Bridging Multiple Dementias
Bridging Multiple Dementias
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缓解多种痴呆症
DOI：
10.1021/acschemneuro.8b00119
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发表时间：
2018
影响因子：
5
通讯作者：
Okazawa Hitoshi
中科院分区：
文献类型：
--
作者：
Ryo Yamasaki;Yinan Zhao;Marion Wijering;Hiroo Yamaguchi;Jun-ichi Kira;小野寺理;Okazawa Hitoshi
Tau磷酸化再次成为人们关注的焦点，这一次是痴呆病理学最早阶段的关键参与者。在多种神经退行性疾病中观察到磷酸化tau蛋白向树突棘的错误定位以及由此产生的突触变性，即使在没有tau蛋白聚集的情况下也是如此。此外，由相同激酶磷酸化的其他分子，如MARCKS，可能通过促进突触功能障碍而导致超早期病理学。
Tau phosphorylation has come into the limelight again, this time as a critical player in the earliest stages of dementia pathology. Mislocalization of phosphorylated tau to dendritic spines and the resultant degeneration of synapses are observed across multiple neurodegenerative diseases, even in the absence of tau aggregation. Moreover, other molecules phosphorylated by the same kinases, such as MARCKS, might contribute to ultra-early phase pathology by promoting synapse dysfunction.