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Long‐term effects of glucocorticoid excess on the brain

The metabolic and cardiovascular clinical manifestations in patients with Cushing's syndrome (CS) are generally well known. However, recent studies have broadened the perspective of the effects of hypercortisolism, showing that both endogenous and exogenous glucocorticoid excess alter brain fun...

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Published in:Journal of neuroendocrinology 2022-08, Vol.34 (8), p.e13142-n/a
Main Authors: Dekkers, Alies J., Miguel Amaya, Jorge, Meulen, Merel, Biermasz, Nienke R., Meijer, Onno C., Pereira, Alberto M.
Format: Article
Language:English
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Summary:The metabolic and cardiovascular clinical manifestations in patients with Cushing's syndrome (CS) are generally well known. However, recent studies have broadened the perspective of the effects of hypercortisolism, showing that both endogenous and exogenous glucocorticoid excess alter brain functioning on several time scales. Consequently, cognitive deficits and neuropsychological symptoms are highly prevalent during both active CS and CS in remission, as well as during glucocorticoid treatment. In this review, we discuss the effects of endogenous hypercortisolism and exogenously induced glucocorticoid excess on the brain, as well as the prevalence of cognitive and neuropsychological deficits and their course after biochemical remission. Furthermore, we propose possible mechanisms that may underly neuronal changes, based on experimental models and in vitro studies. Finally, we offer recommendations for future studies. Preventing neuropsychiatric adverse effects of dexamethasone with co‐administration of cortisol. Dexamethasone suppresses the HPA‐axis and thereby the adrenocortical cortisol production, leaving cortisol‐preferring MRs unoccupied. Re‐activating the MR using cortisol might reduce or prevent neuropsychiatric adverse effects of dexamethasone treatment via activation of brain MR. ACTH, adrenocorticotropic hormone; CRH, corticotrophin‐releasing hormone; GR, glucocorticoid receptor; HPA, hypothalamus‐pituitary‐adrenal; MR, mineralocorticoid receptor
ISSN:0953-8194
1365-2826
1365-2826
DOI:10.1111/jne.13142