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脂膜筏对β淀粉样蛋白质前体代谢的调节
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作者 周剑涛 祁木桥 高原 《生命的化学》 CAS CSCD 2004年第4期319-321,共3页
β淀粉样蛋白质前体 (APP)有α 和 β 裂解途径。细胞膜脂膜筏 (或胆固醇 )对APP代谢有调节作用 ,存在脂膜筏外的APP经α分泌酶发生α 裂解不产生Aβ,结合APP的脂膜筏与含有β分泌酶的脂膜筏经胞吞簇集化使APP发生 β 裂解产生Aβ。
关键词 脂膜筏 β淀粉样蛋白质前体 分泌酶 阿尔茨海默病
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淀粉样前体蛋白(APP)分泌的神经及药物调节
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作者 陈多 吴春福 《沈阳药科大学学报》 CAS CSCD 2001年第1期75-78,共4页
综述了多种神经递质通过兴奋受体参与APP的分泌过程。这些受体包括M1、M3、5 HT2 、5 HT1C,代谢型谷氨酸受体及肽能加压素和缓激肽受体。脑片实验同样表明内源性神经递质和神经调质可调节APP在哺乳动物脑中的代谢。进一步明确神经递质... 综述了多种神经递质通过兴奋受体参与APP的分泌过程。这些受体包括M1、M3、5 HT2 、5 HT1C,代谢型谷氨酸受体及肽能加压素和缓激肽受体。脑片实验同样表明内源性神经递质和神经调质可调节APP在哺乳动物脑中的代谢。进一步明确神经递质在AD中的作用 ,有利于研究开发出更多的针对不同受体亚型或递质系统的药物 。 展开更多
关键词 ALZHEIMER病 β淀粉样蛋白质 APP 神经调节 药物
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早老素与阿尔茨海默病 被引量:5
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作者 王丹玲 王建枝 《生命的化学》 CAS CSCD 2003年第6期416-418,共3页
早老素 (presenilin ,PS)与阿尔茨海默病 (alzheimer′sdisease ,AD)密切相关 ,其基因突变是遗传性家族型AD的主要病因。PS可能作为γ分泌酶和 (或 )通过影响蛋白质的膜转运参与 β淀粉样前体蛋白质 (β amyloidprecursorpro tein ,APP... 早老素 (presenilin ,PS)与阿尔茨海默病 (alzheimer′sdisease ,AD)密切相关 ,其基因突变是遗传性家族型AD的主要病因。PS可能作为γ分泌酶和 (或 )通过影响蛋白质的膜转运参与 β淀粉样前体蛋白质 (β amyloidprecursorpro tein ,APP)代谢生成Aβ42的过程 ,而PS多蛋白质复合物的形成可能是其中的关键步骤 ,突变的PS则通过“获得功能”的方式引起Aβ42的产生和沉积增加。PS还可能通过影响未折叠蛋白质反应等多种途径来影响神经细胞对凋亡的敏感性。 展开更多
关键词 阿尔茨海默病 早老素 β淀粉前体蛋白质 β淀粉 细胞凋亡 病理作用 中枢神经系统退行性疾病
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新法防治老年痴呆
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《发明与创新(大科技)》 2004年第7期46-46,共1页
关键词 防治 老年痴呆 美国哈佛大学 β淀粉样蛋白质
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Effects of free radicals and amyloid β protein on the currents of expressed rat receptors in Xenopus oocytes
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作者 黄福南 李文彬 +6 位作者 张炳烈 崔旭 韩志涛 房征宇 蔡竖平 尹岭 王鲁宁 《Chinese Medical Journal》 SCIE CAS CSCD 2001年第3期20-23,103,共5页
Objective To investigate the effects of free radicals (FRs) and amyloid β protein 1 40 (Aβ 1 40 ) on the functions of expressed neurotransmitter receptors (NRs) in Xenopus oocytes Methods Total RNA and ... Objective To investigate the effects of free radicals (FRs) and amyloid β protein 1 40 (Aβ 1 40 ) on the functions of expressed neurotransmitter receptors (NRs) in Xenopus oocytes Methods Total RNA and messenger RNA (mRNA) was prepared from 3 month old Wistar rat brain tissues with Promega kits and microinjected into maturated Xenopus oocytes (stages Ⅴ Ⅵ) with 50?nl (50?ng) for each oocyte The microinjected oocytes were incubated with modified Bath's solution at 19 0℃±1 0℃ for receptor expression and their currents were recorded with double electrode voltage clamp technique Superoxide anion free radicals (SAFRs) were produced via a reaction system (HPX/XO) with hypoxanthine (HPX, 0 05?mol/L) and xanthine oxidase (XO, 0 1?U/L) In order to observe the effects of Aβ and SAFRs on the expressed glutamate receptor, HPX/XO and Aβ 1 40 were added to incubation solution at 12?h, 24?h and 96?h before recording Results The results showed that the oocytes expressed functional NRs originating from rat brain tissues These NRs included muscarinic acetylcholine (mACh), glutamate (Glu), dopamine (DA), serotonin (5 HT) and γ aminobutyric acid (GABA) The current characteristics of expressed receptors were inward currents carried by chloride ion