Fig. 9: Schematic diagram of CA on the regulation of CEBPβ–NFκB interaction in the AD brain. | Cell Death & Disease

Fig. 9: Schematic diagram of CA on the regulation of CEBPβ–NFκB interaction in the AD brain.

From: Inhibition of the CEBPβ-NFκB interaction by nanocarrier-packaged Carnosic acid ameliorates glia-mediated neuroinflammation and improves cognitive function in an Alzheimer’s disease model

Fig. 9

A The increases of CEBPβ–NFκB interaction enhance NFκB DNA binding activity, facilitating the transcription of NFκB target genes. The upregulation of CEBPβ and NFκB downstream genes, proinflammatory cytokines, could increase the releases of inflammatory factor from the microbubbles or exosomes secreted by microglia or astrocytes. NFκB-mediated increases and activation of BACE1 prompt the amyloidogenic processing of APP, followed by the γ-secretase cleavage, leading to the Aβ production by the neuron. Chronic inflammatory conditions and Aβ depositions exacerbate the binding of CEBPβ-NFκB, deteriorating the AD-like pathology. B CA provides neuroprotective effects by preventing the nucleus translocation of NFκB, reducing the expressions of proinflammatory cytokines. Meanwhile, CA reduces the CEBPβ–NFκB interaction and alleviates Aβ aggregation via inhibiting the amyloidogenic proteolytic pathway of APP.

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