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

N. Ertekin-Taner, L. H. Younkin, D. M. Yager, F. Parfitt, M. C. Baker, S. Asthana, M. L. Hutton, S. G. Younkin, N. R. Graff-Radford

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


OBJECTIVE: Plasma Aβ 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 Aβ 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 Aβ 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 ϵ4 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 Aβ.

Original languageEnglish (US)
Pages (from-to)596-606
Number of pages11
Issue number8
StatePublished - Feb 2008

ASJC Scopus subject areas

  • Clinical Neurology


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