CAMP catabolic process

Abstract: Backgrounds: β-Amyloid (Aβ) is a principal constituent of senile plaques in Alzheimer’s disease (AD) and induces neuronal cell death. The molecular mechanism of how Aβ evokes neuronal cell death remains complicated, which were investigated in the present study. Methods: Using the human neuroblastoma cell line SHSY5Y, we investigated the neurotoxic effects of human β-Amyloid 1–42 (Aβ1–42) aggregates on gene expression profile and protein expression profile by using the Agilent GeneChip Human 1A (V2) Oligo MicroArray, Quantitative Real-time PCR, PF-2D and Western blot analysis. Results: Our results show that Aβ1–42 specifically influences gene and protein expression such as EGR1, eIF5A, PDE8A, ERp57 and ERp5 in pathways associated with apoptotic process, protein translation, cAMP catabolic process and response to endoplasmic reticulum stress. Conclusion: Although Genes with significant changes in transcriptomic analysis matched very few of the proteins identified in proteomics analysis, our findings will strengthen our knowledge concerning the molecular mechanisms underlying AD.