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Cited by 666

The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.

Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”

Open access
·1998·Neurobiology of Aging

Abstract

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.

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Show all 26 references

Research works printed but not linked: 7

  1. Galasko, D.; Chang, L.; Motter, R., et al. High CSF tau and low A(42 in the clinical diagnosis of Alzheimer’s disease and relation to APOE genotype. Arch. Neurol. (in press).
  2. Arai, 1997, Elevated cerebrospinal fluid tau protein level as a predictor of dementia in memory-impaired individuals, Alzheimer’s Res., 3, 211
  3. Clark, C. M.; Ewbank, D.; Lee, V.; Trojanowski, J. Q. Molecular pathology of Alzheimer’s disease: Neuronal cytoskeletal abnormalities. In: Growdon, J. H.; Rossor, M., eds., The Dementias. Newton, MA: Butterworth Heinemann; (in press).
  4. Trojanowski, 1996, Elevated levels of tau in cerebrospinal fluid, Alzheimer’s Disease Review, 1, 77
  5. Gasparini, 1997, Inhibition of energy metabolism alters APP secretion in Alzheimer’s disease fibroblasts, Soc. Neurosci. Abs., 23, 332
  6. Hirashima, 1996, Calcium responses in human fibroblasts, Neurobiol. Aging, 17, 549, 10.1016/0197-4580(96)00074-7 · doi:10.1016/0197-4580(96)00074-7
  7. Zubenko, 1996, Prospective study of increased platelet membrane fluidity as a risk factor for Alzheimer’s disease, Am. J. Psychiatry, 153, 420, 10.1176/ajp.153.3.420 · doi:10.1176/ajp.153.3.420

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Metadata

Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
1998-03
Volume
19
Issue
2
Pages
109-116
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2511246053
Cited by
666
References
26
FWCI
19.37
Type
journal article
Language
en
Open access
hybrid
Licence

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CoChat. (2026). Citation check: Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”. https://app.cochat.ai/papers/10.1016/s0197-4580(98)00022-0
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Consensus Report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer’s Disease”. (1998). Neurobiology of Aging. https://doi.org/10.1016/s0197-4580(98)00022-0

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