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Notably, this occurred in the absence of improved insulin sensitivity, neuroinflammation, brain mTORC1 signaling, or activation of brain autophagy all physiological and molecular changes that have been hypothesized to explain the ability of CR to slow the development or promote the clearance of A plaques

Although the precise molecular mechanisms of the NLRP3 inflammasome activation remain to be fully elucidated, reactive oxygen species (ROS) are widely regarded as essential for NLRP3 inflammasome activation (111)

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