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Differences in dexamethasone-sensitivity between lymphocytes from patients with Alzheimer's disease and patients with

E W Nijhuis1, F Oostervink, B Hinloopen

  • 1Division of Immunological and Infectious Diseases, TNO Prevention and Health, Leiden, 2301 CE, The Netherlands.

Brain, Behavior, and Immunity
|June 1, 1996
PubMed

Insights

Peripheral blood mononuclear cells (PBMC) from Alzheimer's patients show reduced sensitivity to dexamethasone (DEX). This difference, linked to higher bcl-2 expression, suggests PBMC can offer insights into Alzheimer's disease pathogenesis.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Cognitive impairment, including Alzheimer's disease (AD) and multi-infarct dementia (MID), affects millions globally.
  • Understanding the underlying biological mechanisms of different dementia types is crucial for diagnosis and treatment.
  • Peripheral blood mononuclear cells (PBMC) offer a potentially accessible model for studying systemic changes related to neurological disorders.

Purpose of the Study:

  • To investigate the in vitro sensitivity of peripheral blood mononuclear cells (PBMC) to dexamethasone (DEX) across different types of cognitive impairment.
  • To explore potential cellular and molecular factors, such as bcl-2 expression, that may underlie differential DEX sensitivity in patients with senile dementia of the Alzheimer type (SDAT) and multi-infarct dementia (MID).
  • To assess the utility of PBMC as a biomarker for understanding the pathogenesis of Alzheimer's disease.

Main Methods:

  • Peripheral blood mononuclear cells (PBMC) were isolated from 40 patients with cognitive impairment.
  • PBMC were studied in vitro for their proliferation response to phytohemagglutinin and sensitivity to dexamethasone (DEX).
  • Flow cytometry was used to analyze CD4(+) T cell populations, glucocorticoid receptor expression, and bcl-2 expression.

Main Results:

  • PBMC from patients with senile dementia of the Alzheimer type (SDAT) exhibited significantly lower sensitivity to DEX inhibition compared to those from multi-infarct dementia (MID) patients.
  • PBMC from patients with mixed dementia (MIXED) showed intermediate DEX sensitivity.
  • Higher expression of bcl-2 was observed in PBMC from SDAT patients, correlating inversely with DEX sensitivity. No significant differences were found in CD4(+) T cell composition or IL-2/IL-4 production.
  • Glucocorticoid receptor expression levels did not explain the observed differences in DEX sensitivity.

Conclusions:

  • Differential dexamethasone (DEX) sensitivity of peripheral blood mononuclear cells (PBMC) may distinguish between Alzheimer's disease (AD) and other forms of dementia.
  • Elevated bcl-2 expression in PBMC from AD patients is associated with reduced DEX sensitivity, suggesting a role in disease pathogenesis.
  • PBMC characteristics, particularly bcl-2 expression, may serve as accessible biomarkers reflecting central nervous system changes in Alzheimer's disease, aiding in research and potentially clinical applications.

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