Endocrine Abstracts

Background: Chronically elevated brain glucocorticoid (GC) levels impair cognition. In rodents, raised GC levels prior to lipopolyaccharide (LPS) administration potentiate neuroinflammation although GC suppresses neuroinflammation if administered after LPS. 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1) activity can increase intracellular GC levels, including in the brain, without alteration in circulating levels. 11β-HSD1 deficiency/inhibition protects against a...

Chronically elevated glucocorticoid (GC) levels alter cognition and increase cardio-metabolic disease risk. Negative feedback suppression of the hypothalamic–pituitary–adrenal (HPA) axis, including at the hippocampus, maintains low/basal circulating GC levels. Intracellular GC can be increased, without alteration in circulating levels, by the activity of 11β-hydroxysteroid dehydrogenase type1 (11β-HSD1). In some tissues, 11β-HSD1 expression is increase...

Chronically elevated glucocorticoid (GC) level impairs cognition. In rodents, elevated plasma GC levels, prior to an inflammatory challenge, potentiates neuroinflammation that is abolished by GR but not MR antagonism. 11β-hydroxysteroid dehydrogenase type-1 (11β-HSD1) increases intracellular GC levels by regenerating active GCs from inert forms. Inhibition/deficiency of 11β-HSD1 is protective against age-related cognitive decline presumably by lifelong reduced b...