Amyloid beta (Aββ) is the primary constituent of plaque seen in Alzheimerg disease.APP/PS1 mice, which pos sess the human APP/PS1 mutation, have been shown to demon strate both Aβ plaque pathology and memory deficits in behavior al task.While SAMP8 mice are the strain of animal exhibiting age-related pathological changes in the brain and deficit in learn ing and memory.We crossed APP/PS1 mice with SAMP8 strain mice and generated AD model (P8-APP/PS1) mice expressing human APP/PS1 gene in SAMP8 background.To characterize the P8-APP/PS1 model, behavioral evaluations in a full of sen sorimotor, anxiety, and cognitive tasks were conducted in the new strain mice with same ages of C57 wild, C57 APP/PS1 and SAMP8 wild mice serving as control groups.At the ages of 3, 6and 9 months, P8-APP/PS1 mice exhibited greater open field activity than C57 APP/PS1.The elevated plus maze experiment showed that P8-APP/PS1 mouse spent more time in open arm compared with C57 APP/PS1.The learning memory ability was measured by applying shuttle box and Morris water maze.