在阿尔茨海默氏病中,对mTOR的调节失调

George S Bloom1,2,3, Andrés Norambuena1

  • 1Department of Biology, University of Virginia, Charlottesville, Virginia, USA.

PubMed
概括

异常的陶酸化,由粉样β寡合体触发,导致神经元重新进入细胞循环并死亡,抑制营养诱导的线粒体激活在阿尔茨海默病 (AD). 这种tau驱动的神经退行会影响关键的细胞过程.

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