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

Neuroreport. 1997 Mar 24;8(5):1127-30. doi: 10.1097/00001756-199703240-00013.

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 (A beta) protein, within the brain. It has been postulated that A beta may in some way contribute directly to AD pathogenesis. The epsilon 4 allele of apolipoprotein E (apoE) is a major AD risk factor. Since both apoE and A beta are components of lipoproteins in plasma and cerebrospinal fluid, we asked whether lipoproteins and apoE isoforms would modify the toxicity of A beta (1-42) in cortical cell cultures. We show that high density lipoprotein with or without apoE reduces A beta toxicity and that apoE in the absence of lipoproteins does not affect A beta toxicity. These results suggest that interactions between A beta and lipoproteins in the brain could influence AD pathogenesis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alleles
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / antagonists & inhibitors
  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Apolipoproteins E / analysis
  • Apolipoproteins E / pharmacology*
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Cerebral Cortex / drug effects*
  • Lipoproteins, HDL / chemistry
  • Lipoproteins, HDL / pharmacology*
  • Mice
  • Risk Factors

Substances

  • Amyloid beta-Peptides
  • Apolipoproteins E
  • Lipoproteins, HDL