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

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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NRR-D-14-00520 Pradip Kumar Kamat 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Pradip K. Kamat博士,在《中国神经再生研究(英文版)》2015年第10卷第3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。Dr. Kamat研究显示,微注射/ 脑内/脑室内注射冈...

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
NRR-D-14-00520 Pradip Kumar Kamat 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Pradip K. Kamat博士,在《中国神经再生研究(英文版)》2015年第10卷第3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 关于同志近三年现实表现材料材料类招标技术评分表图表与交易pdf视力表打印pdf用图表说话 pdf 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。Dr. Kamat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: "Okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer’s disease" by Pradip Kumar Kamat1, Chandishwar Nath2 (1Division of Physiology and Biophysics, University of Louisville, School of Medicine, (KY) 40202, USA; 2Division of Pharmacology, Central Drug Research Institute (CDRI), P.O. Box 173, Luck now (U.P.) 226001, India) Kamat PK, Nath C (2015) Okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer’s disease. Neural Regen Res 10(3):365-367. 欲获更多资讯:文章全文请见:Neural Regen Res Okadaic acid: A tool to study regulatory mechanism for neurodegeneration and regeneration in Alzheimer’s disease. SUMMARY Alzheimer’s disease (AD) is a neurodegenerative disorder that affects approximately 36 million people worldwide. Okadaic acid (OKA), a potent selective inhibitor of protein phosphatase, PP1 and PP2A and is a powerful probe for studying the various regulatory mechanisms underlying AD pathology. A very exciting avenue to study molecular mechanism of AD by using OKA as an experimental tool that can offer new strategies for neurodegenerative and regenerative studies and can give path to novel therapeutics. NEWS RELEASE Dr. Pradip Kumar Kamat, an internationally renowned neuroscientist, highlighted his research about importance of Okadaic acid (OKA) for AD pathology in a paper in Neural Regeneration Research (Vol. 10, No. 3, 2015) “Okadaic acid: A tool to study regulatory mechanism for neurodegeneration and regeneration in Alzheimer's disease.”OKA is associated with protein phosphorylation; it is implicated in hyperphosphorylation of tau and in later stage causes Alzheimer’s disease (AD)-like pathology. AD is a progressive neurodegenerative disorder, pathologically cha racterized by extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs) that are associated with cognitive dysfunction. Interestingly, OKA NRR-D-14-00520 Pradip Kumar Kamat 新闻 produces pathological hallmark in in vitro and in vivo as similar to AD. Protein kinases are comprehensively associated with tau hyperphosphorylation and neurodegeneration. OKA induced PP2A gene regulatory mechanism and mediates kinases remodeling which play a vital role in the abnormal hyperphosphorylation of tau resulting in neurodegeneration. Evidences from earlier reports also indicate that serine/threonine protein phosphatases and kinases are potentially used as therapeutic targets in several neurodegenerative diseases. Therefore, OKA can be used as an experimental tool to study regulatory mechanism of AD pathology and can be used for development of novel therapeutics approaches. Article: "Okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer’s disease" by Pradip Kumar Kamat1, Chandishwar Nath2 (1Division of Physiology and Biophysics, University of Louisville, School of Medicine, (KY) 40202, USA; 2Division of Pharmacology, Central Drug Research Institute (CDRI), P.O. Box 173, Luck now (U.P.) 226001, India) Kamat PK, Nath C (2015) Okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer’s disease. Neural Regen Res 10(3):365-367.
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