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Cerebrospinal fluid beta-amyloid(1-42) in Alzheimer disease: differences between early- and late-onset Alzheimer disease and stability during the course of disease.

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OBJECTIVES: To study the diagnostic potential of the 42 amino acid form of beta-amyloid (beta-amyloid(1-42)) in cerebrospinal fluid (CSF) as a biochemical marker for Alzheimer disease (AD), the intra-individual biological variation of CSF-beta-amyloid(1-42) level in patients with AD, and the possible effects of differential binding between beta-amyloid and apolipoprotein E isoforms on CSF-beta-amyloid(1-42) levels.

DESIGN: A 20-month prospective follow-up study.

SETTING: Community population-based sample of consecutive patients with AD referred to the Pitea River Valley Hospital, Pitea, Sweden.

PATIENTS: Fifty-three patients with AD (mean +/- SD age, 71.4 +/- 7.4 years) diagnosed according to the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer’s Disease and Related Disorders Association criteria and 21 healthy, age-matched (mean +/- SD age, 68.8 +/- 8.0 years) control subjects.

MAIN OUTCOME MEASURES: Cerebrospinal fluid beta-amyloid(1-42) level–analyzed using enzyme-linked immunosorbent assay–and severity of dementia–analyzed using the Mini-Mental State Examination.

RESULTS: Mean +/- SD levels of CSF-beta-amyloid(1-42) were decreased (P<.001 in patients with ad pg compared controls most of had reduced levels a highly significant correlation p between baseline and follow-up csf-beta-amyloid was found. there were no correlations level duration or severity dementia. low also found mild dementia state examination score>25).

CONCLUSIONS: The sensitivity of CSF-beta-amyloid(1-42) level as a diagnostic marker for AD is high. The intra-individual biological variation in CSF-beta-amyloid(1-42) level is low. Low CSF-beta-amyloid(1-42) levels are also found in the earlier stages of dementia in patients with AD. These findings suggest that CSF-beta-amyloid(1-42) analyses may be of value in the clinical diagnosis of AD, especially in the early course of the disease, when drug therapy may have the greatest potential of being effective but clinical diagnosis is particularly difficult.

Source: Arch Neurol 1999 Jun;56(6):673-80

PMID: 10369305, UI: 99295979

(Department of Rehabilitation, Pitea River Valley Hospital, Sweden. niels.andreasen@nll.se )

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