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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: The peri-menopause in a woman’s life: a systemic inflammatory phase that enables later neurodegenerative disease

Fig. 2

Putative mechanism of inflammasome activation in the neuron during pre- and peri-menopause. During pre-menopause, cyclic estradiol-17β(E2) maintains expression of nuclear, membrane, and mitochondrial estrogen receptor-beta (ER-β) expression, which in turn inhibits inflammasome activation by regulating mitochondrial functions, regulating biogenesis through cyclic AMP response element binding (CREB), and by reducing mitochondrial reactive oxygen species (ROS) formation. ER-β also increases expression of anti-inflammatory protein expression and reduces pro-inflammatory proteins. Decline in circulating estradiol-17β decreases estrogen receptor-beta (ER-β), causing activation of the inflammasome by reactive oxygen species (ROS). The inflammasome activates pro-caspase-1 into caspase-1, resulting in the processing of pro-IL-1β into IL-1β. Once active, IL-1β is secreted, resulting in a spread of the inflammatory response into neighboring cells. Similarly, extracellular vesicles containing inflammasome proteins get secreted, thus also contributing to the spread of the inflammatory response. ASC, Apoptosis-Associated Speck-Like Protein Containing CARD; ER-β, estrogen receptor subtype beta; ILR, interleukin receptors; IL-1β, interleukin 1β; NLR, nod-like receptor; NF-κB, nuclear factor κB; ROS, reactive oxygen species; TLR, toll-like receptors; TNFα, tumor necrosis factor alpha

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