Objective:　Phosphodiesterase　(PDE)　plays　an　important　role　in　the　pathogenesis　of　Alzheimer＇s　disease　(AD).　Ferulic　acid　(FA)　has　a　therapeutic　benefit　in　the　treatment　of　AD.　We　investigated　whether　this　therapeutic　effect　is　based　on　the　modulation　of　the　PDE/cyclic　adenosine　monophosphate　(cAMP)　pathway.　In　the　present　study,　we　investigated　whether　FA　could　abrogate　A　beta(25-35)-　and　lipopolysaccharide-induced　cellular　damage.　Materials　and　methods:　Cell　viability,　superoxide　production,　and　the　levels　of　inflammatory　factors　were　investigated.　We　further　investigated　the　intracellular　levels　of　cAMP　and　Ca2+,　both　of　which　are　associated　with　PDE　activity.　Furthermore,　molecular　docking　was　used　to　identify　the　binding　mode　between　phosphodiesterase　4B2　(PDE4B2)　and　FA.　Results:　Pretreatment　with　FA　significantly　maintained　cell　viability,　increased　the　levels　of　superoxide　dismutase,　and　inhibited　production　of　TNF-alpha　and　IL-1　beta　induced　by　A　beta(25-35).　Moreover,　pretreatment　with　FA　increased　the　intracellular　levels　of　cAMP　and　decreased　the　intracellular　levels　of　Ca2+.　The　docking　results　also　showed　that　FA　has　the　potential　to　inhibit　PDE4B2　activity.　Conclusions:　Taken　together,　our　results　suggested　that　one　of　the　therapeutic　effects　of　FA　on　AD　was　potentially　mediated　by　modulating　the　PDE/cAMP　pathway.