Abstract
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. 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. 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). Low levels of CSF Abeta42 may predict cognitive decline among older women without dementia.
MeSH Terms
Aged
Aged, 80 and over
Amyloid beta-Peptides/cerebrospinal fluid
Biomarkers/cerebrospinal fluid
Cognition Disorders/cerebrospinal fluid
Dementia/cerebrospinal fluid
Female
Humans
Longitudinal Studies
Mental Status Schedule
Peptide Fragments/cerebrospinal fluid
Predictive Value of Tests
Risk Factors
Chemicals
Amyloid beta-Peptides
Biomarkers
Peptide Fragments
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Gustafson Deborah R
The Institute of Neuroscience and Physiology, Section for Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. deb.gustafson@neuro.gu.se
Skoog Ingmar
Rosengren Lars
Zetterberg Henrik
Blennow Kaj
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