with their equibrilium potentials close to -22?mV The extent of effect on the current of expressed glutamate receptor from rat brain was different among different Aβ concentrations and incubation times Aβ 1 40 at a concentration of 20?nmol/L had little effect on the currents of expressed rat brain glutamate receptors up to 24?h of incubation period; but the currents of glutamate receptor were significantly decreased (25% off, P <0 01) in the treatment of 60?nmol/L Aβ 1 40 over 24?h Moreover, when 20?nmol/L Aβ 1 40 was co incubated over 12?h with SAFRs produced by the reaction system of HPX/XO, it was found that the currents of expressed rat brain glutamate receptors had been changed markedly When the oocytes were co treated with 60?nmol/L Aβ 1 40 and SAFRs over a period of 12?h, the currents of glutamate receptor significantly decreased (21% off, P <0 05), and the decreased percentage reached 52% over 24?h co treatment with 60?nmol/L Aβ 1 40 and SAFRs In addition, vitamin E had a partial effect against this inhibitory effect Conclusion The results suggest that Aβ has a kind of inhibitory effect upon the current of the glutamate receptor, similar to the effects of free radicals The effects can be antagonized by vitamin E These imply that Aβ may play a role via inhibiting receptor function in the pathophysiology of Alzheimer's disease 展开更多
关键词 amyloid β protein · free radicals · neurotransmitter receptor · glutamate · Alzheimer's disease
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Presenilins as endoplasmic reticulum calcium leak channels and Alzheimer's disease pathogenesis 被引量:17
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作者 Charlene SUPNET Ilya BEZPROZVANNY 《Science China(Life Sciences)》 SCIE CAS 2011年第8期744-751,共8页
Alzheimer disease(AD) is the most common neurodegenerative disorder worldwide and is at present,incurable.The accumulation of toxic amyloid-beta(Aβ) peptide aggregates in AD brain is thought to trigger the extensive ... Alzheimer disease(AD) is the most common neurodegenerative disorder worldwide and is at present,incurable.The accumulation of toxic amyloid-beta(Aβ) peptide aggregates in AD brain is thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline,an idea that underlies the'amyloid hypothesis'of AD etiology in both the familal(FAD) and sporadic forms of the disease.Genetic mutations causing FAD also result in the dysregulation of neuronal calcium(Ca2+) handling and may contribute to AD pathogenesis,an idea termed the'calcium hypothesis'of AD.Mutations in presenilin proteins account for majority of FAD cases.Presenilins function as catalytic subunit ofγ-secretase involved in generation of Aβ peptide Recently,we discovered that presenilns function as low-conductance,passive ER Ca2+ leak channels,independent of γ-secretase activity.We further discovered that many FAD mutations in presenilins result in loss of ER Ca2+ leak function activity and Ca2+ overload in the ER.These results provided potential explanation for abnormal Ca2+ signaling observed in FAD cells with mutations in presenilns.Our latest work on studies of ER Ca2+ leak channel function of presenilins and implications of these findings for understanding AD pathogenesis are discussed in this article. 展开更多
关键词 calcium signaling NEURODEGENERATION PRESENILINS Alzheimer's disease GAMMA-SECRETASE AMYLOID
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