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The Journal of Neuroscience, March 26, 2008, 28(13):3474-3478; doi:10.1523/JNEUROSCI.4893-07.2008

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Behavioral/Systems/Cognitive
Glucocorticoid Therapy-Induced Memory Deficits: Acute versus Chronic Effects

Daniel Coluccia,¹ Oliver T. Wolf,² Spyros Kollias,³ Benno Roozendaal,⁵ Adrian Forster,^4,6 and Dominique J.-F. de Quervain¹

¹Department of Psychiatry Research, University of Zürich, 8032 Zürich, Switzerland, ²Faculty of Psychology, Ruhr-University, 44780 Bochum, Germany, ³Institute of Neuroradiology and ⁴Department of Rheumatology and Institute for Physical Medicine, University Hospital of Zürich, 8091 Zürich, Switzerland, ⁵Center for the Neurobiology of Learning and Memory and Department of Neurobiology and Behavior, University of California, Irvine, California 92697-3800, and ⁶Rehabilitation Clinic St. Katharinental, 8253 Diessenhofen, Switzerland

Correspondence should be addressed to Dominique J.-F. de Quervain, Division of Psychiatry Research, University of Zürich, Lenggstrasse 31, 8032 Zürich, Switzerland. Email: quervain{at}bli.unizh.ch

Conditions with chronically elevated glucocorticoid levels are usually associated with declarative memory deficits. Considerable evidence suggests that long-term glucocorticoid exposure may cause cognitive impairment via cumulative and long-lasting influences on hippocampal function and morphology. However, because elevated glucocorticoid levels at the time of retention testing are also known to have direct impairing effects on memory retrieval, it is possible that such acute hormonal influences on retrieval processes contribute to the memory deficits found with chronic glucocorticoid exposure. To investigate this issue, we examined memory functions and hippocampal volume in 24 patients with rheumatoid arthritis who were treated either chronically (5.3 ± 1.0 years, mean ± SE) with low to moderate doses of prednisone (7.5 ± 0.8 mg, mean ± SE) or without glucocorticoids. In both groups, delayed recall of words learned 24 h earlier was assessed under conditions of either elevated or basal glucocorticoid levels in a double-blind, placebo-controlled crossover design. Although the findings in this patient population did not provide evidence for harmful effects of a history of chronic prednisone treatment on memory performance or hippocampal volume per se, acute prednisone administration 1 h before retention testing to either the steroid or nonsteroid group impaired word recall. Thus, these findings indicate that memory deficits observed under chronically elevated glucocorticoid levels result, at least in part, from acute and reversible glucocorticoid effects on memory retrieval.

Key words: glucocorticoids; prednisone; memory; retrieval; hippocampus; MRI

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Received Oct. 30, 2007; revised Jan. 24, 2008; accepted Feb. 4, 2008.

Correspondence should be addressed to Dominique J.-F. de Quervain, Division of Psychiatry Research, University of Zürich, Lenggstrasse 31, 8032 Zürich, Switzerland. Email: quervain{at}bli.unizh.ch

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