3′,4′,7-trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine-induced memory deficit in mice

Abstract

Alzheimer's disease is a major neurodegenerative disorder that leads to dementia, yet specific treatments remain elusive. Although Albizzia julibrissin has been used in traditional oriental medicine to treat insomnia and disorientation by its anti-inflammatory properties, there are currently no studies in animal models. This study aims to identify potential therapeutic candidates for Alzheimer's disease by examining how 3 ',4 ',7-trihydroxy-flavone (THF), isolated from Albizzia julibrissin stem bark, as a potential therapeutic candidate for Alzheimer's disease by examining memory recovery in a scopolamine-induced memory deficit mouse model. THF administration both orally and centrally in scopolamine-induced AD mice led to significant improvements in cognitive performance. Biochemical assays revealed restoration of cholinergic markers (ACh, AChE, ChAT) and an increase in BDNF levels in the hippocampus. Electrophysiological recordings confirmed that THF restored LTP reduced scopolamine, indicating improved synaptic plasticity. These findings suggest that THF has the potential neuropharmacological agent to protect the brain from memory loss induced by Alzheimer's disease through enhancing cholinergic system activity and activating the CREB-BDNF signaling pathway in the hippocampus.