Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'

Peter Davies; Judith Resnick; Burton Resnick; Sid Gilman; John H. Growdon; Zaven S. Khachaturian; Teresa S. Radebaugh; Allen D. Roses; Dennis J. Selkoe; John Q. Trojanowski; John P. Blass; Gary E. Gibson; K. F R Sheu; Kaj Blennow; Andre Delacourte; Giovanni B. Frisoni; Wilfred A. Jefferies; Amanda McRae; H. M. Wisniewski; P. D. Mehta; T. Pirttla; Ram Parshad; Leonard F M Scinto; Philip Scheltens; Paavo J. Riekkinen; Hilkka S. Soininen; Gregory R J Swanwick; Lars Olof Wahlund; S. E. Arnold; Bengt Winblad; Yasuo Ihara; Tsuneo Yamazaki; Hiroyuki Arai; Christopher M. Clark; Douglas C. Ewbank; Sadao Takase; Susumu Higuchi; Masakazu Mirua; Hisatomo Seki; Makoto Higuchi; Toshifumi Matsui; Virginia M Y Lee; Hidetata Sasaki; Norman L. Foster; Douglas Galasko; Christoph Hock; Bradley T. Hyman; P. H. St. George-Hyslop; Takeshi Iwatsubo; Malcolm Kennard; William E. Klunk; Lars Lannfelt; Irene Litvan; Richard Mayeux; Alfredo Robles; V. A. Fabian; T. M. Jones; S. D. Wilton; J. E. Dench; M. R. Davis; L. Lim; B. A. Kakulas; M. L. Kennard; H. Feldman; T. Yamada; R. A. Sweet; G. S. Zubenko

doi:10.1016/S0197-4580(98)00022-0

Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'

Peter Davies, Judith Resnick, Burton Resnick, Sid Gilman, John H. Growdon, Zaven S. Khachaturian, Teresa S. Radebaugh, Allen D. Roses, Dennis J. Selkoe, John Q. Trojanowski, John P. Blass, Gary E. Gibson, K. F R Sheu, Kaj Blennow, Andre Delacourte, Giovanni B. Frisoni, Wilfred A. Jefferies, Amanda McRae, H. M. Wisniewski, P. D. MehtaT. Pirttla, Ram Parshad, Leonard F M Scinto, Philip Scheltens, Paavo J. Riekkinen, Hilkka S. Soininen, Gregory R J Swanwick, Lars Olof Wahlund, S. E. Arnold, Bengt Winblad, Yasuo Ihara, Tsuneo Yamazaki, Hiroyuki Arai, Christopher M. Clark, Douglas C. Ewbank, Sadao Takase, Susumu Higuchi, Masakazu Mirua, Hisatomo Seki, Makoto Higuchi, Toshifumi Matsui, Virginia M Y Lee, Hidetata Sasaki, Norman L. Foster, Douglas Galasko, Christoph Hock, Bradley T. Hyman, P. H. St. George-Hyslop, Takeshi Iwatsubo, Malcolm Kennard, William E. Klunk, Lars Lannfelt, Irene Litvan, Richard Mayeux, Alfredo Robles, V. A. Fabian, T. M. Jones, S. D. Wilton, J. E. Dench, M. R. Davis, L. Lim, B. A. Kakulas, M. L. Kennard, H. Feldman, T. Yamada, R. A. Sweet, G. S. Zubenko

Research output: Contribution to journal › Article › peer-review

583 Scopus citations

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 Aβ₄₂ 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 Aβ₄₂ and high levels of tau come closest to fulfilling criteria for a useful biomarker.

Original language	English (US)
Pages (from-to)	109-116
Number of pages	8
Journal	Neurobiology of Aging
Volume	19
Issue number	2
DOIs	https://doi.org/10.1016/S0197-4580(98)00022-0
State	Published - Mar 1998
Externally published	Yes

ASJC Scopus subject areas

Clinical Neurology
Biological Psychiatry
Developmental Neuroscience
Neurology
General Psychology

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10.1016/S0197-4580(98)00022-0

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Davies, P., Resnick, J., Resnick, B., Gilman, S., Growdon, J. H., Khachaturian, Z. S., Radebaugh, T. S., Roses, A. D., Selkoe, D. J., Trojanowski, J. Q., Blass, J. P., Gibson, G. E., Sheu, K. F. R., Blennow, K., Delacourte, A., Frisoni, G. B., Jefferies, W. A., McRae, A., Wisniewski, H. M., ... Zubenko, G. S. (1998). Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'. Neurobiology of Aging, 19(2), 109-116. https://doi.org/10.1016/S0197-4580(98)00022-0

Davies, P, Resnick, J, Resnick, B, Gilman, S, Growdon, JH, Khachaturian, ZS, Radebaugh, TS, Roses, AD, Selkoe, DJ, Trojanowski, JQ, Blass, JP, Gibson, GE, Sheu, KFR, Blennow, K, Delacourte, A, Frisoni, GB, Jefferies, WA, McRae, A, Wisniewski, HM, Mehta, PD, Pirttla, T, Parshad, R, Scinto, LFM, Scheltens, P, Riekkinen, PJ, Soininen, HS, Swanwick, GRJ, Wahlund, LO, Arnold, SE, Winblad, B, Ihara, Y, Yamazaki, T, Arai, H, Clark, CM, Ewbank, DC, Takase, S, Higuchi, S, Mirua, M, Seki, H, Higuchi, M, Matsui, T, Lee, VMY, Sasaki, H, Foster, NL, Galasko, D, Hock, C, Hyman, BT, St. George-Hyslop, PH, Iwatsubo, T, Kennard, M, Klunk, WE, Lannfelt, L, Litvan, I, Mayeux, R, Robles, A, Fabian, VA, Jones, TM, Wilton, SD, Dench, JE, Davis, MR, Lim, L, Kakulas, BA, Kennard, ML, Feldman, H, Yamada, T, Sweet, RA & Zubenko, GS 1998, 'Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'', Neurobiology of Aging, vol. 19, no. 2, pp. 109-116. https://doi.org/10.1016/S0197-4580(98)00022-0

