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Vol. 15, No. 3, 2003
Issue release date: February 2003
Section title: Original Research Article
Dement Geriatr Cogn Disord 2003;15:169–176
(DOI:10.1159/000068478)

Cerebrospinal Fluid Beta-Amyloid 42 Is Reduced before the Onset of Sporadic Dementia: A Population-Based Study in 85-Year-Olds

Skoog I. · Davidsson P. · Aevarsson Ó. · Vanderstichele H. · Vanmechelen E. · Blennow K.
aInstitute of Clinical Neuroscience, Unit of Neuropsychiatric Epidemiology, University of Göteborg, Sahlgrenska University Hospital, Göteborg, bInstitute of Clinical Neuroscience, Department of Experimental Neuroscience, Unit of Neurochemistry, University of Göteborg, Sahlgrenska University Hospital, Mölndal, and cThe Medical Research Council, Sweden; dInnogenetics, Ghent, Belgium

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Article / Publication Details

First-Page Preview
Abstract of Original Research Article

Received: 9/3/2002
Published online: 2/19/2003

Number of Print Pages: 8
Number of Figures: 1
Number of Tables: 3

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM

Abstract

Deposition of β-amyloid (Aβ) is an early pathogenic event in Alzheimer’s disease (AD). We measured Aβ42 and Aβ40 in cerebrospinal fluid (CSF) in a population-based sample of 85-year-olds, 27 demented and 35 non-demented. During the following 3 years, 7 of the 35 non-demented individuals had developed dementia, while 28 remained non-demented. Reduced CSF levels of both Aβ42 (p = 0.001) and Aβ40 (p = 0.0001) were found in patients with manifest AD and vascular dementia at the age of 85. Non-demented individuals who developed dementia during follow-up had lower levels of CSF- Aβ42 (p = 0.003), but not CSF-Aβ40 (p = 0.96), than those who remained non-demented. The odds ratio for development of dementia was 8.2 (p = 0.027) for individuals in the lower 50th percentile of CSF-Aβ42, while none of those in the highest 33rd percentile of CSF-Aβ42 developed dementia during follow-up. There were no significant differences between carriers and non-carriers of the apolipoprotein E ε4 allele regarding CSF-Aβ42or CSF-Aβ40.Our study suggests that low CSF-Aβ42 is found also in an unselected population-based sample of old demented patients and provides the first evidence of a disturbance in the metabolism of Aβ, specifically involving Aβ42, before the onset of clinical symptoms in AD.


  

Author Contacts

Kaj Blennow, MD, PhD
Department of Experimental Neuroscience, Unit of Neurochemistry
University of Göteborg, Sahlgrenska University Hospital
SE–413 45 Göteborg (Sweden)
Tel. +46 31 343 17 91, Fax +46 31 343 24 26, E-Mail kaj.blennow@neuro.gu.se

  

Article Information

Accepted: September 3, 2002
Number of Figures : 1, Number of Tables : 3, Number of References : 50

  

Publication Details

Dementia and Geriatric Cognitive Disorders

Vol. 15, No. 3, Year 2003 (Cover Date: Released February 2003)

Journal Editor: V. Chan-Palay, New York, N.Y.
ISSN: 1420–8008 (print), 1421–9824 (Online)

For additional information: http://www.karger.com/journals/dem


Article / Publication Details

First-Page Preview
Abstract of Original Research Article

Received: 9/3/2002
Published online: 2/19/2003

Number of Print Pages: 8
Number of Figures: 1
Number of Tables: 3

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM


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