Background. The study is to explore the molecular mechanisms of the inflammation induced by beta-amyloid (A beta) in the tissue of cortex and hippocampus of mice. Methods. The tissue of cortex and hippocampus of mice, were exposed to A beta(1-42) with or without Pyrrolidinedithiocarbamate ammonium (PDTC), then Enzyme linked immunosorbent assay (ELISA) for interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha); Quantitative real time polymerase chain reaction (RT-PCR) for IL-1 beta and TNF alpha mRNA, western blot analyses of I kappa B alpha and NF-kappa B p65. Results. PDTC inhibited the protein expression of IL-1 beta, TNF alpha, IL-1 beta and TNF alpha mRNA, inhibited the decreasion of I kappa B alpha in the cytoplasm, and also inhibited elevation of NF-kappa B p65 in the nucleus in A beta-stimulated tissue of cortex and hippocampus of mice. Conclusion. Our findings suggest that the IL-1 beta, TNF alpha protein and mRNA were induced by A beta via the NF-kappa B signal pathway in the tissue of cortex and hippocampus of mice. [Jun Wu, Zhe Min, Yongjie Xiong, Qiuyue Yan, Yuming Xu, Suming Zhang. Study on the molecular mechanisms of the inflammation induced by beta-amyloid in vivo. Life Science Journal. 2012; 9(1):750-755] (ISSN: 1097-8135). http://www.lifesciencesite.com. 108