Here, we report that anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase, is crucial for the tau-mediated AD pathology. ALK caused abnormal accumulation of highly phosphorylated tau in the somatodendritic region of neurons through its tyrosine kinase activity. ALK-induced LC3-positive axon swelling and loss of spine density, leading to tau-dependent neuronal degeneration. We propose that aberrantly activated ALK is a bona fide mediator of tau proteinopathy that disrupts autophagosome maturation and causes tau accumulation and aggregation, leading to neuronal dysfunction in AD. READ ARTICLE

Molecular Psychiatry DOI: 10.1038/s41380-020-01003-y

Authors: Jisu Park, Hyunwoo Choi, Young Doo Kim, Seo-Hyun Kim, Youbin Kim, Youngdae Gwon, Dong Young Lee, Sung-Hye Park, Won Do Heo & Yong-Keun Jung

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