TABLE 2.

Summary of the regulation of YAP in central nervous system diseases.

CNS Diseases	Mechanism	Influence	References
Glioma	• Decreased cell contact inhibition • mtp53-induced tumor proliferation associated with WIP and YAP • CYR61/CCN1 and miR-296-3p mediate glioma via NF2 inhibition	Tumor proliferation of glioma has a positive correlation with higher expression and nuclear localization of YAP	(Zhao et al., 2007; Lee et al., 2016; Rivas et al., 2018)
Subarachnoid hemorrhage	• Increased Nrg1β1, ErbB4, YAP, and PIK3CB • Decreased MMP-9, degradation of tight junction proteins, and upregulation of Mst1 and NF-κB	ErbB4-YAP and Mst1 respond to early brain injury after SAH through BBB disruption, neuronal cell death, and white matter damage	(Yan et al., 2017; Qu et al., 2018; Qian et al., 2018)
Huntington disease	• A toxic effect causes the transcriptional dysregulation with five approaches • Decreased nuclear YAP induces BCD and TRIAD	Transcriptional alteration leads to mutant Huntington gene with activation of Mst1 and decreased nuclear localization of YAP in HD	(Mao et al., 2016; Mueller et al., 2018)
Alzheimer disease	• The YAP/p73-mediated apoptosis in symptomatic Alzheimer’s disease • The intracellular Aβ aggregation and YAP cytoplasmic sequestration induce Hippo pathway-dependent TRIAD necrosis in the early stage of Alzheimer’s disease	Neuron apoptosis and necrosis increase in AD via intracellular Aβ aggregation and YAP interaction with p73 or TEAD	(Zhang et al., 2011; Tanaka et al., 2020)