Plasma amyloid beta protein is elevated in late-onset Alzheimer disease families

Neurology. 2008 Feb 19;70(8):596-606. doi: 10.1212/01.WNL.0000278386.00035.21. Epub 2007 Oct 3.

Abstract

Objective: Plasma A beta levels are elevated in early-onset Alzheimer disease (AD) caused by autosomal dominant mutations. Our objective was to determine whether similar genetic elevations exist in late-onset AD (LOAD).

Methods: We measured plasma A beta in first-degree relatives of patients with LOAD in a cross-sectional series and in extended LOAD families. We screened these subjects for pathogenic mutations in early-onset AD genes and determined their ApoE genotypes.

Results: Plasma A beta is significantly elevated in the LOAD first-degree relatives in comparison to unrelated controls and married-in spouses. These elevations are not due to ApoE epsilon 4 or pathogenic coding mutations in the known early-onset AD genes.

Conclusions: The findings provide strong evidence for the existence of novel, as yet unknown genetic factors that affect late-onset Alzheimer disease by increasing A beta.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age Factors
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / blood*
  • Alzheimer Disease / genetics
  • Amyloid beta-Peptides / blood*
  • Apolipoprotein E4 / genetics
  • Enzyme-Linked Immunosorbent Assay / methods
  • Family Health*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Peptide Fragments / blood
  • Polymorphism, Genetic
  • Presenilins / genetics
  • Psychiatric Status Rating Scales
  • Sex Factors
  • Time Factors

Substances

  • Amyloid beta-Peptides
  • Apolipoprotein E4
  • Peptide Fragments
  • Presenilins
  • amyloid beta-protein (1-42)