Decreased sensitivity to dexamethasone in lymphocytes from patients with Alzheimer's disease.
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.
Nijhuis
E
E
Section of Immunology, Institute of Aging and Vascular Research TNO, Leiden, The Netherlands.
Hinloopen
B
B
van Duijn
C
C
Hofman
A
A
Rozing
J
J
Nagelkerken
L
L
D000368:Aged; D000544:Alzheimer Disease / Q000097:blood* / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects*; D008297:Male; D010641:Phenotype; D012680:Sensitivity and Specificity; D013601:T-Lymphocytes / Q000276:immunology
D003907:Dexamethasone