1. The effects of synthetic glucocorticoid treatment for inflammatory disease on brain structure, function, and dementia outcomes: A systematic review.
- Author
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Shorey CL, Mulla RT, and Mielke JG
- Subjects
- Humans, Glucocorticoids, Brain, Atrophy drug therapy, Atrophy pathology, Alzheimer Disease, Cognitive Dysfunction chemically induced, Cognitive Dysfunction drug therapy, Cognitive Dysfunction complications
- Abstract
Many regions of the brain have a high density of glucocorticoid receptors, and the prolonged elevation of endogenous glucocorticoids may cause neurotoxicity and increase risk for cognitive decline and dementia. However, despite synthetic glucocorticoids being the first line of treatment for many inflammatory diseases, few studies have addressed whether therapeutic glucocorticoids may have similar undesirable effects on the brain. Thus, our systematic review investigated the impact of long-term glucocorticoid usage on adult brain structure, cognitive function, and dementia risk. We identified 13 studies that met our eligibility criteria and found conflicting results dependent on the outcome studied. In particular, all but one study on hippocampal and amygdalar volumes found significant atrophy of both structures occurred in those who took glucocorticoids. Additionally, executive function, particularly working memory, and global cognitive function were significantly poorer in those taking long-term glucocorticoids. Notably, declines in episodic memory were not associated with long-term usage. Furthermore, most studies of dementia (all-cause) and Alzheimer's disease, excluding vascular dementia, showed null to negative associations with glucocorticoids, suggesting a potential protective effect. Therefore, glucocorticoid therapy in those with inflammatory disease may impair certain brain structures and specific cognitive functions, but could lead to a significantly reduced risk of dementia., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)
- Published
- 2023
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