Abstract
Cytoskeletal and microtubule atrophy are major hallmarks of Alzheimer's disease (AD). A method to investigate endogenous proteins that can interact/stabilize the cytoskeleton (under pathological cues) is rare. Here, we describe how receptor tyrosine kinase-like orphan receptor 1 (ROR1), a receptor tyrosine kinase (RTK), can act as a neuroprotective molecule by promoting neurite outgrowth, stabilizing cytoskeletal components, and altering the dynamics of actin assembly in a cell culture model of AD.
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