Figure 6.

Proposed cascade of the signaling events regulating the pathogenesis of AD by PGI ₂. In detail, elevated levels of PGI ₂ in APP/PS1 transgenic mice will enhance the expression of APP‐1α/1β via the PKA/CREB and JNK/c‐Jun pathways in neuron cells of APP/PS1 transgenic mice, which in turn aggravates the pathogenesis of AD. Moreover, the highly secreted Aβ oligomers from neuron cells are able to reciprocally regulate the expression of APH‐1α/1β, which further aggravate the pathogenesis of AD in vivo. PGI ₂, a metabolic product of COX‐2, inhibition by NS398 administration reversed the effects of APP/PS1 overexpression in stimulating the expression of APH‐1α/1β, which potentially contributes to improvement in study ability and decline in cognitive ability in APP/PS1 transgenic mice.