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Alzheimer’s disease (AD) is one of the common diseases of older people. Although several genes have been identified for Familial Alzheimer’s Disease (FAD), a reliable diagnostic, especially for those patients in their early or intermediate phases of AD, is still not available. There is neither effective treatment nor drugs that can stop or reverse AD progression. Breakthroughs in diagnosis or treatment development likely require understanding of the molecular mechanisms of AD. Studies in FAD have shown that APP, PS1, PS2 and some other genes are related to FAD. Mutations of APP and PS1 lead to amyloid plaque accumulation which is also prominent in Sporadic AD. Transgenic animals closely mimic human AD pathologies in many aspects. A mouse model carrying both APP Swedish mutation and PS1 deltaE9 mutation is used in this study. This mouse model accumulates amyloid plaque rapidly, and the plaque shows up as early as 6 months of age. Using microarrays, we have isolated 176 genes with significant expression changes and 14 turned on/off genes from AD mouse cortex. From this cDNA microarray measurement of global gene expression, several functional groups were regulated significantly in our mouse model of AD pathology. Mt2 and Atp7a were identified and may be candidates for further studies of AD pathology, as well as potential drug targets. Five significant microRNAs were found from AD mouse cortex, providing evidence that microRNAs could play a role in AD. cDNA arrays were also used to identify potential biomarkers from whole blood samples that distinguish AD mice from their non-transgenic littermates.