Plasma amyloid β-protein Aβ42 levels are increased in patients with familial Alzheimer disease (AD) mutations, and high levels reportedly identify individuals at risk to develop AD.
To determine whether there are characteristic changes in plasma Aβ40 and Aβ42 levels in sporadic AD, and to examine the relationship of plasma Aβ measures with clinical, demographic, and genetic variables in a prospectively characterized outpatient clinic population.
A total of 371 outpatients with sporadic AD (n = 146), mild cognitive impairment (n = 37), or Parkinson disease (n = 96) and nondemented control cases (n = 92).
We collected plasma samples and determined Aβ40 and Aβ42 levels by sandwich enzyme-linked immunosorbent assay with the use of the capture antibody BNT77 (anti–Aβ11-28) and the detector antibodies horseradish peroxidase–linked BA27 (anti-Aβ40) and BC05 (anti-Aβ42).
Mean Aβ40 and Aβ42 levels increased significantly with age in each diagnostic group. When covaried for age, mean plasma levels of Aβ40 and Aβ42 did not differ significantly among the 4 diagnostic groups. Within the mild cognitive impairment and AD groups, Aβ40 and Aβ42 levels did not correlate with duration of memory impairment or with cognitive test scores. The Aβ measures were not influenced by family history of AD, apolipoprotein E genotype, or current medication use of cholinesterase inhibitors, vitamin E, statins, nonsteroidal anti-inflammatory drugs, or estrogen.
Plasma Aβ measures increase with age, but, in contrast to reports on familial AD, plasma Aβ measures were neither sensitive nor specific for the clinical diagnosis of mild cognitive impairment or sporadic AD.