Journal
NEUROLOGY
Volume 78, Issue 7, Pages 468-476Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3182477eed
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Funding
- Swedish Brain Power
- Swedish Research Council [14002, 2006-6227, KP2010-63P-21562-01-4, K2011-61X-20401-05-6]
- Alzheimer's Association [NIRG-08-90356]
- cNEUPRO
- Lundbeck Foundation
- Royal Swedish Academy of Sciences
- Sahlgrenska University Hospital
- Sahlgrenska Academy
- Stiftelsen Psykiatriska Forskningsfonden
- Stiftelsen Gamla Tjanarinnor
- Uppsala Universitets Medicinska Fakultet stiftelse for psykiatrisk och neurologisk forskning
- Swedish Brain Fund
- Soderberg Foundation
- Alzheimer Foundation, Sweden
- Dementia Association, Sweden
- Alzheimer's Association
- International College of Geriatric Psychoneuropharmacology
- Schering-Plough Corp.
- AADC Research Trust
- Internationale Stichting Alzheimer Onderzoek
- Center for Translational Molecular Medicine
- American Alzheimer Association
- Alzheimer Drug Discovery Foundation
- Stichting Internationaal Parkinson Fonds
- Hersenstichting Nederland
- Lundbeck, Inc
- Novartis
- GE Healthcare
- GlaxoSmithKline
- DiaGenic ASA
- Lundbeck, Inc.
- Merck Serono
- European Commission
- B.R.A.H.M.S.
- Biotech GmbH
- Janssen
- BMBF (German Ministry for Education and Research)
- Trinity College Dublin, Ireland
- State of Hess, Germany
- Katharina-Hardt-Foundation
- Thea-Goering-Foundation
- Alzheimer Nederland
- Stichting VUmc fonds
- Innovation Fund
- Swedish Research Council
- Swedish municipalities (SKL)
- Swedish Brain Power network
- Gustav V and Queen Victoria's Freemason Foundation
- Pfizer Inc
- Eisai Inc.
- Knut & Alice Wallenberg Foundation
- Bristol-Myers Squibb
- Research Council, Sweden
- Vastra Gotalandsregionen, Sweden
- Swedish Brain Power Project
- Swedish Council for Working Life and Social Research
- Swedish Alzheimer Foundation
- Stiftelsen for Gamla Tjanarinnor
- King Gustaf V and Queen Victoria's Foundation
- Swedish State Support for Clinical Research
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Objectives: Core CSF changes in Alzheimer disease (AD) are decreased amyloid beta(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively. These biomarkers identify AD already at the predementia stage, but their diagnostic performance might be affected by age-dependent increase of AD-type brain pathology in cognitively unaffected elderly. Methods: We investigated effects of age on the diagnostic performance of CSF biomarkers in a uniquely large multicenter study population, including a cross-sectional cohort of 529 patients with AD dementia (median age 71, range 43-89 years) and 304 controls (67, 44-91 years), and a longitudinal cohort of 750 subjects without dementia with mild cognitive impairment (69, 43-89 years) followed for at least 2 years, or until dementia diagnosis. Results: The specificities for subjects without AD and the areas under the receiver operating characteristics curves decreased with age. However, the positive predictive value for a combination of biomarkers remained stable, while the negative predictive value decreased only slightly in old subjects, as an effect of the high AD prevalence in older ages. Conclusion: Although the diagnostic accuracies for AD decreased with age, the predictive values for a combination of biomarkers remained essentially stable. The findings highlight biomarker variability across ages, but support the use of CSF biomarkers for AD even in older populations. Neurology (R) 2012;78:468-476
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