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Neuroimage Clin. 2019 Nov 14;24:102020. doi: 10.1016/j.nicl.2019.102020. [Epub ahead of print]

Interferon-beta-induced changes in neuroimaging phenotypes of appetitive motivation and reactivity to emotional salience.

Author information

1
Institute of Clinical Chemistry and Clinical Pharmacology, University of Bonn, Sigmund-Freud-Str. 25, 53127 Bonn, Germany.
2
Institute of Psychology, University of Innsbruck, Innrain 52, 6020 Innsbruck, Austria; Psychiatry and Psychotherapy Clinic III, University of Ulm, Leimgrubenweg 12, 89075 Ulm, Germany.
3
Department of Research, Federal Institute for Drugs and Medical Devices Kurt-Georg-Kiesinger-Allee 3, 53175 Bonn.
4
Department of Neurology, University of Bonn, Sigmund-Freud-Str. 25, 53127 Bonn, Germany.
5
Institute of Clinical Pharmacology, University Hospital of RWTH Aachen, Wendlingweg 2, 52074 Aachen, Germany. Electronic address: jstingl@ukaachen.de.

Abstract

Treatment with interferon (IFN) has been associated with depressive side effects. Previous neuroimaging studies have provided information about changes in brain activation patterns in patients under treatment with IFN-alpha, but the effect of other IFNs, or the role of the underlying disease, has yet to be clarified. In the present fMRI study, we looked at brain changes after 8 days of IFN-beta treatment in N = =17 healthy volunteers, thus avoiding the possible confound of the effects of underlying pathology in studies of IFN-treated patients with neurological or other medical disorders. We followed a symptom dimensional approach by simultaneously investigating two distinct symptom domains of depressiveness: negative affect (amygdala) and appetitive motivation (ventral striatum). In these early phases of IFN treatment we detected a selective change in neural substrates of appetitive motivation, consistent with the predominant symptomatic change recorded in psychopathology ratings. In contrast, the fMRI phenotype of negative affect, which is known to characterize disorders of affect involving anxiety and depressiveness as well as individual vulnerability to depression, was unchanged after treatment. These findings suggest that IFN may induce an affective syndrome through a mechanism involving down-regulation of appetitive motivation.

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