Neurochemical Research

, Volume 33, Issue 8, pp 1509–1517

Cholesterol Potentiates β-Amyloid-Induced Toxicity in Human Neuroblastoma Cells: Involvement of Oxidative Stress

  • Patricia Ferrera
  • Octavio Mercado-Gómez
  • Martín Silva-Aguilar
  • Mahara Valverde
  • Clorinda Arias
Original Paper

DOI: 10.1007/s11064-008-9623-y

Cite this article as:
Ferrera, P., Mercado-Gómez, O., Silva-Aguilar, M. et al. Neurochem Res (2008) 33: 1509. doi:10.1007/s11064-008-9623-y

Abstract

Alterations in brain cholesterol concentration and metabolism seem to be involved in Alzheimer’s disease (AD). In fact, several experimental studies have reported that modification of cholesterol content can influence the expression of the amyloid precursor protein (APP) and amyloid β peptide (Aβ) production. However, it remains to be determined if changes in neuronal cholesterol content may influence the toxicity of Aβ peptides and the mechanism involved. Aged mice, AD patients and neurons exposed to Aβ, show a significant increase in membrane-associated oxidative stress. Since Aβ is able to promote oxidative stress directly by catalytically producing H2O2 from cholesterol, the present work analyzed the effect of high cholesterol incorporated into human neuroblastoma cells in Aβ-mediated neurotoxicity and the role of reactive oxygen species (ROS) generation. Neuronal viability was studied also in the presence of 24S-hydroxycholesterol, the main cholesterol metabolite in brain, as well as the potential protective role of the lipophilic statin, lovastatin.

Keywords

Cholesterolβ-amyloidNeurotoxicityROSHuman neuroblastoma

Copyright information

© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  • Patricia Ferrera
    • 1
  • Octavio Mercado-Gómez
    • 1
  • Martín Silva-Aguilar
    • 1
  • Mahara Valverde
    • 1
  • Clorinda Arias
    • 1
  1. 1.Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones BiomédicasUniversidad Nacional Autónoma de MéxicoMexicoMexico