Autophagy:华人科学家发现自噬介导淀粉样蛋白降解机制

2017-10-15 海北 MedSci原创

阿尔兹海默病(AD)是以脑淀粉样斑块沉积为特征的非常常见的神经退行性疾病。已有的报导显示,自噬相关的含PIK3C3的磷脂酰肌醇3-激酶(PtdIns3K)复合物能够帮助APP的代谢以及淀粉样蛋白(Aβ)的体内平衡。但是至今为止,人们对其机制还不太了解。

阿尔兹海默病(AD)是以脑淀粉样斑块沉积为特征的非常常见的神经退行性疾病。已有的报导显示,自噬相关的含PIK3C3的磷脂酰肌醇3-激酶(PtdIns3K)复合物能够帮助APP的代谢以及淀粉样蛋白(Aβ)的体内平衡。但是至今为止,人们对其机制还不太了解。 来自澳门大学的研究人员最近发现,NRBF2(核受体结合因子2)是PtdIns3K的关键组分和调节因子。在AD细胞模型中,其在APP-CTFs的体内平衡过程中发挥作用。 研究人员发现,NRBF2在体内能够与APP相互作用,并且其表达水平在5XFAD AD小鼠的海马区中有所降低。研究人员进一步证明,在人突变APP过表达细胞中,NRBF2过表达能够促进APP C末端片段(APP-CTFs)的降解,并降低Aβ1-40和Aβ1-42的水平。相反,在Nrbf2敲低或nrbf2敲除细胞中,APP-CTF,Aβ1-40和Aβ1-42的水平有所升高。 此外,NRBF2能够增强神经元细胞中的自噬,并且,NRBF2介导的APP-CTF水平的降低是自噬依赖性的。Nrbf2敲除能够减弱APP和APP-CTFs在吞噬泡中的募集,以及APP和APP-CTFs向内体腔

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    2017-10-16 yfjms

    学习了

    0

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    2017-10-15 1ddf0692m34(暂无匿称)

    学习了.涨知识

    0

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    2017-10-15 惠映实验室

    新发现.真好

    0

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    2017-10-15 Y—xianghai

    学习了新知识

    0

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    2017-10-15 明月清辉

    谢谢分享.学习了

    0

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阿尔兹海默症等神经退行性疾病已经成为药物研发的重灾区。几十年来药企在这一领域不断受挫也让情况更显恶劣。随着AI技术的兴起,阿尔兹海默症领域的疗法开发似乎出现了一丝曙光。最近一家名为MyndYou的公司希望利用AI技术结合诊断工具通过追踪患者语言模式变化的方法来确定阿尔兹海默症患者的病情发展。

JAMA Neurol:载脂蛋白E亚型与阿尔兹海默性别差异

研究发现,与长期以来的认知不同,55-85岁女性APOE ε3/ε4基因携带不会导致患者阿尔兹海默风险提高

JACS:抑制阿尔茨海默症发展分子机制被发现!

众所周知,饮用绿茶对大脑具有很大的益处。绿茶提取物的抗氧化和解毒特性有助于抵抗阿尔茨海默病等重大疾病。然而,科学家至今没有完全了解绿茶发挥作用的分子机制,以及如何利用它们来寻找更好的治疗方法。