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These inflammation modifying roles of nrf2 demonstrate redox-neuroinflammation crosstalk at the transcriptional level which highlights nrf2 as an important therapeutic target for controlling both ROS-mediated damage and activation of proinflammatory cascades

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Over-activation of NMDARs leads to calcium overload of postsynaptic neurons, inducing excitatory toxicity, neuronal apoptosis, and neurodegeneration