High density lipoprotein decreases β-amyloid toxicity in cortical cell culture

Z. Shadi Farhangrazi, Howard Ying, Guojun Bu, Laura L. Dugan, Anne M. Fagan, Dennis W. Choi, David M. Holtzman

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

A hallmark of Alzheimer's disease (AD) is the extracellular deposition and accumulation of a 39-43 amino peptide, known as the amyloid beta (Aβ) protein, within the brain. It has been postulated that Aβ may in some way contribute directly to AD pathogenesis. The ε4 allele of apolipoprotein E (apoE) is a major AD risk factor. Since both apoE and Aβ are components of lipoproteins in plasma and cerebrospinal fluid, we asked whether lipoproteins and apoE isoforms would modify the toxicity of Aβ(1-42) in cortical cell cultures. We show that high density lipoprotein with or without apoE reduces Aβ toxicity and that apoE in the absence of lipoproteins does not affect Aβ toxicity. These results suggest that interactions between Aβ and lipoproteins in the brain could influence AD pathogenesis.

Original languageEnglish
Pages (from-to)1127-1130
Number of pages4
JournalNeuroReport
Volume8
Issue number5
DOIs
StatePublished - Jan 1 1997

Keywords

  • Alzheimer's disease
  • apolipoprotein E
  • high density lipoprotein
  • β-amyloid

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