Trazodone attenuates the neuroinflammation signaling mechanism and restores the activity of BACE 1 and ChAT in scopolamine-induced AD-like symptoms in male wistar rats

Abstract

Abstract Trazodone, an antidepressant may play a role in attenuating neuroinflammation induced by scopolamine. We propose the potential novel mechanistic insights that link up between neuroinflammation and memory biomarkers modulate the pathogenesis of AD. Docking studies and histopathological alterations were performed against scopolamine toxicity. Scopolamine was administered into the brain through the peritoneal cavity for the establishment of the AD model. Trazodone (TRAZ) was administered orally used to treat AD-like symptoms in male wistar rats aged between 200–250 g. We confirmed that TRAZ administration significantly attenuates the SCOP-induced cognitive decline targeted neuroinflammation-mediated age-dependent disease progression. TRAZ attenuates the activity of TNF-α, ChAT, and BACE1 and inhibits apoptosis. These findings confirmed that TRAZ has the potential efficacy to modulate the interference in cognitive decline induced by scopolamine. TRAZ is the controlling candidate that regulates the neuroinflammation-dependent memory biomarkers activity response pathway that positively manages apoptosis.