@article{96e2117408e94293915b106291d94b1a,

title = "Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'",

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 Aβ42 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 Aβ42 and high levels of tau come closest to fulfilling criteria for a useful biomarker.",

author = "Peter Davies and Judith Resnick and Burton Resnick and Sid Gilman and Growdon, {John H.} and Khachaturian, {Zaven S.} and Radebaugh, {Teresa S.} and Roses, {Allen D.} and Selkoe, {Dennis J.} and Trojanowski, {John Q.} and Blass, {John P.} and Gibson, {Gary E.} and Sheu, {K. F R} and Kaj Blennow and Andre Delacourte and Frisoni, {Giovanni B.} and Jefferies, {Wilfred A.} and Amanda McRae and Wisniewski, {H. M.} and Mehta, {P. D.} and T. Pirttla and Ram Parshad and Scinto, {Leonard F M} and Philip Scheltens and Riekkinen, {Paavo J.} and Soininen, {Hilkka S.} and Swanwick, {Gregory R J} and Wahlund, {Lars Olof} and Arnold, {S. E.} and Bengt Winblad and Yasuo Ihara and Tsuneo Yamazaki and Hiroyuki Arai and Clark, {Christopher M.} and Ewbank, {Douglas C.} and Sadao Takase and Susumu Higuchi and Masakazu Mirua and Hisatomo Seki and Makoto Higuchi and Toshifumi Matsui and Lee, {Virginia M Y} and Hidetata Sasaki and Foster, {Norman L.} and Douglas Galasko and Christoph Hock and Hyman, {Bradley T.} and {St. George-Hyslop}, {P. H.} and Takeshi Iwatsubo and Malcolm Kennard and Klunk, {William E.} and Lars Lannfelt and Irene Litvan and Richard Mayeux and Alfredo Robles and Fabian, {V. A.} and Jones, {T. M.} and Wilton, {S. D.} and Dench, {J. E.} and Davis, {M. R.} and L. Lim and Kakulas, {B. A.} and Kennard, {M. L.} and H. Feldman and T. Yamada and Sweet, {R. A.} and Zubenko, {G. S.}",

year = "1998",

month = mar,

doi = "10.1016/S0197-4580(98)00022-0",

language = "English (US)",

volume = "19",

pages = "109--116",

journal = "Neurobiology of Aging",

issn = "0197-4580",

publisher = "Elsevier Inc.",

number = "2",

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T1 - Consensus report of the working group on

T2 - 'Molecular and biochemical markers of Alzheimer's disease'

AU - Davies, Peter

AU - Resnick, Judith

AU - Resnick, Burton

AU - Gilman, Sid

AU - Growdon, John H.

AU - Khachaturian, Zaven S.

AU - Radebaugh, Teresa S.

AU - Roses, Allen D.

AU - Selkoe, Dennis J.

AU - Trojanowski, John Q.

AU - Blass, John P.

AU - Gibson, Gary E.

AU - Sheu, K. F R

AU - Blennow, Kaj

AU - Delacourte, Andre

AU - Frisoni, Giovanni B.

AU - Jefferies, Wilfred A.

AU - McRae, Amanda

AU - Wisniewski, H. M.

AU - Mehta, P. D.

AU - Pirttla, T.

AU - Parshad, Ram

AU - Scinto, Leonard F M

AU - Scheltens, Philip

AU - Riekkinen, Paavo J.

AU - Soininen, Hilkka S.

AU - Swanwick, Gregory R J

AU - Wahlund, Lars Olof

AU - Arnold, S. E.

AU - Winblad, Bengt

AU - Ihara, Yasuo

AU - Yamazaki, Tsuneo

AU - Arai, Hiroyuki

AU - Clark, Christopher M.

AU - Ewbank, Douglas C.

AU - Takase, Sadao

AU - Higuchi, Susumu

AU - Mirua, Masakazu

AU - Seki, Hisatomo

AU - Higuchi, Makoto

AU - Matsui, Toshifumi

AU - Lee, Virginia M Y

AU - Sasaki, Hidetata

AU - Foster, Norman L.

AU - Galasko, Douglas

AU - Hock, Christoph

AU - Hyman, Bradley T.

AU - St. George-Hyslop, P. H.

AU - Iwatsubo, Takeshi

AU - Kennard, Malcolm

AU - Klunk, William E.

AU - Lannfelt, Lars

AU - Litvan, Irene

AU - Mayeux, Richard

AU - Robles, Alfredo

AU - Fabian, V. A.

AU - Jones, T. M.

AU - Wilton, S. D.

AU - Dench, J. E.

AU - Davis, M. R.

AU - Lim, L.

AU - Kakulas, B. A.

AU - Kennard, M. L.

AU - Feldman, H.

AU - Yamada, T.

AU - Sweet, R. A.

AU - Zubenko, G. S.

PY - 1998/3

Y1 - 1998/3

N2 - 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 Aβ42 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 Aβ42 and high levels of tau come closest to fulfilling criteria for a useful biomarker.

AB - 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 Aβ42 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 Aβ42 and high levels of tau come closest to fulfilling criteria for a useful biomarker.

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Consensus report of the working group on: 'Molecular and biochemical markers of Alzheimer's disease'

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