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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Getting a diagnosis

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

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 Piteå River Valley Hospital, Piteå, 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 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.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Andreasen, N., Hesse, C., Davidsson, P., Minthon, L., Wallin, A., Winblad, B., et al. (1999). Cerebrospinal fluid beta-amyloid(1-42) in Alzheimer disease: differences between early- and late-onset Alzheimer disease and stability during the course of disease. Archives of neurology. https://doi.org/10.1001/archneur.56.6.673

Vancouver

Andreasen N, Hesse C, Davidsson P, Minthon L, Wallin A, Winblad B, et al. Cerebrospinal fluid beta-amyloid(1-42) in Alzheimer disease: differences between early- and late-onset Alzheimer disease and stability during the course of disease. Archives of neurology. 1999. doi:10.1001/archneur.56.6.673. PMID: 10369305.

BibTeX

@article{andreasen1999-10369305,
  author  = {Andreasen, N. and Hesse, C. and Davidsson, P. and Minthon, L. and Wallin, A. and Winblad, B. and Vanderstichele, H. and Vanmechelen, E. and others},
  title   = {{Cerebrospinal fluid beta-amyloid(1-42) in Alzheimer disease: differences between early- and late-onset Alzheimer disease and stability during the course of disease}},
  journal = {Archives of neurology},
  year    = {1999},
  doi     = {10.1001/archneur.56.6.673},
  pmid    = {10369305},
  url     = {https://doi.org/10.1001/archneur.56.6.673}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Why it matters

In this 20-month follow-up of 53 people with Alzheimer's disease and 21 healthy people of similar age at one Swedish hospital, the authors concluded that the level of beta-amyloid(1-42) in spinal fluid had "high" sensitivity as a diagnostic marker, varied little within the same patient over time, and was low even "in the earlier stages of dementia". Our copy of the abstract has lost its results figures, so no sensitivity, specificity or level values can be shown here, and the stated questions about ApoE and early- versus late-onset disease have no reported answer. It is a test-measurement study: it does not show that amyloid causes the disease or that any treatment works.

Study details

How this study scored 51/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 4 of 6; Cited by studies here 4 of 6; Still being cited 3 of 4; Senior author's track record 4 of 4; Institution's track record left out, no data; Multicenter collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. 49 of the 97 points it could be judged on, which is 51 of 100. Total 51 of 100.49 of the 97 points we could judge = 51 of 100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on institution's track record, so that was left out: it earned 49 of the 97 points we could judge it on, which is 51 out of 100.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Archives of neurology)
Journal's citation record 3 / 4 Archives of Neurology: journal h-index 353 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 1 / 5 1999 — older than 20 years, still counted
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded 0 / 2 No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 6 / 7 Cited 661 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 22.8 citations a year over 29 year(s) since 1999
Impact for its field and year 4 / 6 Cited 14.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 4 / 6 Cited by 67 other studies in this library
Still being cited 3 / 4 Cited 51 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Kaj Blennow: h-index 220 (OpenAlex, whole career)
Institution's track record — / 3 No institution listed in OpenAlex — left out of this score
Multicenter collaboration 0 / 3 OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 10369305)
Free to read 0 / 2 Behind a paywall — scores zero
Points 49 / 97 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 49 of the 97 points we could judge it on is 51 out of 100.
Total 51 / 100 —

What each of these 20 components measures, and what this score is not →

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