1. Consensus Report of the Working Group on: 'Molecular and Biochemical Markers of Alzheimer’s Disease'
- Author
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Kwan-Fu Rex Sheu, Masakazu Mirua, Philip Scheltens, Toshifumi Matsui, Howard Feldman, M. L. Kennard, Bradley T. Hyman, Burton Resnick, S. D. Wilton, Irene Litvan, Lars Lannfelt, Douglas Galasko, T. Pirttla, Wilfred A. Jefferies, Malcolm L. Kennard, L. Lim, Dennis J. Selkoe, Christoph Hock, Amanda McRae, Sadao Takase, Hilkka Soininen, Giovanni B. Frisoni, B. A. Kakulas, Gary E. Gibson, Ram Parshad, J. E. Dench, Gregory R J Swanwick, Hidetata Sasaki, John Q. Trojanowski, M. R. Davis, Teresa S. Radebaugh, Sid Gilman, Christopher M. Clark, John H. Growdon, Steven E. Arnold, T. M. Jones, Leonard F. M. Scinto, Makoto Higuchi, Bengt Winblad, G. S. Zubenko, Hiroyuki Arai, Virginia M. Y. Lee, H. M. Wisniewski, Takeshi Iwatsubo, Allen D. Roses, Yasuo Ihara, T. Yamada, Hisatomo Seki, Lars-Olof Wahlund, Robert A. Sweet, Paavo Riekkinen, Judith Resnick, V. A. Fabian, John P. Blass, Norman L. Foster, P. St. George-Hyslop, Douglas C. Ewbank, Richard Mayeux, William E. Klunk, Tsuneo Yamazaki, Pankaj D. Mehta, Alfredo Robles, Zaven S. Khachaturian, André Delacourte, Susumu Higuchi, Peter Davies, and Kaj Blennow
- Subjects
Apolipoprotein E ,Aging ,Pathology ,medicine.medical_specialty ,biology ,Amyloid ,business.industry ,General Neuroscience ,Neuropathology ,medicine.disease ,Bioinformatics ,Presenilin ,Degenerative disease ,Amyloid precursor protein ,biology.protein ,Medicine ,Biomarker (medicine) ,Neurology (clinical) ,Geriatrics and Gerontology ,Alzheimer's disease ,business ,Developmental Biology - 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.
- Published
- 1998
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