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 journalArticlepeer-review

583 Scopus citations


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 languageEnglish (US)
Pages (from-to)109-116
Number of pages8
JournalNeurobiology of Aging
Issue number2
StatePublished - Mar 1998
Externally publishedYes

ASJC Scopus subject areas

  • Clinical Neurology
  • Biological Psychiatry
  • Developmental Neuroscience
  • Neurology
  • General Psychology


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