Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1006/clin.1994.1168

Type

Journal article

Journal

Clinical immunology and immunopathology

Publication Date

10/1994

Volume

73

Pages

45 - 52

Addresses

Section of Immunology, Institute of Aging and Vascular Research TNO, Leiden, The Netherlands.

Keywords

Lymphocytes, T-Lymphocytes, Humans, Alzheimer Disease, Dexamethasone, Sensitivity and Specificity, Lymphocyte Activation, Phenotype, Aged, Female, Male