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Taken together, disturbed Li homeostasis may contribute to early AD biology (potentially via GSK3/-catenin signaling and microglial/myelin vulnerability), but lithium is not an established AD therapy
Additionally, BACH1 disappeared at a slower rate in HUVECs after protein synthesis was inhibited with CHX (Fig
Phenylbutyrate up-regulates the DJ-1 protein and protects neurons in cell culture and in animal models of Parkinson disease
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