Prognostic neuroimaging biomarkers of trauma-related psychopathology: resting-state fMRI shortly after trauma predicts future PTSD and depression symptoms in the AURORA study

Harnett, Nathaniel G.; Rooij, Sanne J.H. van; Ely, Timothy D.; Lebois, Lauren A. M.; Murty, Vishnu P.; Jovanović, Tanja; Hill, Sarah B.; Dumornay, Nathalie M.; Merker, Julia; Bruce, Steve; House, Stacey L.; Beaudoin, Francesca L.; An, Xiuli; Zeng, Donglin; Neylan, Thomas C.; Clifford, Gari D.; Linnstaedt, Sarah D.; Germine, Laura; Bollen, Kenneth A.; Rauch, Scott L.; Lewandowski, Christopher; Hendry, Phyllis L.; Sheikh, Sophia; Storrow, Alan B.; Musey, Paul I.; Haran, John P.; Jones, Christopher W.; Punches, Brittany E.; Swor, Robert A.; McGrath, Meghan E.; Pascual, José L.; Seamon, Mark J.; Mohiuddin, Kamran; Chang, Anna Marie; Pearson, Claire; Peak, David A.; Domeier, Robert M.; Rathlev, Niels K.; Sánchez, León D.; Pietrzak, Robert H.; Joormann, Jutta; Deanna, M; Pizzagalli, Diego A.; Sheridan, John F.; Harte, Steven E.; Elliott, James M.; Kessler, Ronald C.; Koenen, Karestan C.; McLean, Samuel A.; Ressler, Kerry J.; Stevens, Jennifer

doi:10.1038/s41386-020-00946-8

Cited by 42 publications

(44 citation statements)

References 82 publications

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“…Individuals during the COVID-19 epidemic have higher negative emotions ( Li et al, 2020a ; Wang et al, 2021a ), which can have an impact on a variety of cognitive domains, including working memory ( Cesare et al, 2018 ). We suggest that disruptions across these functional networks reflect a general posttraumatic psychopathology ( Harnett et al, 2021 ) which in vicarious traumatization is associated with cognitive, emotional and self-social deficits.…”

Section: Discussionmentioning

confidence: 92%

“…Neurofunctionally, a significant component of the variance in general distress could be explained by the functional connectome. Although few studies have investigated the relationship between functional connectome and general distress, there is abundant evidence for a role of functional connectivity in depression, anxiety and stress ( Harnett et al, 2021 ; van Oort et al, 2020 ), which are increasingly understood as network-based disorders ( Bao et al, 2021 ; Mulders et al, 2015 ; Xu et al, 2019 ). For example, functional connectivity within DMN, and between DMN and SN/FPN, are altered in depression ( Mulders et al, 2015 ); anxiety is characterized by hypo-connectivity of multiple brain networks, notably the FPN, DMN, SN and motor network ( Xu et al, 2019 ); stress can be linked to the balance between FPN and SN ( Hermans et al, 2014 ; Hermans et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

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COVID‐19 vicarious traumatization links functional connectome to general distress

et al. 2022

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

COVID‐19 vicarious traumatization links functional connectome to general distress

et al. 2022

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“…Post-trauma DMN-amygdala FC predicts PTSD severity at time of scan, and negatively correlates with resilience months later [ 62 ]. Early post-trauma connectivity between DMN nodes and rACC, periaqueductal grey, inferior frontal gyrus, and thalamus also are all negatively associated with subsequent resilience [ 62 , 65 , 80 , 81 ]. Further, reduced centrality of the PCC/precuneus in sexual assault victims peri-trauma is reported in those who did not develop PTSD, compared to non-trauma exposed controls [ 82 ].…”

Section: Peri-trauma To Long-term Predictors Of Resiliencementioning

confidence: 99%

“…These patterns suggest that growth of the dlPFC early after a traumatic event may be a positive adaptation. The dlPFC may engage in the regulation of emotional arousal responses during the early recovery period, as its connectivity with a threat network overlapping the bilateral amygdala and brainstem 2 weeks post-trauma predicts subsequent resilience to PTSD and depressive symptoms months later [ 74 , 80 ]. This suggests the DLPFC as an interesting target for early intervention, following current neuromodulation treatments for chronic PTSD and MDD which typically target the dlPFC.…”

Section: Peri-trauma To Long-term Predictors Of Resiliencementioning

confidence: 99%

Neural contributors to trauma resilience: a review of longitudinal neuroimaging studies

et al. 2021

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Resilience in the face of major life stressors is changeable over time and with experience. Accordingly, differing sets of neurobiological factors may contribute to an adaptive stress response before, during, and after the stressor. Longitudinal studies are therefore particularly effective in answering questions about the determinants of resilience. Here we provide an overview of the rapidly-growing body of longitudinal neuroimaging research on stress resilience. Despite lingering gaps and limitations, these studies are beginning to reveal individual differences in neural circuit structure and function that appear protective against the emergence of future psychopathology following a major life stressor. Here we outline a neural circuit model of resilience to trauma. Specifically, pre-trauma biomarkers of resilience show that an ability to modulate activity within threat and salience networks predicts fewer stress-related symptoms. In contrast, early post-trauma biomarkers of subsequent resilience or recovery show a more complex pattern, spanning a number of major circuits including attention and cognitive control networks as well as primary sensory cortices. This novel synthesis suggests stress resilience may be scaffolded by stable individual differences in the processing of threat cues, and further buttressed by post-trauma adaptations to the stressor that encompass multiple mechanisms and circuits. More attention and resources supporting this work will inform the targets and timing of mechanistic resilience-boosting interventions.

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“…Particularly, GRs are expressed in many different brain regions and cell types 2,3 . Glucocorticoid effects in hippocampus, amygdala and prefrontal cortex 4,5 are subject to extensive research in relation to cognitive and emotional functioning 6 . In the hypothalamus, glucocorticoids are pivotal for the negative feedback regulation of the hypothalamus pituitary adrenal axis.…”

Section: Introductionmentioning

confidence: 99%

Gene expression changes in the brain of a Cushing's syndrome mouse model

Amaya

Viho

Sips

et al. 2022

J Neuroendocrinology

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Excess glucocorticoid exposure affects emotional and cognitive brain functions. The extreme form, Cushing's syndrome, is adequately modelled in the AdKO 2.0 mouse, consequential to adrenocortical hypertrophy and hypercorticosteronemia. We previously reported that the AdKO 2.0 mouse brain undergoes volumetric changes that resemble closely those of Cushing's syndrome human patients, as well as changes in expression of glial related marker proteins. In the present work, the expression of genes related to glial and neuronal cell populations and functions was assessed in regions of the anterior brain, hippocampus, amygdala and hypothalamus. Glucocorticoid target genes were consistently regulated, including CRH mRNA suppression in the hypothalamus and induction in amygdala and hippocampus, even if glucocorticoid receptor protein was downregulated. Expression of glial genes was also affected in the AdKO 2.0 mouse brain, indicating a different activation status in glial cells. Generic markers for neuronal cell populations, and cellular integrity were only slightly affected. Our findings highlight the vulnerability of glial cell populations to chronic high levels of circulating glucocorticoids.

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Prognostic neuroimaging biomarkers of trauma-related psychopathology: resting-state fMRI shortly after trauma predicts future PTSD and depression symptoms in the AURORA study

Cited by 42 publications

References 82 publications

COVID‐19 vicarious traumatization links functional connectome to general distress

COVID‐19 vicarious traumatization links functional connectome to general distress

Neural contributors to trauma resilience: a review of longitudinal neuroimaging studies

Gene expression changes in the brain of a Cushing's syndrome mouse model

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