Alzheimer＇s　disease　(AD)　is　an　extremely　complex　disease,　characterized　by　several　pathological　features　including　oxidative　stress　and　amyloid-beta　(A　beta)　aggregation.　Blockage　of　A　beta-induced　injury　has　emerged　as　a　potential　therapeutic　approach　for　AD.　Our　previous　efforts　resulted　in　the　discovery　of　Monascus　pigment　rubropunctatin　derivative　FZU-H　with　potential　neuroprotective　effects.　This　novel　lead　compound　significantly　diminishes　toxicity　induced　by　A　beta(1-42)　in　Neuro-2A　cells.　Our　further　mechanism　investigation　revealed　that　FZU-H　inhibited　A　beta(1-42)-induced　caspase-3　protein　activation　and　the　loss　of　mitochondrial　membrane　potential.　In　addition,　treatment　of　FZU-H　was　proven　to　attenuate　A　beta(1-42)-induced　cell　redox　imbalance　and　Tau　hyperphosphorylation　which　caused　by　okadaic　acid　in　Neuro-2A　cells.　These　results　indicated　that　FZU-H　shows　promising　neuroprotective　effects　for　AD.