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Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”
The Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association and, National Institute on Aging Working Group. Neurobiology of Aging, 1998-03-01
Topic: Amyloid, tau and blood-test diagnosis
The ideal biomarker for Alzheimer’s disease (AD) should detect a fundamental feature of neuropathology and be validated in neuropathologically-confirmed cases; it should have a sensitivity >80% for detecting AD and a specificity of >80% for distinguishing other dementias; it should be reliable, reproducible, non-invasive, simple to perform, and inexpensive. Recommended steps to establish a biomarker include confirmation by at least two independent studies conducted by qualified investigators with the results published in peer-reviewed journals. Our review of current candidate markers indicates that for suspected early-onset familial AD, it is appropriate to search for mutations in the presenilin 1, presenilin 2, and amyloid precursor protein genes. Individuals with these mutations typically have increased levels of the amyloid Aβ 42 peptide in plasma and decreased levels of APPs in cerebrospinal fluid. In late-onset and sporadic AD, these measures are not useful, but detecting an apolipoprotein E e4 allele can add confidence to the clinical diagnosis. Among the other proposed molecular and biochemical markers for sporadic AD, cerebrospinal fluid assays showing low levels of Aβ 42 and high levels of tau come closest to fulfilling criteria for a useful biomarker.
Why it matters
A working group stated that an ideal Alzheimer's biomarker should have a sensitivity above 80% for detecting the disease and a specificity above 80% for distinguishing other dementias, and be reliable, non-invasive, simple and inexpensive. Of the candidates reviewed, low cerebrospinal fluid levels of Aβ42 and high levels of tau came closest to meeting the criteria for sporadic Alzheimer's.
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How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on strength of evidence, senior author's track record and institution's track record, so those were left out: it earned 39 of the 88 points we could judge it on, which is 44 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of Aging) |
| Journal's citation record | 3 / 4 | Neurobiology of Aging: journal h-index 263 (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 | — / 5 | No evidence rating recorded — left out of this score |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 1998 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 668 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.3 citations a year over 30 year(s) since 1998 |
| Impact for its field and year | 4 / 6 | Cited 19.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 2 / 2 | Free to read |
| Points | 39 / 88 | Scored on 17 of 20 parts. We have no data for the rest, so they are left out: 39 of the 88 points we could judge it on is 44 out of 100. |
| Total | 44 / 100 | — |
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Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
The Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association and, & National Institute on Aging Working Group. (1998). Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”. Neurobiology of Aging. https://doi.org/10.1016/s0197-4580(98)00022-0
Vancouver
The Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association and, National Institute on Aging Working Group. Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”. Neurobiology of Aging. 1998. doi:10.1016/s0197-4580(98)00022-0.
BibTeX
@article{study1998-73d1d490,
author = {{The Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association and} and {National Institute on Aging Working Group}},
title = {{Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”}},
journal = {Neurobiology of Aging},
year = {1998},
doi = {10.1016/s0197-4580(98)00022-0},
url = {https://doi.org/10.1016/s0197-4580(98)00022-0}
}
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