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.

50-02-2 (Dexamethasone), Aged, Alzheimer Disease/*blood/genetics, Dexamethasone/*pharmacology, Female, Human, Lymphocyte Activation/drug effects, Lymphocytes/*drug effects, Male, Phenotype, Sensitivity and Specificity, Support, Non-U.S. Gov't, T-Lymphocytes/immunology, dementia
dx.doi.org/10.1006/clin.1994.1168, hdl.handle.net/1765/5813
Clinical Immunology and Immunopathology
Erasmus MC: University Medical Center Rotterdam

Nijhuis, E, Hinloopen, B, van Duijn, C.M, Rozing, J, Nagelkerken, L, & Hofman, A. (1994). Decreased sensitivity to dexamethasone in lymphocytes from patients with Alzheimer's disease. Clinical Immunology and Immunopathology, 73(1), 45–52. doi:10.1006/clin.1994.1168