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AGING CELL:研究人员发现改善阿尔茨海默病树突异常的途径

2019-02-10 海北 MedSci原创

研究人员在许多神经退行性疾病中发现了树突树和树突脊的损伤,包括阿尔茨海默氏病(AD)。已有的研究还显示,AD中具有褪黑激素信号通路的缺陷。褪黑激素受体2(MT2)在海马中广泛表达,并介导褪黑激素的生物学功能。

研究人员在许多神经退行性疾病中发现了树突树和树突脊的损伤,包括阿尔茨海默氏病(AD)。已有的研究还显示,AD中具有褪黑激素信号通路的缺陷。褪黑激素受体2(MT2)在海马中广泛表达,并介导褪黑激素的生物学功能。

已知褪黑激素对AD中的树突异常具有保护作用。然而至今为止,MT2是否参与神经保护及其潜在机制尚不清楚。

最近,研究人员首次发现MT2在低聚物Aβ的损伤下在树突室中显着减少。MT2的激活阻止了Aβ诱导的树突复杂性和树突脊的破坏。重要的是,MT2的激活降低了cAMP,反过来使转录因子CCAAT /增强子结合蛋白α(C /EBPα)失活,从而抑制miR-125b的表达,并提高其靶标GluN2A的表达。

此外,miR-125b类似物完全阻断了MT2激活对树突树和脊的保护作用。将含有miR-125b海绵的慢病毒注射到APP / PS1小鼠的海马中,可以有效地挽救了树突异常和学习/记忆障碍。

因此,这些数据表明cAMP-C /EBPα/ miR-125b / GluN2A信号通路对Aβ诱导的树突损伤和学习/记忆障碍,以及MT2激活的神经保护作用很重要,这为AD提供了新的治疗靶点。 


原始出处:

Hui Tang et al. Activation of MT2 receptor ameliorates dendritic abnormalities in Alzheimer’s disease via C/EBPα/miR‐125b pathway. Aging Cell, 2019; doi: https://doi.org/10.1111/acel.12902


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    2019-10-08 维他命
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    2019-02-11 1e145228m78(暂无匿称)

    学习了,谢谢作者分享!

    0

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    2019-02-10 坚强007

    向科研人员致敬!!!

    0

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    2019-02-10 1e145228m78(暂无匿称)

    学习了,谢谢作者分享!

    0

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