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首页 冈田酸:研究阿尔茨海默病神经退行性变化及再生机制的工具

冈田酸:研究阿尔茨海默病神经退行性变化及再生机制的工具.doc

冈田酸:研究阿尔茨海默病神经退行性变化及再生机制的工具

江湖一孤猪小童鞋
2019-05-01 0人阅读 举报 0 0 0 暂无简介

简介:本文档为《冈田酸:研究阿尔茨海默病神经退行性变化及再生机制的工具doc》,可适用于医药卫生领域

NRRDPradipKumarKamat新闻冈田酸:研究阿尔茨海默病神经退行性变化及再生机制的工具美国路易斯维尔大学医学院生理学系PradipKKamat博士,在《中国神经再生研究(英文版)》年第卷第期杂志发文介绍他有关冈田酸在阿尔茨海默病病理意义的研究。以往研究表明,冈田酸可以快速的代谢改变体内磷酸化去磷酸化速率,导致细胞死亡。冈田酸导致β淀粉样蛋白沉积和随后的神经元变性、突触损失和记忆障碍。DrKamat研究显示,微注射脑内脑室内注射冈田酸到啮齿动物的大脑会引起β淀粉样蛋白沉积和tau蛋白磷酸化,导致认知缺陷。蛋白激酶和蛋白磷酸酶调节蛋白的磷酸化状态在生理过程起着重要作用。冈田酸诱导的神经毒性模型能够同时检测药物对蛋白磷酸化和存储器过程的作用。因此,冈田酸可以用来作为实验工具研究神经变性的机制和解开阿尔茨海默病的病理研究靶标,并可用于临床药物的开发。Article:"Okadaicacid:atooltostudyregulatorymechanismsforneurodegenerationandregenerationinAlzheimer’sdisease"byPradipKumarKamat,ChandishwarNath(DivisionofPhysiologyandBiophysics,UniversityofLouisville,SchoolofMedicine,(KY),USADivisionofPharmacology,CentralDrugResearchInstitute(CDRI),POBox,Lucknow(UP),India)KamatPK,NathC()Okadaicacid:atooltostudyregulatorymechanismsforneurodegenerationandregenerationinAlzheimer’sdiseaseNeuralRegenRes():欲获更多资讯:文章全文请见:NeuralRegenResOkadaicacid:AtooltostudyregulatorymechanismforneurodegenerationandregenerationinAlzheimer’sdiseaseSUMMARYAlzheimer’sdisease(AD)isaneurodegenerativedisorderthataffectsapproximatelymillionpeopleworldwideOkadaicacid(OKA),apotentselectiveinhibitorofproteinphosphatase,PPandPPAandisapowerfulprobeforstudyingthevariousregulatorymechanismsunderlyingADpathologyAveryexcitingavenuetostudymolecularmechanismofADbyusingOKAasanexperimentaltoolthatcanoffernewstrategiesforneurodegenerativeandregenerativestudiesandcangivepathtonoveltherapeuticsNEWSRELEASEDrPradipKumarKamat,aninternationallyrenownedneuroscientist,highlightedhisresearchaboutimportanceofOkadaicacid(OKA)forADpathologyinapaperinNeuralRegenerationResearch(Vol,No,)“Okadaicacid:AtooltostudyregulatorymechanismforneurodegenerationandregenerationinAlzheimer'sdisease”OKAisassociatedwithproteinphosphorylationitisimplicatedinhyperphosphorylationoftauandinlaterstagecausesAlzheimer’sdisease(AD)likepathologyADisaprogressiveneurodegenerativedisorder,pathologicallycharacterizedbyextracellularamyloidbeta(Aβ)plaquesandintracellularneurofibrillarytangles(NFTs)thatareassociatedwithcognitivedysfunctionInterestingly,OKANRRDPradipKumarKamat新闻producespathologicalhallmarkininvitroandinvivoassimilartoADProteinkinasesarecomprehensivelyassociatedwithtauhyperphosphorylationandneurodegenerationOKAinducedPPAgeneregulatorymechanismandmediateskinasesremodelingwhichplayavitalroleintheabnormalhyperphosphorylationoftauresultinginneurodegenerationEvidencesfromearlierreportsalsoindicatethatserinethreonineproteinphosphatasesandkinasesarepotentiallyusedastherapeutictargetsinseveralneurodegenerativediseasesTherefore,OKAcanbeusedasanexperimentaltooltostudyregulatorymechanismofADpathologyandcanbeusedfordevelopmentofnoveltherapeuticsapproachesArticle:"Okadaicacid:atooltostudyregulatorymechanismsforneurodegenerationandregenerationinAlzheimer’sdisease"byPradipKumarKamat,ChandishwarNath(DivisionofPhysiologyandBiophysics,UniversityofLouisville,SchoolofMedicine,(KY),USADivisionofPharmacology,CentralDrugResearchInstitute(CDRI),POBox,Lucknow(UP),India)KamatPK,NathC()Okadaicacid:atooltostudyregulatorymechanismsforneurodegenerationandregenerationinAlzheimer’sdiseaseNeuralRegenRes():

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