
关键词 telencephalin/intercellular adhesion molecule 5 amyloid beta protein ezrin/radixin/moesin familyproteins/phosphatidylinositol-3-kinase/protein kinase B signal transduction neural regeneration
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LPS Regulates Apolipoprotein E and A<i>β</i>Interactionswith Effects on Acute Phase Proteins and Amyloidosis
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作者 Ian James Martins 《Advances in Aging Research》 2015年第2期69-77,共9页
Interactions between apolipoprotein E (apo E) and amyloid beta (Aβ) are associated with the peripheral clearance of Aβ and are important to the development of neurodegenerative diseases. Interests in acute phase pro... Interactions between apolipoprotein E (apo E) and amyloid beta (Aβ) are associated with the peripheral clearance of Aβ and are important to the development of neurodegenerative diseases. Interests in acute phase proteins (APP) as biomarkers for the early progression of Alzheimer’s disease indicate that the peripheral Aβ metabolism is perturbed and the role of nutritional diets are important to reduce APPs to maintain peripheral Aβ clearance with relevance to hepatic cholesterol homeostasis and brain amyloidosis. The role of nutriproteomic diets that reverse the effects of high fat diets are associated with the reduction in APPs, cholesterol homeostasis and improved clearance of Aβ. Nutritional diets that reduce the increase in plasma endotoxins (gut microbiotica) such as lipopolysaccarides (LPS) reduce the effects of LPS on cell membranes and increase the cellular uptake of Aβ by interactions with apo E. LPS alter hepatic lipid metabolism with an increase hepatic cytokines and APPs in plasma. Interactions between apo E and Aβ are altered by LPS with increased binding of LPS to apo E with effects on electrostatic alterations in Aβ oligomers. The role of LPS in neurodegenerative diseases includes the effects of LPS on alpha-synuclein metabolism with relevance to Parkinson’s disease and Alzheimer’s 展开更多
关键词 LIPOPOLYSACCHARIDES apOLIPOprotein E amyloid Beta Acute Phase protein Diet
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Effects of amyloid precursor protein peptide APP96-110,alone or with human mesenchymal stromal cells,on recovery after spinal cord injury
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作者 Stuart I.Hodgetts Sarah J.Lovett +4 位作者 D.Baron-Heeris A.Fogliani Marian Sturm C.Van den Heuvel Alan R.Harvey 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第6期1376-1386,共11页
Delivery of a peptide(APP96-110),derived from amyloid precursor protein(APP),has been shown to elicit neuroprotective effects following cerebral stroke and traumatic brain injury.In this study,the effect of APP96-110 ... Delivery of a peptide(APP96-110),derived from amyloid precursor protein(APP),has been shown to elicit neuroprotective effects following cerebral stroke and traumatic brain injury.In this study,the effect of APP96-110 or a mutant version of this peptide(mAPP96-110)was assessed following moderate(200 kdyn,(2 N))thoracic contusive spinal cord injury(SCI)in adult Nude rats.Animals received a single tail vein injection of APP96-110 or mAPP96-110 at 30 minutes post-SCI and were then assessed for functional improvements over the next 8 weeks.A cohort of animals also received transplants of either viable or non-viable human mesenchymal stromal cells(hMSCs)into the SC lesion site at one week post-injury to assess the effect of combining intravenous APP96-110 delivery with hMSC treatment.Rats were perfused 8 weeks post-SCI and longitudinal sections of spinal cord analyzed for a number of factors including hMSC viability,cyst size,axonal regrowth,glial reactivity and macrophage activation.Analysis of sensorimotor function revealed occasional significant differences between groups using Ladderwalk or Ratwalk tests,however there were no consistent improvements in functional outcome after any of the treatments.mAPP96-110 alone,and APP96-110 in combination with both viable and non-viable hMSCs significantly reduced cyst size compared to SCI alone.Combined treatments with donor hMSCs also significantly increased βIII tubulin^(+),glial fibrillary acidic protein(GFAP^(+))and laminin+expression,and decreased ED1^(+)expression in tissues.This preliminary study demonstrates that intravenous delivery of APP96-110 peptide has selective,modest neuroprotective effects following SCI,which may be enhanced when combined with hMSC transplantation.However,the effects are less pronounced and less consistent compared to the protective morphological and cognitive impact that this same peptide has on neuronal survival and behaviour after stroke and traumatic brain injury.Thus while the efficacy of a particular therapeutic approach in one CNS injury model may provide justification for its use in other neurotrauma models,similar outcomes may not necessarily occur and more targeted approaches suited to location and severity are required.All animal experiments were approved by The University of Western Australia Animal Ethics Committee(RA3/100/1460)on April 12,2016. 展开更多
关键词 amyloid precursor protein cell transplantation combination CONTUSION functional recovery mesenchymal stromal cells NEUROPROTECTION REGENERATION spinal cord injury tissue sparing
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太子参改善斑马鱼和APP/PS 1小鼠学习记忆
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作者 丰心月 王奕霏 +3 位作者 邓嘉航 何传统 蒋嘉慧 杨志友 《食品与发酵工业》 CAS CSCD 北大核心 2024年第8期55-61,共7页
太子参是一种可用于保健食品的传统中药,具有抗疲劳和调节免疫等作用,但神经保护和改善记忆作用报道较少。为探究太子参改善记忆和认知障碍的有效成分及作用机制,利用Aβ1-42脑室显微注射斑马鱼模型初步探究太子参醇提物对记忆的改善作... 太子参是一种可用于保健食品的传统中药,具有抗疲劳和调节免疫等作用,但神经保护和改善记忆作用报道较少。为探究太子参改善记忆和认知障碍的有效成分及作用机制,利用Aβ1-42脑室显微注射斑马鱼模型初步探究太子参醇提物对记忆的改善作用;CCK8试剂盒测定太子参水提物、醇提物、多糖、皂苷、环肽对Aβ25-35诱导皮层神经元存活率的影响;荧光定量PCR测定太子参环肽B(heterophyllin B,HB)对神经元中凋亡相关基因的表达,免疫细胞化学染色探究HB对神经元的保护作用;利用APP/PS 1转基因小鼠探究HB对痴呆样行为和记忆的改善作用。太子参醇提物给药后,斑马鱼新臂和奖励臂探寻的潜伏期显著降低,在新臂和奖励臂游动时间和总路程增加。HB显著增加神经元存活率及β3-tubulin、MAP2阳性突起的表达,并改善APP/PS 1转基因小鼠记忆障碍。综上,太子参的神经保护作用可能通过HB减少突起萎缩,从而改善认知功能障碍和记忆缺陷。 展开更多
关键词 阿尔兹海默症 Β-淀粉样蛋白 太子参环肽B 神经突起 记忆障碍
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