Vitamin E protects nerve cells from amyloid beta protein toxicity

Biochem Biophys Res Commun. 1992 Jul 31;186(2):944-50. doi: 10.1016/0006-291x(92)90837-b.

Abstract

The amyloid beta protein (ABP) is a 40 to 42 amino acid peptide which accumulates in Alzheimer's disease plaques. It has been demonstrated that this peptide and a fragment derived from it are cytotoxic for cultured cortical nerve cells. It is shown here that ABP and an internal fragment encompassing residues 25 to 35 (beta 25-35) are cytotoxic to a clone of PC12 cells at concentrations above 1 x 10(-9)M and to several other cell lines at higher concentrations. Between 10(-9) and 10(-11) M beta 25-35 protects PC12 cells from glutamate toxicity. The antioxidant and free radical scavenger vitamin E inhibits ABP induced cell death. These results have implications regarding the prevention and treatment of Alzheimer's disease.

Publication types

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

MeSH terms

  • Amyloid beta-Peptides / pharmacology*
  • Amyloid beta-Peptides / toxicity
  • Animals
  • Cell Line
  • Cell Survival / drug effects*
  • Central Nervous System
  • Dose-Response Relationship, Drug
  • Glioma
  • Humans
  • Nerve Growth Factors / pharmacology*
  • Neuroblastoma
  • Neurons
  • PC12 Cells
  • Peptide Fragments / pharmacology*
  • Peptides / chemical synthesis
  • Peptides / pharmacology
  • Propyl Gallate / pharmacology
  • Vitamin E / pharmacology*

Substances

  • Amyloid beta-Peptides
  • Nerve Growth Factors
  • Peptide Fragments
  • Peptides
  • Vitamin E
  • Propyl Gallate