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Age but Not Diagnosis Is the Main Predictor of Plasma Amyloid -Protein Levels

Hiroaki Fukumoto, PhD; Marsha Tennis, RN; Joseph J. Locascio, PhD; Bradley T. Hyman, MD, PhD; John H. Growdon, MD; Michael C. Irizarry, MD

Arch Neurol. 2003;60:958-964.

Background  Plasma amyloid -protein A42 levels are increased in patients with familial Alzheimer disease (AD) mutations, and high levels reportedly identify individuals at risk to develop AD.

Objectives  To determine whether there are characteristic changes in plasma A40 and A42 levels in sporadic AD, and to examine the relationship of plasma A measures with clinical, demographic, and genetic variables in a prospectively characterized outpatient clinic population.

Patients  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).

Methods  We collected plasma samples and determined A40 and A42 levels by sandwich enzyme-linked immunosorbent assay with the use of the capture antibody BNT77 (anti–A11-28) and the detector antibodies horseradish peroxidase–linked BA27 (anti-A40) and BC05 (anti-A42).

Results  Mean A40 and A42 levels increased significantly with age in each diagnostic group. When covaried for age, mean plasma levels of A40 and A42 did not differ significantly among the 4 diagnostic groups. Within the mild cognitive impairment and AD groups, A40 and A42 levels did not correlate with duration of memory impairment or with cognitive test scores. The A 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.

Conclusions  Plasma A measures increase with age, but, in contrast to reports on familial AD, plasma A measures were neither sensitive nor specific for the clinical diagnosis of mild cognitive impairment or sporadic AD.

From the Department of Neurology, Massachusetts General Hospital, Boston.

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