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Aβ-induced astrocytic dysfunctions leading to excitotoxicity and AD pathogenesis. iNOS, inducible nitric oxide synthase; NO, nitric oxide; SR, serine racemase; GS, glutamine synthetase; CaN/NFAT—calcineurin/nuclear factor of activated T cells; GluT, glutamate transporters; GluR, glutamate receptors.
