Aims: Abnormal metal accumulation is associated with Alzheimer's disease and plays a relevant role in affecting amyloid-β (Aβ) peptide aggregation and neurotoxicity. Material & Methods: In the present study, employing a microarray analysis of 35,129 genes, we analyzed gene expression profile changes due to exposure to Aβ 1-42 -Zn or Aβ 1-42 -Cu complexes in neuronal-like cells (SH-SY5Y). Results: Microarray data indicated that Aβ-Zn or Aβ-Cu complexes selectively alter expression of genes mainly related to cell death, inflammatory responses, cytoprotective mechanisms and apoptosis. Conclusions: Taken together, these findings indicate that Aβ 1-42 -Zn or Aβ 1-42 -Cu show some commonalities in affecting Alzheimer's disease-related target functions. The overall modulatory activity on these genes supports the idea of a possible net effect resulting in the activation of pathways that counteract toxic effects of Aβ-Zn or Aβ-Cu.

Microarray analysis of gene expression profiles in human neuroblastoma cells exposed to Aβ-Zn and Aβ-Cu complexes

Bolognin, Silvia;
2012

Abstract

Aims: Abnormal metal accumulation is associated with Alzheimer's disease and plays a relevant role in affecting amyloid-β (Aβ) peptide aggregation and neurotoxicity. Material & Methods: In the present study, employing a microarray analysis of 35,129 genes, we analyzed gene expression profile changes due to exposure to Aβ 1-42 -Zn or Aβ 1-42 -Cu complexes in neuronal-like cells (SH-SY5Y). Results: Microarray data indicated that Aβ-Zn or Aβ-Cu complexes selectively alter expression of genes mainly related to cell death, inflammatory responses, cytoprotective mechanisms and apoptosis. Conclusions: Taken together, these findings indicate that Aβ 1-42 -Zn or Aβ 1-42 -Cu show some commonalities in affecting Alzheimer's disease-related target functions. The overall modulatory activity on these genes supports the idea of a possible net effect resulting in the activation of pathways that counteract toxic effects of Aβ-Zn or Aβ-Cu.
Alzheimer's disease; amyloid-β 1-42; apoptosis; copper; gene expression; inflammation; microarray; oxidative stress; zinc
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11562/518152
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