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We suggest that inhibition of mast cells activation and brain cells associated inflammatory pathways in the brain injuries, stress, and PTSD can be explored as a new therapeutic target to delay or prevent the pathogenesis and severity of AD

These effects are mediated through inhibition of the NF-B/NLRP3/caspase-1 and Bax/Bcl-2/caspase-3 pathways, alongside activation of Nrf2/HO-1, p-AMPK, and -Klotho signaling (Khallaf et al

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