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Intriguingly, the neuroinflammatory response to DOX results in the overexpression of the nuclear factor kappa-B (NF-B) gene and enhanced release of proinflammatory mediators, including IL-1 and TNF- [6], alongside the signaling pathways of Protein Kinase B (AKT)/Glycogen Synthase Kinase-3 beta (GSK-3) and the Wingless-related integration site (Wnt)/-catenin [7, 8]

Lebourgeois S, GonzlezMarn MC, Jeanblanc J, Naassila M, Vilpoux C

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