Fig. 7From: Zerumbone ameliorates behavioral impairments and neuropathology in transgenic APP/PS1 mice by suppressing MAPK signalingSchematic drawing depicting the suppression of MAPK signaling in microglia to alleviate AD by zerumbone. In the Alzheimer’s disease (AD) brain, β-amyloid (Aβ) induces the release of interleukin-1β (IL-1β), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) and activates inflammatory microglia, suppressing Aβ phagocytosis and promoting behavioral impairments (left, red). In this study, zerumbone inhibited the production of prostaglandin E2 (PGE2), cyclooxygenase-2 (Cox-2), and microsomal prostaglandin E synthase-1 (mPGEs-1). It also increased the proportion of anti-inflammatory microglia and ameliorated behavioral impairments and neuropathological changes in transgenic APP/PS1 mice by suppressing mitogen-activated protein kinase (MAPK) signaling (green). The inhibition of p-extracellular signal-related kinase (p-ERK), p-p38, and nuclear factor-kappa B (NF-κB) was a critical mechanism underlying the neuroprotective effect of zerumbone in microglia (right)Back to article page