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Potential senotherapeutic interventions in AD and the steps at which they may operate. NLRP3 end products, IL-1β, IL-18, and caspase-1, inhibit autophagy and mitophagy, contributing to the accumulation of senescent cells and damaged mitochondria. These, in turn, alter biological barriers, enabling microbial translocation and AG loss. Excess iron induces DNA and mtDNA damage, activating NLRP3 with subsequent cellular senescence.
