Abstract
Inhibition of 11β-HSD1, a key enzyme in the stress management, improves cognition by RL-118 drug treatment
Highlights
Inhibition of 11β-HSD1, a key enzyme in the stress management, improves cognition by RL-118 drug treatment
Once the stressful stimulus is perceived, the hypothalamus secretes the corticotropin-releasing hormone (CRH), which acts on the pituitary gland, activating the release of adrenocorticotropic hormone (ACTH) that binds to the adrenal glands, promoting GC secretion and conforming the hypothalamus-hypophysis-adrenal (HPA) axis
GC secretion follows a robust circadian oscillation with a peak around the onset of the active period of the day, i.e., about 1 hour before arising [1]. This basal level of GC secretion is important in exerting tonic effects upon metabolic, immune and neuronal pathways, involving gluconeogenesis stimulation, protein degradation and lipolysis increase, priming of neural regions involved in sensory processing, attention and adaptive responding, as well as accounting for immunosuppressive and anti-inflammatory actions [2]
Summary
Inhibition of 11β-HSD1, a key enzyme in the stress management, improves cognition by RL-118 drug treatment. It has been described that chronic stress in midlife exerts persisting effects leading to cognitive and affective dysfunctions in old age via mechanisms that depend, at least in part, on brain GCs generated locally by 11β-HSD1 [4].
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