Magnolol Ameliorates Behavioral Impairments and Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease

Figure 11

Schematic drawing depicting the molecular mechanisms associated with the cognitive deficits improving effects of MN on TgCRND8 mice. The results of this present study demonstrated that MN could inhibit the activation of microglia and astrocytes to reduce the Aβ deposit, as well as suppress the release of proinflammatory cytokines such as IL-1β, IL-6, and TNF-α, while promoting the production of the anti-inflammatory mediators such as IL-10. Moreover, MN increased the protein expressions of the functional synaptic proteins such as PSD93, PSD95, SYN 1, SYT 1, and SYN in the brains of TgCRND8 mice. Changes of the PI3K/Akt/GSK-3β and NF-κB pathways also occurred in the brains of TgCRND8 mice. MN treatment reduced Aβ deposit, inhibited neuroinflammation, and reversed the synaptic deficits via regulating the PI3K/Akt/GSK-3β and NF-κB pathways. These cellular actions of MN collectively contribute to the therapeutic effects on AD in TgCRND8 mice as evidenced by the improvement in the spatial learning and memory functions.