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The traditional view posits that microglia activated around senile plaques accelerate disease progression by releasing ROS, neurotoxins, and pro-inflammatory cytokines, thereby directly linking Aβ deposition to neurodegeneration (145, 146)
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Both EDS1 and PAD4 are also important activators of SA signaling and mediate antagonism between JA and ET pathways during defense responses [57]
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