[Objective] To investigate the effect of mitogen-activated protein kinases (MAPK) on cerebral ischemia induced by photothrombosis in Swedish amyloid precursor protein (APP/SWE) transgenic mice.[Methods] In APP/SWE transgenic mice and non-transgenic mice (n ＝ 12,respectively),photothrombotic stroke was induced,on 7 d after cerebral ischemia,the amount of the survival neuron in the penumbra was counted using Nissl staining (n ＝ 6),and the activities of p38MAPK and JNK were measured by Western blot (n ＝ 6).[Results] On 7 d after cerebral ischemia,ratio of amount of survival neuron over the penumbra in hippocampus in the ischemic side to that in the non-ischemic side in the non-transgenic mice group (78.3 ± 1.3)% was significantly higher than that in the APP/SWE transgenic mice group (70.5 ± 1.4)% (P ＜ 0.05);compared with the non-ischemic hemisphere,the activities of p38 MAPK and JNK increased significantly in the ischemic hemisphere in the APP/SWE transgenic mice group (P ＜ 0.05),whereas,there was no significant difference between ischemic and non-ischemic hemisphere in the non-transgenic mice group (P ＞ 0.05).[Conclusion] Photothrombosis causes more severe damage in the APP/SWE transgenic mice group than that in the non-transgenic mice group.The possible mechanism includes the increased activities of MAPK which enhance the process of neuronal cell apoptosis.