The neural basis of hot and cold cognition in depressed patients, unaffected relatives, and low-risk healthy controls: An fMRI investigation.

Autor: Cl N; Institute of Cognitive Neuroscience, University College London, London, UK; MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK. Electronic address: Camilla.Nord@mrc-cbu.cam.ac.uk., Dc H; Institute of Cognitive Neuroscience, University College London, London, UK; Department of Psychiatry, University of Oxford, Oxford, UK., N L; Institute of Cognitive Neuroscience, University College London, London, UK; Warwick Medical School, University of Warwick, Coventry, UK; Experimental Therapeutics & Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, 20892, USA., T L; Camden and Islington NHS Foundation Trust, London, UK., S P; Department of Clinical, Educational, and Health Psychology, University College London, London, UK., Jp R; Institute of Cognitive Neuroscience, University College London, London, UK.
Jazyk: angličtina
Zdroj: Journal of affective disorders [J Affect Disord] 2020 Sep 01; Vol. 274, pp. 389-398. Date of Electronic Publication: 2020 May 21.
DOI: 10.1016/j.jad.2020.05.022
Abstrakt: Background: Modern cognitive neuropsychological models of depression posit that negatively biased emotional ("hot") processing confers risk for depression, while preserved executive function ("cold") cognition promotes resilience.
Methods: We compared neural responses during hot and cold cognitive tasks in 99 individuals: those at familial risk for depression (N = 30 unaffected first-degree relatives of depressed individuals) and those currently experiencing a major depressive episode (N = 39 unmedicated depressed patients) with low-risk healthy controls (N = 30). Primary analyses assessed neural activation on two functional magnetic resonance imaging tasks previously associated with depression: dorsolateral prefrontal cortex (DLPFC) responsivity during the n-back working memory task; and amygdala and subgenual anterior cingulate cortex (sgACC) responsivity during incidental emotional face processing.
Results: Depressed patients exhibited significantly attenuated working memory-related DLPFC activation, compared to low-risk controls and unaffected relatives; unaffected relatives did not differ from low-risk controls. We did not observe a complementary pattern during emotion processing. However, we found preliminary support that greater DLPFC activation was associated with lower amygdala response during emotion processing.
Limitations: These findings require confirmation in a longitudinal study to observe each individual's risk of developing depression; without this, we cannot identify the true risk level of the first-degree relative or low-risk control group.
Conclusions: These findings have implications for understanding the neural mechanisms of risk and resilience in depression: they are consistent with the suggestion that preserved executive function might confer resilience to developing depression in first-degree relatives of depressed patients.
Competing Interests: Conflict of interest JPR consults for Cambridge Cognition, Takeda Ltd and GE. The other authors report no conflict of interest.
(Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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