Decreased sensitivity to dexamethasone in lymphocytes from patients with Alzheimer's disease

Clin Immunol Immunopathol. 1994 Oct;73(1):45-52. doi: 10.1006/clin.1994.1168.

Abstract

Cortisol levels in patients with Alzheimer's disease (AD) are relatively unaffected by a challenge with dexamethasone (DEX) in vivo. The present study demonstrates that DEX is less inhibitory for phytohemagglutinin (PHA)-induced T cell proliferation in AD patients as compared to age-matched controls. Since no significant differences were found between AD patients and age-matched controls with regard to the fraction of CD45RA+ or CD45RO+ CD4+ T cells nor the ability of peripheral blood mononuclear cells to produce IL-2 or IL-4, it is unlikely that the difference in DEX sensitivity is due to a changed lymphokine profile or a changed composition of the CD4+ T cell population. Sensitivity to DEX was negatively correlated with the ability to produce IL-2 and IL-4 in the controls but not in AD patients. This suggests that IL-2 and IL-4 synthesis in AD patients is less sensitive to regulation by glucocorticoids.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alzheimer Disease / blood*
  • Alzheimer Disease / genetics
  • Dexamethasone / pharmacology*
  • Female
  • Humans
  • Lymphocyte Activation / drug effects
  • Lymphocytes / drug effects*
  • Male
  • Phenotype
  • Sensitivity and Specificity
  • T-Lymphocytes / immunology

Substances

  • Dexamethasone