Local and systemic GM-CSF increase in Alzheimer's disease and vascular dementia

Acta Neurol Scand. 2001 Mar;103(3):166-74. doi: 10.1034/j.1600-0404.2001.103003166.x.

Abstract

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. The aim of the present study was to investigate patterns of local and systemic cytokine release in patients with Alzheimer's disease (AD) and vascular dementia (VAD). The intrathecal levels of cytokines were related to neuronal damage and cerebral apoptosis. Twenty patients with early AD and 26 patients with VAD were analyzed with respect to cerebrospinal fluid (CSF) and serum levels of pro- and anti-inflammatory cytokines. In addition, CSF levels of Fas/APO-1 and bcl-2, a measure for apoptosis, and Tau protein, a marker for neuronal degradation, were studied. Significantly increased CSF levels of GM-CSF but not of other cytokines were observed in both dementia groups. These patients displayed a significant correlation between the GM-CSF levels and the levels of Fas/APO-1 and Tau protein in CSF. Our study demonstrates an intrathecal production of GM-CSF, a cytokine stimulating microglial cell growth and exerting inflammatogenic properties. It is suggested that GM-CSF once secreted induces programmed cell death in the brain tissue of patients with dementia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alzheimer Disease / pathology*
  • Apoptosis*
  • Brain / pathology*
  • Dementia, Vascular / pathology*
  • Female
  • Granulocyte-Macrophage Colony-Stimulating Factor / blood*
  • Granulocyte-Macrophage Colony-Stimulating Factor / cerebrospinal fluid*
  • Humans
  • Male
  • Microglia
  • Middle Aged
  • Neurons / pathology

Substances

  • Granulocyte-Macrophage Colony-Stimulating Factor