Cerebrospinal fluid S100B is elevated in the earlier stages of Alzheimer's disease

Elaine R. Peskind, W. Sue T. Griffin, Keith T. Akama, Murray A. Raskind, Linda J. Van Eldik

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170 Scopus citations


Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. The hypothesis that the overexpression of S100B in Alzheimer brain is related to the progression of clinical symptoms was addressed in living persons by measuring S100B concentrations in cerebrospinal fluid (CSF) from AD patients with a broad range of clinical dementia severity and from healthy older persons. The effect of normal aging on CSF S100B concentrations also was estimated. CSF S100B did not differ between all 68 AD subjects (0.98±0.09 ng/ml (mean±S.E.M.)) and 25 healthy older subjects (0.81±0.13 ng/ml). When AD subjects were divided into mild/moderate stage and advanced stage clinical dementia severity by the established Clinical Dementia Rating Scale (CDR) criteria, S100B was significantly higher in the 46 mild/moderate stage AD subjects (1.17±0.11 ng/ml) than in either the 22 advanced stage AD subjects (0.60±0.12 ng/ml) or the healthy older subjects. Consistent with higher CSF S100B in mild to moderate AD, there was a significant correlation among all AD subjects between CSF S100B and cognitive status as measured by the Mini Mental State Exam (MMSE) score. CSF S100B did not differ between healthy older subjects and healthy young subjects. These results suggest increased CNS expression of S100B in the earlier stages of AD, and are consistent with a role for S100B in the initiation and/or facilitation of neuritic plaque formation in AD brain.

Original languageEnglish
Pages (from-to)409-413
Number of pages5
JournalNeurochemistry International
Issue number5-6
StatePublished - 2001

Bibliographical note

Funding Information:
These studies were supported in part by NIH grants AG13939 and AG15501 (LVE), AG12411 (WSTG), AG05136 and AG08419 (ERP and MAR), NIH training grant GM08061 (KA), the Department of Veterans Affairs and the Donald W. Reynolds Foundation (WSTG). The authors wish to acknowledge Sharon Murray, R.N., Molly Wamble, and Sally Swedine for their excellent technical assistance, Robert E. Mrak, MD, PhD, for helpful suggestions on the manuscript, and Susan Martin and Rebekah Rein for manuscript preparation.


  • Alzheimer's disease
  • Cerebrospinal fluid S100B
  • Earlier stages
  • Elevated

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology


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