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Furthermore, a number of beta-thalassemia patients fail to achieve significant increases in HbF levels and clinical improvement on this treatment [44], [189]

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Jin et al., 2017) show that sodium selenate reduces Tau phosphorylation in vivo and in vitro by activating serine/threonine-specific protein phosphatase 2A (PP2A), rescuing cognitive deficits in Tau transgenic mice (e.g., P301L, K369I, and Tau441 models)