Cited by 214Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsCerebrospinal fluid and hydrocephalus

Cerebrospinal fluid -amyloid 1-42 concentration may predict cognitive decline in older women

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Gustafson, D. R, Skoog, I., Rosengren, L., Zetterberg, H., Blennow, K.·2006·Journal of Neurology, Neurosurgery & Psychiatry

Abstract

BACKGROUND: Low levels of cerebrospinal fluid (CSF) beta-amyloid 1-42 (Abeta42) and high total tau (T-tau) are diagnostic for manifest Alzheimer's disease. It is not known, however, whether these biomarkers may be risk indicators for cognitive decline in otherwise healthy older people. METHODS: The longitudinal relationship between CSF markers, Abeta42 and T-tau, measured in 1992, and change in Mini-Mental State Examination (deltaMMSE) score between 1992 and 2002 were investigated in 55 women (aged 70-84 years, mean (SD) MMSE score = 28.3 (1.5)), who were participants in the Prospective Population Study of Women in Gothenburg, Sweden. These women did not have dementia when they experienced lumbar puncture in 1992-3. RESULTS: Over the 8-year follow-up period, deltaMMSE (range = +3 to -21 points) was correlated with Abeta42 (Spearman's r = 0.40, p = 0.002), such that lower levels of Abeta42 were related to greater decline. This was also observed after excluding 4 women who developed dementia between 1992 and 2002 (Spearman's r = 0.34, p = 0.019). A multivariate logistic regression model predicting a decline of > or = 5 points on the MMSE (observed in six women), or a risk of developing dementia over the 8-year follow-up period (observed in four women), including age, education, Abeta42 and T-tau as covariates, showed that Abeta42 was the sole predictor of significant cognitive decline or dementia (OR per 100 pg/ml Abeta42 = 2.24, 95% CI 1.19 to 4.22, p = 0.013). CONCLUSIONS: Low levels of CSF Abeta42 may predict cognitive decline among older women without dementia.

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Crossref · 10.1136/jnnp.2006.100529

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  • Cognitively unimpaired individuals with abnormal amyloid biomarkers have more rapid progression of atrophy, hypometabolism, and clinical/cognitive decline than individuals without biomarker evidence of Aβ deposition.

    “Numerous studies have shown that CU individuals with abnormal amyloid biomarkers have more rapid progression of atrophy, hypometabolism, and clinical/cognitive decline than individuals without biomarker evidence of Aβ deposition [13,33,80,93–99]”

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Authors
Gustafson, D. R., Skoog, I., Rosengren, L., Zetterberg, H., & Blennow, K.
Affiliations
University of Gothenburg (SE)
Corresponding author
Gustafson, D. R
Venue
Journal of Neurology, Neurosurgery & Psychiatry
Publisher
BMJ
Published
2006-10-20
Volume
78
Issue
5
Pages
461-464
ISSN
0022-3050 (ISSN-L)
OpenAlex
W2075275965
Cited by
214
References
2
Citations by year
2026: 1 · 2025: 3 · 2024: 6 · 2023: 5 · 2022: 12 · 2021: 8 · 2020: 11 · 2019: 9 · 2018: 8 · 2017: 8 · 2016: 7 · 2015: 21 · 2014: 16 · 2013: 16 · 2012: 23
FWCI
6.17
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurology Neurosurgery & Psychiatry (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Institutes of Health (5r03ag026098-02)
  • National Institute on Aging (1R03AG026098-01A1, R03 AG026098)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
Keywords
cerebrospinal fluid, amyloid-beta 42, total tau, cognitive decline, dementia risk, Alzheimer's disease biomarkers, older women, Mini-Mental State Examination, lumbar puncture, dementia prediction
MeSH terms
Aged, Aged, 80 and over, Cognition Disorders, Dementia, Female, Humans, Longitudinal Studies, Mental Status Schedule, Peptide Fragments, Predictive Value of Tests, Risk Factors, Biomarkers, Amyloid beta-Peptides

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