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Beta amyloid (Aβ) is a key pathological hallmark of Alzheimer disease (AD) and plays key roles the progressive process of this disease. However the involved biological processes or pathways that triggered by Aβ in the progress of AD are still unclear. To answer this question, Aβ25-35 was bilaterally injected into the rats’ bilateral hippocampus and to accelerate the brain aging, d-gal was subcutaneously administrated, so as to set up the combined AD model rats and further explore the gene expression profile of the rats. The results demonstrated that the d-gal and Aβ treatment led to learning and memory impairment in behavioral test and neuronal cells damage in the brain, which validated the establishment of AD model rats. These verified genes may provide a new insight for elucidating Aβ cascade hypothesis in AD and its progression.

Memory Impairment in A?' (25-35) and D-Galactose Induced Alzheimerrs Disease Model Rat