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Beta-Amyloid accumulation induces the secretory pathway stress response in murine neuroblastoma cells.
The major component of the senile plaques that forms in the brains of Alzheimer patients is amyloid beta-protein (Abeta). It accumulates into neurofibrillary tangles and is associated with progressive neurological dysfunction. We have developed a novel in vitro model of Abeta accumulation in murine neuroblastoma cells, which serves as a system for the analysis of biochemical responses associated with Abeta accumulation. Sublethal treatment of these cells with oligomeric Abeta(1-42) induced a stress response, characterized by an early increase in activation of the unfolded protein response and the induction of genes encoding molecular chaperones and endoplasmic reticulum (ER) membrane-associated proteins. Under these conditions, up-regulation of DnaJ-related heat shock protein 47 (DjhrtA) was also detected. Cells overexpressing the wild-type apolipoprotein E4 allele displayed an abnormal accumulation of Abeta and an increased activation of the unfolded protein response and stress-induced genes after Abeta treatment. These findings indicate that Abeta accumulation can trigger ER-associated stress responses in neural cells, which may contribute to the disease process.Q:

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