Biochemical evidence for the long-tail form (A beta 1-42/43) of amyloid beta protein as a seed molecule in cerebral deposits of Alzheimer's disease

Biochem Biophys Res Commun. 1994 Nov 30;205(1):834-42. doi: 10.1006/bbrc.1994.2740.

Abstract

We measured the amounts of total A beta, A beta 1-40 and A beta 1-42/43 in brain tissues using a newly developed ELISA assay and found that the amounts of insoluble A beta 1-42/43 and insoluble A beta 1-40 were linearly related to the amount of A beta deposits or total insoluble A beta at their lower and higher concentrations, respectively. In an experiment to characterize the A beta species in brain homogenates with buffered saline, we unexpectedly detected soluble A beta which was derived from the insoluble amyloid deposits in brain tissue, indicating reversible depolymerization of A beta from insoluble amyloid deposits. To confirm this finding, we performed 5 consecutive washes of insoluble precipitates of AD brains with buffered saline. Both species of A beta were found in all 5 supernatant fractions and their amounts were gradually decreased. The ratio of A beta 1-42/43 to A beta 1-40 was increased with the numbers of washes, indicating that A beta 1-40 existed in an exposed manner as compared to A beta 1-42/43. Thus the present finding is the first biochemical evidence that A beta 1-40 was the predominant species involved in the reversible exchanging reaction on seeding A beta 1-42/43 between the soluble and the insoluble forms (amyloid fibrils).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / isolation & purification
  • Amyloid beta-Peptides / metabolism*
  • Brain / metabolism*
  • Humans
  • Peptide Fragments / isolation & purification
  • Peptide Fragments / metabolism

Substances

  • Amyloid beta-Peptides
  • Peptide Fragments