HIV-1-induced amyloid beta accumulation in brain endothelial cells is attenuated by simvastatin

Ibolya E. András, Sung Yong Eum, Wen Huang, Yu Zhong, Bernhard Hennig, Michal Toborek

Research output: Contribution to journalArticlepeer-review

41 Scopus citations


HIV-1-infected brains are characterized by increased amyloid deposition. To study the influence of HIV-1 on amyloid beta (Aβ) homeostasis at the blood-brain barrier (BBB) level, we employed a model of brain microvascular endothelial cells exposed to HIV-1 in the presence or absence of Aβ. HIV-1 markedly increased endogenous Aβ levels and elevated accumulation of exogenous Aβ. Simvastatin, the HMG-CoA reductase inhibitor, blocked these effects. We next evaluated the effects of HIV-1 and/or simvastatin on expression of the receptor for lipoprotein related protein (LRP1) and the receptor for advanced glycation end products (RAGE), known to regulate Aβ transport across the BBB. LRP1 expression was not affected by HIV-1; however, it was increased by simvastatin. Importantly, simvastatin attenuated HIV-1-induced RAGE expression. These results suggest that HIV-1 may directly contribute to Aβ accumulation at the BBB level. In addition, statins may protect against increased Aβ levels associated with HIV-1 infection in the brain.

Original languageEnglish (US)
Pages (from-to)232-243
Number of pages12
JournalMolecular and Cellular Neuroscience
Issue number2
StatePublished - Feb 2010
Externally publishedYes


  • Amyloid beta
  • Blood-brain barrier
  • HIV-1
  • Human brain microvascular endothelial cells
  • Statins

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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